Science Brain and Behavior contiuned 21

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HOW DO DRUGS AND HORMONES INFLUENCE THE BRAIN AND BEHAVIOR? ! 241
what were these receptors doing in the brain? Opiates, such as morphine, after all,
are not naturally occurring brain chemicals. This question was answered by Scottish
pharmacologists John Hughes and Hans Kosterlitz (1977), who identified two short
peptides that had opioid properties and appeared to be neurotransmitters (see Figure
5-12). They called these opiate-like transmitters endorphins, an abridgement of the
phrase endogenous morphine-like substances.
We now know that there are endorphin-containing neurons in many brain regions
and that morphine is similar enough to endorphins to mimic their action in the brain.
Researchers have extensively studied whether endorphins can be used as drugs to relieve
pain. The answer is so far mixed.
Although synthetic endorphins do alleviate pain, they also cause other effects, including
nausea, and they are difficult to deliver to the brain. Consequently, morphine
remains a preferred pain treatment. Morphine acts on three opioid-receptor classes:
mu, delta, and kappa receptors. Findings from studies
on mice in which the genes that produce these receptors
have been knocked out show that the mu receptor
is critical both for morphine’s effects on pain and
for its addictive properties. Thus, the objectives of
pain research in producing an analgesic that does not
produce addiction may be difficult to realize.
Stimulants
This diverse group of drugs increases the activity of neurons in a number of ways.
Stimulants are subdivided into three groups: behavioral stimulants, general stimulants,
and psychedelics.
BEHAVIORAL STIMULANTS
Behavioral stimulants are drugs that increase motor behavior as well as elevate a person’s
mood and level of alertness. Two examples are cocaine and amphetamine. Cocaine
is a powder extracted from the Peruvian coca shrub, shown in Figure 7-13. The
indigenous people of Peru have chewed coca leaves through the generations to increase
their stamina in the harsh environment of the high elevations at which they live.
Refined cocaine can either be sniffed (snorted) or injected. Cocaine users who do
not like to inject cocaine intravenously or cannot afford it in powdered form, sniff or
smoke “rocks,” a potent, highly concentrated form also called “crack.” Crack is chemically
altered so that it vaporizes at low temperatures, and the vapors are inhaled.
Cocaine was originally popularized as an antidepressant by Viennese
psychoanalyst Sigmund Freud. In an 1884 paper titled “In Praise of Coca,”
Freud (1974) concluded: “The main use of coca will undoubtedly remain
that which the Indians have made of it for centuries: it is of value in all
cases where the primary aim is to increase the physical capacity of the
body for a given short period of time and to hold strength in reserve to
meet further demands—especially when outward circumstances exclude
the possibility of obtaining the rest and nourishment normally necessary
for great exertion.”
Cocaine was once widely used in the manufacture of soft drinks and wine mixtures,
which were promoted as invigorating tonics. It is the origin of the trade name Coca-
Cola, because this soft drink once contained cocaine, as suggested by the advertisement
in Figure 7-14. The addictive properties of cocaine soon became apparent, however.
Sigmund Freud
(1856–1939)
Figure 7-13
Behavioral Stimulant Cocaine (left) is
obtained from the leaves of the coca
plant (center). Crack cocaine (right) is
chemically altered to form “rocks” that
vaporize when heated.
Figure 7-14
Warning Label Cocaine was once an
ingredient in a number of invigorating
beverages, including Coca-Cola.
Gregory G. Dimijian/Photo Researchers
Timothy Ross/The Image Works
Tek Image/Science Photo Library/
Photo Researchers
Granger Collection
Endorphin. Peptide hormone that acts as
a neurotransmitter and may be associated
with feelings of pain or pleasure;
mimicked by opioid drugs such as
morphine, heroin, opium, and codeine.
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Freud had recommended cocaine to a close friend who, in an attempt to relieve excruciating
pain after the amputation of his thumb, had become addicted to morphine.
The euphoric effects of cocaine helped the friend withdraw from the morphine, but
soon he required larger and larger doses of cocaine. Eventually, he experienced euphoric
episodes followed by a sudden crash after each injection. He continued to use
larger and larger doses and eventually developed schizophrenia. Similar experiences by
others led to an escalating negative view of cocaine use.
Freud also recommended that cocaine could be used as a local anesthetic. Cocaine
did prove valuable as a local anesthetic, and many derivatives, such as Novocaine, are
used for this purpose today.
Amphetamine is a synthetic compound that was discovered in attempts to
synthesize the neurotransmitter epinephrine. Both amphetamine and cocaine are
dopamine agonists that act first by blocking the dopamine reuptake transporter. Interferring
with the reuptake mechanism leaves more DA available in the synaptic
cleft. Amphetamine also stimulates the release of DA from presynaptic membranes.
Both mechanisms increase the amount of DA available in synapses to stimulate DA
receptors.
Amphetamine was first used as a treatment for asthma. A form of amphetamine,
Benzedrine, was sold in inhalers as a nonprescription drug through the 1940s. Soon
people discovered that they could open the container and ingest its contents to obtain
an energizing effect. In 1937, an article in the Journal of the American Medical Association
reported that Benzedrine tablets improved performance on mental-efficiency
tests. This information was quickly disseminated among students, who began to use
the drug as an aid to study for examinations.
Amphetamine was widely used in World War II to help keep troops and pilots
alert (and is still used by the U.S. Air Force for this purpose today) and to improve the
productivity of wartime workers. It is also used as a weight-loss aid. Many over-thecounter
compounds marked as stimulants or weight-loss aids have amphetamine-like
pharmacological actions.
In the 1960s, drug users discovered that they could obtain an immediate pleasurable
“rush,” often described as a whole-body orgasm, by the intravenous injection
of amphetamine. People who took amphetamine in this way and were called “speed
freaks” would inject the drug every few hours for days, remaining in a wide-awake,
excited state without eating. They would then crash in exhaustion and hunger and,
after a few days of recovery, would begin the cycle again. One explanation for repeated
injections was to prevent the depressive crash that occurred when the drug
wore off.
Today, an amphetamine derivative, methamphetamine (also known as meth,
speed, crank, smoke, or crystal ice) is in widespread use. About 2 percent of the U.S.
population have used it. The widespread use of methamphetamine is related to its ease
of manufacture in illicit laboratories and to its potency, thus making it a relatively
inexpensive, yet potentially devastating, drug (Anglin, Burke, Perrochet, Stamper, &
Dawud-Noursi, 2000).
GENERAL STIMULANTS
General stimulants are drugs that cause a general increase in the metabolic activity of
cells. Caffeine, a widely used stimulant, inhibits an enzyme that ordinarily breaks down
the second messenger cyclic adenosine monophosphate (cAMP), discussed in relation
to learning at the synapse in Chapter 5. The resulting increase in cAMP leads to an increase
in glucose production within cells, thus making more energy available and allowing
higher rates of cellular activity.
242 ! CHAPTER 7
Amphetamine. Drug that releases the
neurotransmitter dopamine into its
synapse and, like cocaine, blocks
dopamine reuptake.
Psychedelic drug. Drug that can alter
sensation and perception; lysergic acid
dielthylmide, mescalin, and psilocybin
are examples.
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HOW DO DRUGS AND HORMONES INFLUENCE THE BRAIN AND BEHAVIOR? ! 243
PSYCHEDELICS
Psychedelic drugs alter sensory perception and cognitive processes. There are four
major types of psychedelics:
1. Acetylcholine psychedelics either block or facilitate transmission at acetylcholine
synapses in the brain.
2. Norepinephrine psychedelics include mescaline, obtained from the peyote cactus,
which is legal in the United States for use by Native Americans for religious practices.
3. Tetrahydrocannabinol (THC), the active ingredient in marijuana, is obtained from
the hemp plant Cannabis sativa. There is growing evidence that cannabis acts on
endogenous THC receptors called the CB1 and CB2 receptors thought by scientists
to be the receptors for an endogenous neurotransmitter called anandamide. Surprisingly,
results from a number of lines of research suggest that anandamide plays
a role in enhancing forgetting. The idea is that anandamide prevents memory systems
of the brain from being overwhelmed by the information to which the brain
is exposed each day. Thus, THC use may have a detrimental effect on memory.
4. Serotonin psychedelics likely achieve part of their psychedelic action by affecting
serotonin neurons. Lysergic acid diethylamide (LSD) and psilocybin (obtained
from a certain mushroom) stimulate postsynaptic receptors of some serotonin
synapses and block the activity of other serotonin neurons through serotonin autoreceptors.
Psychedelics may stimulate other transmitter systems, including norepinephrine
receptors.
DRUGS, EXPERIENCE, CONTEXT, AND GENES
Many behaviors trigger very predictable results. When you strike the same piano key
repeatedly, you hear the same note each time.When you flick a light switch over and
over again, the same bulb goes on exactly as before. This cause-and-effect consistency
of many things in our world does not extend to psychoactive drugs.
In Review .
Classifying psychoactive drugs by their principal behavioral effects yields seven major categories:
sedative hypnotics and antianxiety agents, antipsychotic agents, antidepressants,
mood stabilizers, narcotic analgesics, psychomotor stimulants, and stimulants that have
psychedelic and hallucinogenic effects. Researchers are still learning how these drugs act
on the nervous system. Sedative hypnotics and antianxiety agents, including alcohol, barbiturates,
and benzodiazepines, affect receptor sites for the neurotransmitter GABA. Although
the therapeutic actions of antianxiety agents are still not understood, one of those
actions is to block a certain kind of DA receptor. Antidepressants, including the SSRIs and
MAO inhibitors, are thought to act by improving chemical transmission in serotonin, noradrenaline,
histamine, and acetylcholine receptors. The narcotic analgesics derived from
opium produce their effects by binding to special receptors for naturally occurring brain
chemicals called endorphins. Cocaine and amphetamine are psychomotor stimulants that
act as DA agonists, making more DA available in synapses. As scientists continue to study
the actions of psychoactive drugs, they will also learn much more about neuropsychological
disorders and possible treatments.
Peyote cactus
Marijuana leaf
Psilocybe
mushroom
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A drug will not produce the same effects every time that it is
taken, for several reasons. For one thing, a drug may be taken in different
contexts with different accompanying behaviors, which cause
the brain to respond to it differently. The actions of a drug on one
person may be quite different from its actions on someone else because
a person’s experience and the influence of genes also determine
drug reactions. Finally, with repeated use by the same person, the effect
of a drug can be dramatically different from the effect obtained
with the first use. The reasons are tolerance and sentization: many
drugs produce an enduring change in the brain that, in time, can be
quite substantial and can alter what subsequent doses do. In the following
sections, we consider a number of ways in which repeated use
of drugs changes the brain and behavior.
Tolerance
Two college freshman roommates, B. C. and A. S., went to a party,
then to a bar, and by 3 AM were in a restaurant ordering pizza. A. S.
decided that he wanted to watch the chef make his pizza, and off he
went to the kitchen. A long and heated argument ensued between
A. S., the chef, and the manager.
The two roommates then got into A. S.’s car and were leaving the
parking lot when a police officer, called by the manager, drove up and
stopped them. A. S. failed a breathalyzer test, which estimates bodyalcohol
content, and was taken into custody; but, surprisingly, B. C.
passed the test, even though he had consumed the same amount of
alcohol as A. S. had. Why this difference in their responses to the
drinking bout?
The reason for the difference could be that B. C. had developed
greater tolerance for alcohol than A. S. had. Isbell and coworkers
(1955) showed how such tolerance comes about. These researchers
gave volunteers in a prison enough alcohol daily in a 13-week period
to keep them in a constant state of intoxication. Yet they found that
the subjects did not stay drunk for 3 months straight.
When the experiment began, all the subjects showed rapidly rising
levels of blood alcohol and behavioral signs of intoxication, as
shown in the Results section of Experiment 7-1. Between the 12th
and 20th days of alcohol consumption, however, blood alcohol and
the signs of intoxication fell to very low levels, even though the subjects
maintained a constant alcohol intake. Interestingly, too, although
blood-alcohol levels and signs of intoxication fluctuated in subsequent days
of the study, one did not always correspond with the other. A relatively high bloodalcohol
level was sometimes associated with a low outward appearance of intoxication.
Why?
These results were likely the products of three different kinds of tolerance:
1. In the development ofmetabolic tolerance, the number of enzymes needed to break
down alcohol in the liver, blood, and brain increases. As a result, any alcohol that
is consumed is metabolized more quickly, and so blood-alcohol levels are reduced.
2. In the development of cellular tolerance, the activities of brain cells adjust to minimize
the effects of alcohol present in the blood. This kind of tolerance can help
244 ! CHAPTER 7
1.0
2.0
Average blood-alcohol
level (mg/ ml)
1
2
3
Average degree
of intoxication
200
400
0
Days
5 10
Days
10
Days
10
15 20
0 5 15 20
0 5 15 20
Alcohol intake
(ml/day)
When the experiment
began, all the subjects
increased their intake
of alcohol.
Subjects were given
alchohol every day for
13 weeks —enough to
keep them intoxicated.
Because of tolerance, much more alcohol was required
by the end of the study to obtain the same level of
intoxication that was produced at the beginning.
Conclusion
Question: Will the consumption of alcohol produce tolerance?
EXPERIMENT 7-1
Procedure
Results
After 15–20 days of
alcohol consumption,
blood-alcohol levels
fell…
…and the signs of
intoxication fell,
too.
Adapted from “An Experimental Study of the
Etiology of ‘Rum Fits’ and Delirium Tremens,” by
H. Isbell, H. F. Fraser, A. Winkler, R. E. Belleville, and
A. J. Eisenman, 1955, Quarterly Journal of Studies
on Alcohol, 16, pp. 1–21.
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explain why the behavioral signs of intoxication may be very low despite a relatively
high blood-alcohol level.
3. Learned tolerance, too, can help explain a drop in the outward signs of intoxication.
As people learn to cope with the daily demands of living while under the influence
of alcohol, they may no longer appear to be drunk.
That learning plays a role in tolerance to alcohol may surprise you, but this role
has been confirmed in many studies. In an early description of the effect,Wenger and
his coworkers (1981) trained rats to walk on a narrow conveyor belt to prevent electric
shock to their feet from a grid over which the belt slid. One group of rats received alcohol
after training in walking the belt, whereas another group received alcohol before
training.A third group received training only, and a fourth group received alcohol only.
After several days of exposure to their respective conditions, all groups were given
alcohol before a walking test. The rats that had received alcohol before training performed
well, whereas those that had received training and alcohol separately performed
just as poorly as those that had never had alcohol before or those that had not
been trained. Apparently, animals can acquire the motor skills needed to balance on a
narrow belt despite alcohol intoxication. Over time, in other words, they can learn to
compensate for being drunk.
The results of these experiments are relevant to our story of A. S. and B. C. A. S.
came from a large city and worked for long hours assisting his father with his plumbing
business. He seldom attended parties and was unaccustomed to the effects of alcohol.
B. C., in contrast, came from a small town, where he was the acclaimed local pool
shark. He was accustomed to “sipping a beer” both while waiting to play and during
play, which he did often. B. C.’s body, then, was prepared to metabolize alcohol, and his
experience in drinking while engaging in a skilled sport had prepared him to display
controlled behavior under the influence of alcohol. Enhanced metabolism and controlled
behavior are manifestations of tolerance to alcohol.
Tolerance can develop not only to alcohol but also to many other drugs, such as
barbiturates, amphetamine, and narcotics. In humans, for instance, a dose of 100 mg
of morphine is sufficient to cause profound sedation and even death in some firsttime
users, but those who have developed tolerance to this drug have been known to
take 4000 mg without adverse effects. Similarly, long-time users of amphetamine may
take doses 100 or more times as great as the doses that they initially took to produce
the same effect. In other words, with repeated administration of a drug, the effect produced
by that drug may progressively diminish owing to metabolic tolerance, cellular
tolerance, and learned tolerance.
Sensitization
Repeated exposure to the same drug does not always result in tolerance. Tolerance
resembles habituation (recall the learning experiments in Chapter 5). The drug
taker may experience the opposite reaction, an increased responsiveness to successive
equal doses, called sensitization. Whereas tolerance
generally develops with repeated use of a drug, sensitization
is much more likely to develop with occasional
use.
To demonstrate drug sensitization, Terry Robinson
and Jill Becker (1986) isolated rats in observation
boxes and recorded their reactions to an injection of
amphetamine, especially reactions such as increases
HOW DO DRUGS AND HORMONES INFLUENCE THE BRAIN AND BEHAVIOR? ! 245
Terry Robinson
Jill Becker
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in sniffing, rearing, and walking, which are typical rat
responses to this drug. Every 3 or 4 days, the investigators
repeated the procedure, shown in the Procedure
1 section of Experiment 7-2. The graph in the
Results 1 section of the experiment shows that the behavior
of the rats was more vigorous each time they
received the drug.
This increased response on successive tests was not
due to the animals becoming comfortable with the
test situation. Control animals that received no drug
did not display a similar escalation in sniffing, rearing,
and walking. Moreover, the sensitization to amphetamine
was enduring. Even when two injections of amphetamine
were separated by months, the animals still
showed an increased response to the drug. It is noteworthy
also that a single exposure to the drug produced
sensitization.
Remember that amphetamine is a DA agonist and
acts both by stimulating the release of DA from the
axon terminals of dopamine neurons and by blocking
its reuptake into those terminals. Which of these two
actions might underlie sensitization to amphetamine?
One possibility is that sensitization is due to the release
of DA. Perhaps with each successive dose of amphetamine,
more DA is released, causing a progressively increasing
behavioral response to the drug.
This explanation was confirmed by another experiment
on rats, some of which had been sensitized
to amphetamine and others of which had never been
given the drug (Casteñeda, Becker,& Robinson, 1988).
The basal ganglia, which are rich in DA synapses, were
removed from the brain of each rat and placed in a
fluid-filled container. Then the tissue was treated with
amphetamine. An analysis of the fluid that bathed the
tissue showed that the basal ganglia from sensitized
rats released more DA than did the basal ganglia of
nonsensitized rats. This increased release of DA can
explain sensitization to amphetamine.
Sensitization also develops to drugs with depressant
effects, such as the major tranquilizer Flupentixol,
which is a DA antagonist that blocks DA receptors.
Procedure 2, on the right in Experiment 7-2, shows the
effect of Flupentixol on the swimming behavior of rats
in another study (Whishaw, Mittleman, & Evenden,
1989). The researchers trained the rats to swim a short
distance to a platform in a swimming pool.When the
rats were able to reach the platform within 1 to 2 seconds,
they were given an injection of Flupentixol that
remained active through a single day’s testing.
On the first few swims after the injection of the
drug, the rats swam normally, but then they began
to slow down. After about 12 swims, they simply sank
246 ! CHAPTER 7
EXPERIMENT 7-2
Number of injections
Number of incidents
of rearing
12
24
1 3 5 9
Number of trials
Time to platform (s)
3
60
1 4 8 12
Question: Does the injection of a drug always produce the same behavior?
Reuptake
transporter
Dopamine blocked
Flupentixol
Receptor
blocked
Release
enhanced
Amphetamine
Agonist
Flupentixol
Antagonist
Sensitization is also dependent on
the occurrence of the behavior. The
number of swims, not the spacing
of swims or the treatment, causes
an increase in the time it takes for
the rat to reach the platform.
Conclusion 2
Sensitization, as indicated by
increased rearing, develops with
periodic repeated injections.
Procedure 1
Results 1
Procedure 2
Results 2
Conclusion 1
In the Robinson and Becker study,
animals were given periodic
injections of the same dose of
amphetamine. Then the researchers
measured the number of times each
rat reared in its cage.
In the Whishaw study, animals
were given different numbers of
swims after being injected with
Flupentixol. Then the researchers
measured their speed to escape to
a platform in a swimming pool.
(Left) Adapted from “Enduring Changes in Brain and Behavior Produced by Chronic
Amphetamine Administration: A Review and Evaluation of Animal Models of Amphetamine
Psychosis,” by T. E. Robinson and J. B. Becker, 1986, Brain Research Reviews, 397, pp. 157–198.
(Right) Adapted from “Training-Dependent Decay in Performance Produced by the Neuroleptic
cis(Z)-Flupentixol on Spatial Navigation by Rats in a Swimming Pool,” by I. Q. Whishaw, G.
Mittelman, and J. L. Evenden, 1989, Pharmacology, Biochemistry, and Behavior, 32, pp. 211–220.
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when placed in the water and had to be removed to prevent them
from drowning. This effect was not just the result of administering
12 successive swimming trials on the same day. If the rats were
both injected with the drug and given only one swim trial each day
for 12 days, the same results were obtained. On the first few days,
the rats swam normally, but thereafter they began to slow down
until, by the 12th day, they sank when placed into the water. Thus,
it was not the drug alone, but the swimming experience under the
influence of the drug that was critical to the drug’s effect on performance.
Sensitization to the drug depended on the number of swims, regardless of the
spacing between swims or the number of drug injections. Presumably, Flupentixol
blocks DA synapses in the brain more effectively after sensitization in a way that accounts
for these results.
Sensitization can be very selective with respect to the behavior affected, and it is
detected only if tests are always given under the same conditions. For example, if rats
are given amphetamine in their home cage on a number of occasions before a sensitization
experiment starts, their behavior in the test situation does not reveal their previous
drug experience. Sensitization develops as if the animals were receiving the drug
for the first time.
Furthermore, sensitization is difficult to achieve in an animal that is tested in its
home cage. Fraioli and coworkers (1999) gave amphetamine to two groups of rats and
recorded the rats’ behavioral responses to successive injections. One group of rats lived
in the test apparatus; so, for that group, home was the test box. The other group of rats
was taken out of its normal home cage and placed in the test box for each day’s experimentation.
The “home” group showed no sensitization to amphetamine, whereas the
“out” group displayed robust sensitization.
At least part of the explanation of the “home–out” effect is that the animals are accustomed
to engaging in a certain repertoire of behaviors in their home environment,
and so it is difficult to get them to change that behavior even in response to a drug. It
is likewise difficult to condition new behavior to their familiar home cues.
When animals are placed in novel environments and receive spaced injections of a
drug, however, their response to the drug may increase, showing sensitization. Presumably,
humans, too, show sensitization to a drug when they periodically take it in
novel contexts where new cues can be readily associated with the novel cognitive and
physiological effects of the drug.
Addiction and Dependence
B. G. started smoking when she was 13 years old.Now a university lecturer, she has one
child and is aware that smoking is not good for her own health or for the health of her
family. She has quit smoking many times without success. Recently, she used a nicotine
patch taped to her skin. The patch provides the nicotine without the smoke.
After successfully abstaining from cigarettes for more than 6 months with this
treatment, she began to smoke again. Because the university where she works has a nosmoking
policy, she has to leave the campus and stand across the street from the building
in which she works to smoke.Her voice has developed a rasping sound, and she has
an almost chronic “cold.” She says that she used to enjoy smoking but does not any
more. Concern about quitting dominates her thoughts.
B. G. has a drug problem. She is one of approximately 25 to 35 percent of North
Americans who smoke. Most begin smoking between the ages of 15 and 35, and each
consumes an average of about 18 cigarettes a day, nearly a pack-a-day habit. Like B. G.,
HOW DO DRUGS AND HORMONES INFLUENCE THE BRAIN AND BEHAVIOR? ! 247
Ian Whishaw
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most smokers realize that smoking is a health hazard, have experienced unpleasant side
effects from it, and have attempted to quit but cannot. B. G. is exceptional only in her
white-collar occupation. Today, most smokers are found within blue-collar occupations
rather than among professional workers.
Substance abuse is a pattern of drug use in which people rely on a drug chronically
and excessively, allowing it to occupy a central place in their lives.A more advanced state
of abuse is substance dependence, popularly known as addiction. Addicted people are
physically dependent on a drug in addition to abusing it. They have developed tolerance
for the drug, and so an addict requires increased doses to obtain the desired effect.
Users may also experience unpleasant, sometimes dangerous withdrawal symptoms
if they suddenly stop taking the abused drug. These symptoms can include muscle aches
and cramps, anxiety attacks, sweating, nausea, and, for some drugs, even convulsions
and death.Withdrawal symptoms from alcohol or morphine can begin within hours of
the last dose and tend to intensify over several days before they subside.
Although B. G. abuses the drug nicotine, she is not physically dependent on it. She
smokes approximately the same number of cigarettes each day (she has not developed
tolerance to nicotine) and she does not get sick if she is deprived of cigarettes (she does
not suffer severe sickness on withdrawal from nicotine but does display some physical
symptoms—irritability, anxiety, and increases in appetite and insomnia). B. G. illustrates
that the power of psychological dependence can be as influential as the power of
physical dependence.
Many different kinds of abused or addictive drugs—including sedative hypnotics,
antianxiety agents, narcotics, and stimulants—have a common property: they produce
psychomotor activation in some part of their dose range. That is, at certain levels of
consumption, these drugs make the user feel energetic and in control. This common
effect has led to the hypothesis that all abused drugs may act on the same target in the
brain. One proposed target is dopamine neurons, because their stimulation is associated
with psychomotor activity. Recall “The Neural Basis of Drug Cravings” at the beginning
of this chapter, describing an experiment illustrating one relation between DA
and drug consumption.
Three lines of evidence support a central role for DA in drug abuse:
1. Animals will press a bar for electrical stimulation of the mesolimbic dopamine system
in the brain, and they will no longer press it if the dopamine system is blocked
or damaged. This finding suggests that the release of DA is somehow rewarding.
2. Abused drugs seem to cause the release of DA or to prolong its availability in synaptic
clefts. Even drugs that have no primary action on DA synapses have been found
to increase its level.Apparently, when activated,many brain regions that contain no
DA neurons themselves may stimulate DA neurons elsewhere in the brain.
3. Drugs such as major tranquilizers, that block DA receptors or decrease its availability
at DA receptors, are not abused substances.
Explaining Drug Abuse
Why do people become addicted to drugs? According to an early explanation, habitual
users of a drug experience psychological or physiological withdrawal symptoms when
the effects of the drug wear off. They feel anxious, insecure, or just plain sick in the absence
of the drug, and so they take the drug again to alleviate those symptoms. In this
way, they get “hooked” on the drug.
Although this dependency hypothesis may account for part of drug-taking behavior,
it has shortcomings as a general explanation. For example, an addict may abstain
248 ! CHAPTER 7
Substance abuse. Use of a drug for the
psychological and behavioral changes
that it produces aside from its therapeutic
effects.
Addiction. Desire for a drug manifested
by frequent use of the drug, leading to the
development of physical dependence in
addition to abuse; often associated with
tolerance and unpleasant, sometimes
dangerous, withdrawal symptoms on
cessation of drug use. Also called
substance dependence.
Withdrawal symptoms. Physical and
psychological behaviors displayed by an
addict when drug use ends.
Psychomotor activation. Increased
behavioral and cognitive activity; at
certain levels of consumption, the drug
user feels energetic and in control.
Visit the Brain and Behavior Web site
(www.worthpublishers.com/kolb)
and go to the Chapter 7 Web links to
learn more about substance abuse and
addiction.
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from a drug for months, long after any withdrawal symptoms have abated, and yet still
be drawn back to using the drug. In addition, some drugs, such as the tricyclic antidepressants,
produce withdrawal symptoms when discontinued, but these drugs are not
abused.
Researchers currently see addiction as a series of stages. The first stage is the activation
of pleasure by the consequences of drug taking. Using the drug produces in the
person a positive subjective sensation. In other words, the user likes the experience.
In the second stage, pleasure is linked through associative learning with mental representations
of drug cues, the objects, acts, places, and events related to taking the drug.
This associative learning may be achieved through classical conditioning (also called
Pavlovian conditioning). You may recall from your introductory psychology course that
classical conditioning consists of learning to associate some formerly neutral stimulus
(such as the sound of a bell for a dog) with a stimulus (such as food in the mouth) that
elicits some involuntary response (such as salivation).
The pairing of the two stimuli continues until the formerly neutral stimulus is
alone able to trigger the involuntary reaction. In drug use, the sight of the drug and the
drug-taking context and equipment are repeatedly paired with administering the drug,
which produces a pleasurable reaction. Soon the visual cues alone are enough to elicit
pleasure.
The third stage is attributing incentive salience to the cues associated with drug use.
In other words, those cues become highly desired and sought-after incentives in their
own right. Stimuli that signal the availability of these incentives also become attractive.
For instance, acts that led to the drug-taking situation in the past become attractive, as
do acts that the drug taker predicts will lead again to the drug.
Drug users may even begin to collect objects that remind them of the drug. Pipe
collecting by pipe smokers and decanter collecting by drinkers are examples. In this sequence
of events, then, a number of repetitions of the drug-taking behavior lead from
liking that act to seeking it out or wanting it, regardless of its current consequences.
A number of findings are in keeping with this explanation of drug addiction. For
one thing, ample evidence reveals that abused drugs initially have a pleasurable effect.
There is also evidence that a habitual user continues to use his or her drug of choice
even though taking it no longer produces any pleasure. Heroin addicts sometimes report
that they are miserable, that their lives are in ruins, and that the drug is not even
pleasurable anymore, but they still want it. Furthermore, desire for the drug is often
greatest just when the addicted person is maximally high on the drug, not when he or
she is withdrawing from it.
To account for all the facts about drug abuse and addiction, Terry Robinson and
Kent Berridge (1993) proposed the incentive-sensitization theory. This perspective is
also called the wanting-and-liking theory because, according to Robinson and Berridge,
wanting and liking are produced by the effect of a drug on two different brain systems,
as illustrated in Figure 7-15. Robinson and Berridge define wanting as equivalent to
craving for a drug, whereas liking is defined as the pleasure that drug taking produces.
They propose that the road to drug dependence begins at the initial experience
when the drug affects a neural system associated with “pleasure.” At this time, the user
may experience liking the substance. With repeated use, liking the drug may decline
from its initial level. Now the user may also begin to show tolerance to the drug’s effects
and so may begin to increase the dosage to increase liking.
The drug also affects a different neural system—that associated with wanting.With
each use, the user increasingly associates the cues related to drug use—for example, an
injection needle, the room in which the drug is taken, people with whom the drug is
taken—with the drug-taking experience. The user makes this association because he
or she has become classically conditioned to all the cues associated with drug taking.
HOW DO DRUGS AND HORMONES INFLUENCE THE BRAIN AND BEHAVIOR? ! 249
Incentive salience. Quality acquired
by drug cues that become highly desired
and sought-after incentives in their own
right.
Incentive-sensitization theory. When
a drug is associated with certain cues, the
cues themselves elicit desire for the drug;
also called wanting-and-liking theory.
Initial
use
Liking
Wanting
Use
Effect
Figure 7-15
Incentive-Sensitization Theory When
first used, a psychoactive drug produces
moderate wanting and liking. With
repeated use, tolerance for liking
develops, and consequently the
expression of liking decreases. In
contrast, the system that mediates
wanting sensitizes, and wanting the
drug increases. Wanting is associated
with drug cues.
Peter Dokus/Stone
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According to Robinson and Berridge, later encounters with these wanting cues, rather
than the expected liking (the pleasure from the drug), initiates wanting.
How can the wanting-and-liking theory explain B.G.’s behavior in regard to smoking?
B. G. reports that her most successful period of abstinence from cigarettes coincided
with moving to a new town. She stopped smoking for 6 months and, during that
time, felt as if she were free and in command of her life again. The wanting-and-liking
theory would argue that her ability to quit at this time was increased because she was
separated from the many cues that had previously been associated with smoking.
Then one night after going out to dinner, B. G. and a few of her new colleagues
went to a bar, where some of them began to smoke. B. G. reported that her desire for
a cigarette became overpowering. Before the evening was over, she bought a package of
cigarettes and smoked more than half of it.
On leaving the bar, she left the remaining cigarettes on the table, intending that
this episode would be only a one-time lapse. Shortly thereafter, however, she resumed
smoking. The wanting-and-liking theory suggests that her craving for a cigarette was
strongly conditioned to certain social cues that she encountered again on her visit to
the bar, which is why the wanting suddenly became overwhelming.
The neural basis for liking and wanting are not completely understood. Robinson
and Berridge believe that liking may be due to the activity of opioid neurons, whereas
wanting may be due to activity in the mesolimbic dopamine system. In these dopamine
pathways, recall, the axons of DA neurons in the midbrain project to the nucleus accumbens,
the frontal cortex, and the limbic system (see Figure 7-1).
When cues that have previously been associated with drug taking are encountered,
the mesolimbic system becomes active, producing the subjective experience of wanting.
That desire for the drug is not a conscious act. Rather, the craving derives from unconsciously
acquired associations between drug taking and various cues related to it.
We can extend the wanting-and-liking explanation of drug addiction to many
other life situations. Cues related to sexual activity, food, and even sports can induce a
state of wanting, sometimes in the absence of liking.We frequently eat when prompted
by the cue of other people eating, even though we may not be hungry and derive little
pleasure from eating at that time.
Behavior on Drugs
Ellen is a healthy, attractive, intelligent 19-year-old university freshman. In her highschool
health class, she learned about the sexual transmission of HIV and other diseases.
More recently, in her college orientation, senior students presented a seminar
about the dangers of having unprotected sexual intercourse and provided the freshmen
in her residence with free condoms and “safe sex” literature.
It is certain that Ellen knows the facts about unprotected sexual intercourse and is
cognizant of the associated dangers. Indeed, she holds negative attitudes toward having
unprotected sexual intercourse, does not intend to have unprotected sexual intercourse,
and has always practiced safe sex. She and her former boyfriend were always
careful to use latex condoms during intercourse.
At a homecoming party in her residence, Ellen has a great time, drinking and dancing
with her friends and meeting new people. She is particularly taken with Brad, a
sophomore at her college, and the two of them decide to go back to her room to order
a pizza. One thing leads to another, and Ellen and Brad have sexual intercourse without
using a condom. The next morning, Ellen wakes up, dismayed and surprised at her
behavior, and very concerned that she may be pregnant or may have contracted a sexually
transmitted disease. Even worse, she is terrified that she may have contracted
AIDS (MacDonald, Zanna, & Fong, 1998).
250 ! CHAPTER 7
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What happened to Ellen? What is it about drugs, especially alcohol, that makes
people do things that they would not ordinarily do? Ellen is not alone in engaging in
risky behavior under the influence of alcohol. Alcohol is associated with many harmful
behaviors that are costly both to individual people and to society. These behaviors
include not only unprotected sexual activity but also drinking and driving, date rape,
spousal or child abuse, and other forms of aggression and crime.
An early and still widely held explanation of the effects of alcohol is the disinhibition
theory. It holds that alcohol has a selective depressant effect on the cortex, the region of
the brain that controls judgment, while sparing subcortical structures, those areas of the
brain responsible for more-primitive instincts, such as desire. Stated differently, alcohol
presumably depresses learned inhibitions based on reasoning and judgment while releasing
the “beast”within.
This theory often excuses alcohol-related behavior with such statements as, “She
was too drunk to know better,” or “The boys had a few too many and got carried away.”
Does such disinhibition explain Ellen’s behavior? Not really. Ellen had used alcohol in
the past and managed to practice safe sex despite the effects of the drug. The disinhibition
theory cannot explain why her behavior was different on this occasion. If alcohol
is a disinhibitor, why is it not always so?
Craig MacAndrew and Robert Edgerton (1969) questioned the disinhibition theory
along just these lines in their book titled Drunken Comportment. They cite many
instances in which behavior under the influence of alcohol changes from one context
to another. People who engage in polite social activity at home when consuming alcohol
may become unruly and aggressive when drinking in a bar.
Even their behavior at the bar may be inconsistent. For example, while drinking
one night at a bar, Joe becomes obnoxious and gets into a fight; but on another occasion
he is charming and witty, even preventing a fight between two friends, whereas on
a third occasion he becomes depressed and only worries about his problems. McAndrew
and Edgerton also cite examples of cultures in which people are disinhibited when
sober only to become inhibited after consuming alcohol and cultures in which people
are inhibited when sober and become more inhibited when drinking.How can all these
differences in alcohol’s effects be explained?
MacAndrew and Edgerton suggest that behavior under the effects of alcohol represents
“time out” from the rules of daily life that would normally apply. This time out
takes into consideration learned behavior that is specific to the culture, group, and setting.
Time out can help explain Ellen’s decision to sleep with Brad. In our culture, alcohol
is used to facilitate social interactions, and so behavior while intoxicated represents
time out from more-conservative rules regarding dating. But time-out theory has more
difficulty explaining Ellen’s lapse in judgment regarding safe sex. Ellen had never practiced
unsafe sex before and had never made it a part of her time-out social activities. So
why did she engage in it with Brad?
Tara MacDonald and her coworkers (1998) suggest an explanation
for alcohol-related lapses in judgment like Ellen’s.
Alcohol myopia (nearsightedness) is the tendency for people
under the influence of alcohol to respond to a restricted set of
immediate and prominent cues while ignoring more remote
cues and potential consequences. Immediate and prominent
cues are very strong and obvious and are close at hand.
In an altercation, the person with alcohol myopia will be
quicker than normal to throw a punch because the cue of the fight is so strong and immediate.
Similarly, at a raucous party, the myopic drinker will be more eager than usual
to join in because the immediate cue of boisterous fun dominates the person’s view. In
regard to Ellen and Brad, once they arrived at Ellen’s room, the sexual cues of the moment
were far more immediate than concerns about long-term safety. As a result, Ellen
HOW DO DRUGS AND HORMONES INFLUENCE THE BRAIN AND BEHAVIOR? ! 251
Disinhibition theory. Explanation that
attributes alcohol’s selective depressant
effect on the cortex, the region of the
brain that controls judgment, while
sparing subcortical structures responsible
for more-primitive instincts, such as
desire.
Alcohol myopia. “Nearsighted”
behavior displayed under the influence of
alcohol: local and immediate cues
become prominent, and remote cues and
consequences are ignored.
Tara MacDonald
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responded to those immediate cues and behaved as she normally would not. Such alcohol
myopia can explain many other lapses in judgment that lead to risky behavior,
including aggression, date rape, and reckless driving under the influences of alcohol.
Why Doesn’t Everyone Abuse Drugs?
Observing that some people are more prone to drug abuse and dependence than other
people are, scientists have wondered if this difference might be genetically based. Three
lines of evidence suggest a genetic contribution.
1. The results of twin studies show that, if one of two twins abuses alcohol, the other
is more likely to abuse it if those twins are identical (have the same genetic
makeup) than if they are fraternal (have only some of their genes in common).
2. The results of studies of people adopted shortly after birth reveal that they are
more likely to abuse alcohol if their biological parents were alcoholic, even though
they have had almost no contact with those parents.
3. Although most animals do not care for alcohol, the selective breeding of mice, rats,
and monkeys can produce strains that consume large quantities of it.
There are problems with all these lines of evidence, however. Perhaps identical
twins show greater concordance for alcohol abuse because they are exposed to more
similar environments than fraternal twins are. And perhaps the link between alcoholism
in adoptees and their biological parents has to do with nervous system changes
due to prebirth exposure to the drug. Finally, the fact that animals can be selectively
bred for alcohol consumption does not mean that human alcoholics have a similar genetic
makeup. The evidence for a genetic basis of alcohol abuse will become compelling
only when a gene or set of genes related to alcoholism is found.
Another avenue of research into individual differences associated with drug abuse
has been to search for personality traits that drug abusers tend to have in common.One
such trait is unusual risk taking. Consider Frenchman Bruno Gouvy, the daredevil who
was the first person to jump out of a helicopter and surf the sky on a snowboard (Figure
7-16). He also set a world speed record on a monoski and was the first person to
snowboard down Mont Blanc, the highest peak in Europe.He set a windsurfing record
across the Mediterranean Sea and a free-fall speed record after jumping out of a plane.
In an attempt to snowboard down three major peaks in one day, he hit black ice and
fell 3000 feet to his death.
Do people who love high-risk adventure have a genetic predisposition toward risk
taking that will also lead them to experiment with drugs (Comings et al., 1996)? In an
attempt to find out if certain behavioral traits are related to drug abuse, Pier Vincenzo
Piassa and his coworkers (1989) gave rats an opportunity to self-administer
amphetamine. Some rats were very quick to become amphetamine
“junkies,” giving themselves very large doses, whereas other rats
avoided the drug.
By examining the behavior of the rats in advance of the drug-taking
opportunity, the researchers were able to identify characteristics associated
with becoming an amphetamine user. In particular, those rats
that ran around the most when placed in an open area, thus seeming
less cautious and self-restrained than other rats, were also the most
likely to become addicted. Perhaps, the researchers concluded, such behavioral
traits make some rats more prone to drug use.
Although research on the characteristics that might influence becoming
a drug user continues, no unequivocal evidence suggests that
252 ! CHAPTER 7
Figure 7-16
Bruno Gouvy in Flight
Redneck/Liaison
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a specific gene determines substance abuse. Nor is there unequivocal evidence that differences
in the dopamine system make some people more prone to drug abuse than
others.And, even if a particular substance-abuse gene or genes could be found, that genetic
factor would not provide a full explanation of drug addiction. Identical twins
have all their genes in common, and yet, when one becomes a drug abuser, the other
does not necessarily become one, too. Clearly, learning also plays an important role in
developing drug abuse and addiction.
Can Drugs Cause Brain Damage?
Table 7-1 on page 233 shows that many substances produced by plants and animals, including
domoic acid, the causative agent in mussel poisoning, can act as neurotoxins.
Given the widespread use of psychoactive drugs in our society, it is important to
ask whether these substances can do the same. In this section, we examine the evidence
that commonly used psychoactive drugs can act as neurotoxins and investigate the
processes by which they might have toxic effects.
SOLVING THE DOMOIC ACID MYSTERY
Let us first consider how domoic acid acts as a toxin on the nervous system. The chemical
structure of domoic acid is similar to that of the neurotransmitter glutamate. Because
of its structural similarity to glutamate, domoic acid is referred to as a glutamate
analogue. It is also a glutamate agonist because, like glutamate, it binds to glutamate receptors
and affects them in the same way.
As described in Chapter 5, each neurotransmitter can attach to a number of different
types of receptors. Domoic acid acts to stimulate one of the three types of glutamate
receptors, the kainate receptor, so named because kainate, a chemical used
in fertilizer, binds very potently to it. Domoic acid, it turns out, binds to the kainate
receptor even more potently than does kainate itself. (Because receptors are usually
named for the compound that most potently binds to them, had domoic acid
been discovered earlier, the kainate receptor would have been called the domoic acid
receptor.)
The distribution of the different glutamate receptor subtypes in the brain varies
from region to region. Kainate receptors are especially numerous in the hippocampus.
If domoic acid reaches these receptors in high enough concentrations, it overexcites
the receptors, initiating a series of biochemical reactions that results in the death of
the postsynaptic neuron. Consequently, domoic acid is more toxic to the hippocampus
than it is to other brain regions.
Figure 7-17 shows a section through the brain of a rat that has been given an injection
of domoic acid. The brain is colored with a silver stain that accumulates in damaged
neurons. Tissue in the hippocampus exhibits the greatest amount of damage,
although there is also sparse damage elsewhere in the brain.
It may seem surprising that a chemical that mimics a neurotransmitter can cause
memory problems and brain damage. To understand how domoic acid can act as a
neurotoxin requires that we temporarily turn to a different story, that of monosodium
glutamate (MSG). The plot of this second story eventually links up with the plot of the
domoic acid story.
In the late 1960s, there were many reports that MSG, a salty-tasting, flavorenhancing
food additive, produced headaches in some people. In the process of investigating
why this effect happened, scientists placed large doses of MSG on cultured
neurons and noticed that the neurons died. Subsequently, they injected monosodium
glutamate into the brains of experimental animals, where it also produced neuron
death.
HOW DO DRUGS AND HORMONES INFLUENCE THE BRAIN AND BEHAVIOR? ! 253
Hippocampus
Domoic acid produces
hippocampal damage, as
shown by a dark silver stain
that highlights degeneration.
Domoic acid Kainic acid
Figure 7-17
Neurotoxicity Domoic acid damage is
not restricted to the hippocampus; it can
be seen to a lesser extent in many other
brain regions. Micrograph from NeuroScience
Associates.
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These findings raised the question of whether large doses of the neurotransmitter
glutamate, which MSG resembles structurally,might also be toxic to neurons. It turned
out that it is. This finding suggested that a large dose of any substance that acts like glutamate
might be toxic.
Now the toxic action of domoic acid can be explained. Domoic acid in large quantities
excessively stimulates the glutamate receptors of certain brain cells, and this activation
is related to neuronal death. Glutamate-receptor activation results in an influx
of Ca2! into the cell, and the influx of excessive Ca2! may through second messengers
activate a “suicide gene” in a cell’s DNA. Such apoptosis, as you learned in Chapter 6,
may be a mechanism by which the brain disposes of sick cells.
This is not to say that people should totally avoid MSG, which is similar in chemical
structure to glutamate. Only very large doses of these substances are harmful, just
as glutamate itself is not harmful except in large doses. Glutamate, in fact, is an essential
chemical in the body.
Recent findings show that we even have taste-bud receptors for glutamate on our
tongues, in addition to our receptors for sweet, salty, bitter, and sour. The glutamate
taste-bud receptor, mGluR4, most likely functions to encourage us to eat foods containing
glutamate, especially high-protein foods such as meat. Clearly, glutamate in
doses typically found in food is required by the body and is not toxic. Only excessive
doses of glutamate or its analogues cause harm.
POTENTIAL HARMFULNESS OF RECREATIONAL DRUGS
What about the many recreational drugs that affect the nervous system? Are any of
them potentially harmful? The answer is not always easy to determine, as Una McCann
and her coworkers (1997) found in their review of research.
For one thing, there is the problem of sorting out the effects of the drug itself from
the effects of other factors related to taking the drug. For instance, although chronic
alcohol use can be associated with damage to the thalamus and limbic system, producing
severe memory disorders, it is not the alcohol itself that seems to cause this damage
but rather related complications of alcohol abuse, including vitamin deficiencies due
to poor diet. For example, not only do alcoholics obtain reduced amounts of thiamine
(vitamin B1) in their diets, but alcohol also interferes with the absorption of thiamine
by the intestine. Thiamine plays a vital role in maintaining cell-membrane structure.
Similarly, there are many reports of people who suffer some severe psychiatric disorder
subsequent to their abuse of certain recreational drugs, but, in most cases, it is
difficult to determine whether the drug initiated the condition or just aggravated an
existing problem. It is also hard to determine exactly whether the drug itself or some
contaminant in the drug is related to a harmful outcome. Recall the development of
Parkinson’s disease after the use of synthetic heroin, described in Chapter 5, which was
caused by a contaminant (MPTP) rather than by the heroin itself.
A number of cases of chronic use of marijuana have been associated with psychotic
attacks, as “Drug-Induced Psychosis” describes. But the marijuana plant contains at
least 400 chemicals, 60 or more of which are structurally related to its active ingredient
tetrahydrocannabinol. Clearly, it is almost impossible to determine whether the
psychotic attacks are related to THC or to some other ingredient contained in marijuana
or to aggravation of an existing condition.
There is growing evidence that some recreational drugs can cause brain damage
and cognitive impairments. MDMA, also called ecstasy, is a widely used synthetic amphetamine.
Although MDMA is structurally related to amphetamine, it produces hallucinogenic
effects and is referred to as a “hallucinogenic amphetamine.”Findings from
animal studies show that doses of MDMA approximating those taken by human users
result in the degeneration of very fine serotonergic nerve terminals.
254 ! CHAPTER 7
Monosodium glutamate
Domoic acid Glutamate
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Drug-Induced Psychosis
Focus on Disorders
At age 29, R. B. S. was a chronic marijuana smoker. For years,
he had been selectively breeding a particularly potent strain
of marijuana in anticipation of the day when it would be legalized.
R. B. S. made his living as a pilot, flying small freight
aircraft into coastal communities in the Pacific Northwest.
One evening, R. B. S. experienced a sudden revelation
that he was no longer in control of his
life. Convinced that he was being manipulated
by a small computer that had
been implanted into his brain when he
was 7 years old, he confided in a close
friend, who urged him to consult a doctor.
R. B. S. insisted that he had undergone the
surgery when he participated in an experiment
at a local university. He also
claimed that all the other children who
participated in the experiment had been
murdered.
The doctor told R. B. S. that it was unlikely
that he had a computer implanted
in his brain, but called the psychology department
at the university and got confirmation
that children had in fact taken part in an experiment
conducted years before. The records of the study had long
since been destroyed. R. B. S. believed that this information
completely vindicated his story. His delusional behavior persisted
and cost him his pilot’s license.
The delusion seemed completely compartmentalized in
R. B. S.’s mind. When asked why he could no longer fly, he
intently recounted the story of the implant and the murders,
asserting that its truth had cost him the medical certification
needed for a license. Then he happily discussed other topics
in a normal way.
R. B. S. was suffering from a mild focal psychosis: he
was losing contact with reality. In some cases, this loss of
contact is so severe and the capacity to respond to the environment
is so impaired and distorted that the person can no
longer function in the world. People in a state of psychosis
may experience hallucinations (false sensory perceptions) or
delusions (false beliefs) or they may withdraw into a private
world isolated from people and events around them.
A variety of drugs can produce psychosis, including
LSD, amphetamine, cocaine, and, as shown by this case,
marijuana. The active ingredient in marijuana is D-9-tetrahydrocannabinol
(THC). At low doses, THC has mild sedativehypnotic
effects, similar to those of alcohol. At high doses, it
can produce euphoria and hallucinations.
The marijuana that R. B. S. used so
heavily comes from the leaves of the hemp
plant Cannabis sativa, perhaps the oldest
cultivated nonfood plant. Humans have
used hemp for thousands of years to make
rope, paper, cloth, and a host of products.
And marijuana has beneficial medical effects:
THC alleviates nausea and vomiting
associated with chemotherapy in cancer
and AIDS patients, controls the brain
seizures symptomatic of epilepsy, reduces
intraocular pressure in patients with glaucoma,
and relieves the symptoms of some
movement disorders. But marijuana’s psychedelic
effect has, to date, prevented its
legalization in the United States.
There is little cross-tolerance between THC and other
drugs, which suggests that THC has its own brain receptor.
THC may mimic a naturally occurring substance called
anandamide, which acts on a THC receptor that naturally inhibits
adenyl cyclase, part of one of the second-messenger
systems active in sensitization (see Chapter 5).
R. B. S.’s heavy marijuana use certainly raises the suspicion
that the drug had some influence on his delusional condition.
Henquet et al. (2004) report that cannabis use
moderately increases the risk of psychotic symptoms in
young people and has a much stronger effect in those with
evidence of predisposition for psychosis. There is no evidence
that marijuana use produces brain damage. It is possible
that R. B. S.’s delusions might have eventually occurred
anyway, even if he had not used marijuana. Furthermore,
marijuana contains about 400 compounds besides THC, any
of which could trigger psychotic symptoms. Approximately
10 years after his initial attack, R. B. S.’s symptoms subsided,
and he returned to flying.
Cannabis sativa is an annual herb that
reaches a height between 3 and 15
feet. Hemp grows in a wide range of
altitudes, climates, and soils and has
myriad practical uses.
Phil Schermeister/Stone
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In rodents, these terminals regrow within a few months after drug use is
stopped, but, in monkeys, the terminal loss may be permanent, as shown in
Figure 7-18. Memory impairments have been reported in users of MDMA,
which may be a result of similar neuronal damage (Morgan, 1999). But researchers
still want to know if people’s use of MDMA is associated with the
same loss of serotonergic terminals as it is in rodents and monkeys. Answering
this question is complicated by the fact that many MDMA users
have also used other drugs. In addition, the types of anatomical analysis used
with other animals cannot be used with humans.
The finding that MDMA can be toxic to neurons has led to investigations
into whether amphetamine itself also is toxic.The results of studies in rodents
have shown that high doses of amphetamine can result in the loss of DA terminals.
One form of amphetamine—methamphetamine, one of the most
widely used recreational drugs—has been found to produce both brain damage,
as revealed by brain-imaging studies, and impaired memory performance, as indicated
by neuropsychological tests (Thompson et al., 2004). The subjects used in this
study had been using the drug for about 10 years, and so the study does not produce evidence
that a single or only a few uses of the drug have similar detrimental brain and behavioral
effects but that in some way repeated use can permanently damage neurons.
The psychoactive properties of cocaine are similar to those of amphetamine, and
its possible deleterious effects have been subjected to intense investigation. The results
of many studies show that cocaine use is related to the blockage of cerebral blood flow
and other changes in blood circulation.Whether cocaine causes these abnormalities or
aggravates preexisting conditions is not clear.
Phencyclidine (PCP), or “angel dust,” is an NMDA-receptor blocker that was originally
developed as an anesthetic. Its use was discontinued after about half of treated
patients were found to display psychotic symptoms for as long as a week after coming
out of anesthesia. PCP users report perceptual changes and the slurring of speech after
small doses, with high doses producing perceptual disorders and hallucinations. Some
of the symptoms can last for weeks. The mechanisms by which PCP produces enduring
behavioral changes are unknown, but John Olney and his colleagues (1971) reported
that, after rats are given a related drug (MK-801), they undergo abnormal changes in
neurons, as well as loss of neurons. This finding suggests that the altered behavior of
PCP users may be related to neuron damage.
Some drugs that produce altered perceptual experiences and changes in mood do
not appear linked to brain damage. For instance, LSD, a drug believed to act on serotonergic
neurons, produces hallucinations but does not seem to cause enduring brain
changes in rats. Similarly, although opiates produce mood changes, the results of longterm
studies of opiate users have not revealed persistent cognitive impairments or
brain damage.
In Review .
Behavior may change in a number of ways with the repeated use of a drug. These changes
include tolerance, in which a behavioral response decreases; sensitization, in which a behavioral
response increases; and substance dependence, or addiction, in which the desire
to use a drug increases as a function of experience with it. Today, many researchers believe
that it is not so much avoidance of withdrawal symptoms that keeps people using a
drug as it is a set of powerful learned incentives associated with drug taking. Individual
differences in experience and genetic makeup, as well as the context in which a drug is
taken, influence that drug’s effects on behavior. Disinhibited behavior while a person is
256 ! CHAPTER 7
Figure 7-18
Drug Damage Treatment with MDMA
changes the density of serotonin axons
in the neocortex of a squirrel monkey:
(left) normal monkey; (right) monkey 18
months after treatment. From “Long-Lasting
Effects of Recreational Drugs of Abuse on the
Central Nervous System,” by U. D. McCann, K. A.
Lowe, and G. A. Ricaurte, 1997, The Neurologist,
3, p. 401.
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HOW DO DRUGS AND HORMONES INFLUENCE THE BRAIN AND BEHAVIOR? ! 257
HORMONES
In 1849, European scientist A. A. Berthold performed the first experiment to demonstrate
the existence and function of hormones, chemicals released by an endocrine
gland. Endocrine glands are cell groups in the body that secrete hormones into the
bloodstream to circulate to a body target and affect it. Berthold removed the testes of
a rooster and found that the rooster no longer crowed; nor did it engage in sexual or
aggressive behavior. Berthold then reimplanted one testis in the rooster’s body cavity.
The rooster began crowing and displaying normal sexual and aggressive behavior
again. The reimplanted testis did not establish any nerve connections, and so Berthold
concluded that it must release a chemical into the rooster’s circulatory system to influence
the animal’s behavior.
That chemical, we now know, is testosterone, the sex hormone secreted by the testes
and responsible for the distinguishing characteristics of the male. The effect that
Berthold produced by reimplanting the testis can be mimicked by administering testosterone
to a castrated rooster, or capon. The hormone is sufficient to make the capon behave
like a rooster with testes.
Testosterone’s influence on the rooster illustrates some of the ways that this hormone
produces male behaviors. Testosterone also initiates changes in the size and appearance
of the mature male body. In a rooster, for example, testosterone produces the
animal’s distinctive plumage and crest, and it activates other sex-related organs.
Hormones, like other drugs, are used to treat or prevent disease. People take synthetic
hormones as a replacement therapy because of the removal of glands that produce
those hormones or because of their malfunction. People also take hormones,
especially sex hormones, to counteract the effects of aging, and they take them to increase
physical strength and endurance and to gain an advantage in sports.
As many as 100 hormones in the human body are classified as either steroids or
peptides. Steroid hormones are synthesized from cholesterol and are lipid (fat) soluble.
Steroids diffuse away from their site of synthesis in glands, including the gonads,
adrenal cortex, and thyroid, easily crossing the cell membrane. They enter target cells
in the same way and act on the cells’ DNA to increase or decrease the production of
proteins. Peptide hormones, such as insulin and growth hormone, are made by cellular
DNA in the same way that other proteins are made, and they influence their target
cell’s activity by binding to metabotropic receptors on the cell membrane, generating
a second messenger that affects the cell’s physiology.
Hormones fall into one of three main groups with respect to their behavioral functions,
and they may function in more than one of these groups:
1. Hormones that maintain homeostasis, a state of internal metabolic balance and
regulation of physiological systems in an organism, form one group. (The term
homeostasis comes from the Greek words homeo, meaning “the same place,” and
stasis, meaning “standing.”) Homeostatic mineralocorticoids (e.g., aldosterone)
control the concentration of water in blood and cells; control the levels of sodium,
potassium, and calcium in the body; and promote digestive functions.
2. Gonadal (sex) hormones control reproductive functions. They instruct the body
to develop as male (e.g., testosterone) or female (e.g., estrogen), influence sexual
.
under the influence of alcohol can often be explained by the concepts of time out and alcohol
myopia. Scientists are still investigating the potential deleterious effects on the brain
of different psychedelic drugs. So far, their findings have been mixed, with some drugs
producing brain damage and others apparently not doing so.
Steroid hormone. Fat-soluble chemical
messenger synthesized from cholesterol.
Peptide hormone. Chemical messenger
synthesized by cellular D NA that acts to
affect the target cell’s physiology.
Homeostasis. State of internal metabolic
balance and regulation of physiological
systems in an organism.
Gonadal (sex) hormone. One of a
group of hormones, such as testosterone,
that control reproductive functions and
bestow sexual appearance and identity as
male or female.
Normal rooster
Rooster who has had
gonads removed
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behavior and the conception of children, and, in women, control the menstrual
cycle (e.g., estrogen and progesterone), the birthing of babies, and the release of
breast milk (e.g., prolactin, oxytocin).
3. Hormones activated in psychologically challenging events or emergency situations
prepare the body to cope by fighting or fleeing. Glucocorticoids (cortisol and corticosterone
are examples), a group of steroid hormones secreted in times of stress,
are important in protein and carbohydrate metabolism, controlling sugar levels in
the blood and the absorption of sugar by cells.
Hierarchical Control of Hormones
Figure 7-19 shows that the control and action of hormones are organized into a fourlevel
hierarchy consisting of the brain, the pituitary and remaining endocrine glands,
and the target cells affected by the hormones. As detailed in Chapter 11, the brain,
mainly the hypothalamus, releases neurohormones that stimulate the pituitary to
pump hormones into the circulatory system. The pituitary hormones, in turn, influence
the endocrine glands to release appropriate hormones into the bloodstream.
These hormones then act on various targets in the body, also providing feedback to the
brain about the need for more or less hormone release.
Although many questions remain about how hormones produce complex behavior,
they not only affect body organs but also target the brain and activating systems
there.Almost every neuron in the brain contains receptors on which various hormones
can act. In addition to influencing sex organs and physical appearance in a rooster,
testosterone may have neurotransmitter-like effects on the brain cells that it targets, especially
neurons that control crowing, male sexual behavior, and aggression.
In these neurons, testosterone is transported into the cell nucleus, where it activates
genes. The genes, in turn, trigger the synthesis of proteins needed for cellular
processes that produce the rooster’s male behaviors. Thus, the rooster receives not only
a male body but a male brain as well.
258 ! CHAPTER 7
Glucocorticoid. One of a group of
steroid hormones, such as cortisol,
secreted in times of stress; important in
protein and carbohydrate metabolism.
In response to sensory stimuli and
cognitive activity, the hypothalamus
produces neurohormones that enter
the anterior pituitary through veins
and the posterior pituitary through
axons.
On instructions from these releasing
hormones, the pituitary sends
hormones into the bloodstream to
target endocrine glands.
In response to pituitary hormones,
the endocrine glands release their
own hormones that stimulate target
organs, including the brain. In
response, the hypothalamus and the
pituitary decrease hormone
production.
Sensory
stimuli
Pituitary
gland
Target
endocrine
gland
Target
endocrine
gland
Target organs
and tissues
Endocrine
hormones
(A) (B) (C)
Pituitary
gland
Hypothalamus
Figure 7-19
Hormonal Hierarchy
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The diversity of testosterone’s functions clarifies why the body uses hormones as
messengers: their targets are so widespread that the best possible way of reaching all of
them is to travel in the bloodstream, which goes everywhere in the body. In subsequent
chapters, we will take up the story of hormones again, as we examine motivation and
the relation between learning and memory.
Homeostatic Hormones
The body’s internal environment must remain within relatively constant parameters in
order for us to function. An appropriate balance of sugars, proteins, carbohydrates,
salts, and water is required in the bloodstream, in the extracellular compartments of
muscles, in the brain and other body structures, and within all body cells. Homeostasis
of the internal environment must be maintained regardless of a person’s age, activities,
or conscious state. As children or adults, at rest or in strenuous work, when we
have overeaten or when we are hungry, to survive, we need a relatively constant internal
environment. Thus, the homeostatic hormones are essential to life itself.
Insulin is a homeostatic hormone. The normal concentration of glucose in the
bloodstream varies between 80 and 130 milligrams per 100 milliliters of blood. One
group of cells in the pancreas releases insulin, which causes blood sugar to fall by instructing
the liver to start storing glucose rather than releasing it and by instructing
cells to increase glucose uptake. The resulting decrease in glucose then decreases the
stimulation of pancreatic cells so that they stop producing insulin.
Diabetes mellitus is caused by a failure of these pancreatic cells to secrete enough
or any insulin. As a result, blood-sugar levels can fall (hypoglycemia) or rise (hyperglycemia).
In hyperglycemia, blood-glucose levels rise because insulin does not instruct
cells of the body to take up that glucose. Consequently, cell function, including neural
function, can fail through glucose starvation, even in the presence of high levels of glucose
in the blood. In addition, chronic high blood-glucose levels cause damage to the
eyes, kidneys, nerves, heart, and blood vessels. In hypoglycemia, inappropriate diet can
lead to to low blood sugar, which can be so severe as to cause fainting.
Gonadal Hormones
We are prepared for our adult reproductive roles by the gonadal hormones that give us
our sexual appearance, mold our identity as male or female, and allow us to engage in
sex-related behaviors. Sex hormones begin to act on us even before we are born and
continue their actions throughout our lives (see Chapters 6, 11, and 13).
For males, sex hormones produce the male body and male behaviors. The Y chromosome
of males contains a gene called the sex-determining region or SRY gene. If
cells in the undifferentiated gonads of the early embryo contain an SRY gene, they will
develop into a testes and, if they do not, they will develop into an ovary. In the male,
the testes produce the hormone testosterone,which in turn masculinizes the body, producing
the male body and genital organs and the male brain.
The organizational hypothesis proposes that actions of hormones during development
alter tissue differentiation. Thus, testosterone masculinizes the brain early in
life by being taken up in brain cells where it is converted into estrogen by the enzyme
aromatase. Estrogen then acts on estrogen receptors to initiate a chain of events that
include the activation of certain genes in the cell nucleus. These genes then contribute
to the masculinization of brain cells and their interactions with other brain cells.
Hormones play a somewhat lesser role in producing the female body, but they control
menstrual cycles, regulate many facets of pregnancy and birth, and stimulate milk
HOW DO DRUGS AND HORMONES INFLUENCE THE BRAIN AND BEHAVIOR? ! 259
Organizational hypothesis. Proposal
that actions of hormones during
development alter tissue differentiation;
for example, testosterone masculinizes
the brain.
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production for breast-feeding babies. It might seem surprising that estrogen, a hormone
usually associated with the female, masculinizes the male brain. Estrogen does
not have the same effect on the female brain, because females have a blood enzyme that
binds to estrogen and prevents its entry into the brain.
Hormones contribute to surprising differences in the brain and in cognitive behavior.
The male brain is slightly larger than the female brain after corrections are made for
body size, and the right hemisphere is somewhat larger than the left in males.The female
brain has a higher rate both of cerebral blood flow and of glucose utilization. There are
also a number of differences in brain size in different regions of the brain including nuclei
in the hypothalamus that are related to sexual function, parts of the corpus callosum
that are larger in females, and a somewhat larger language region in the female brain.
Three lines of evidence, summarized by Elizabeth Hampson and Doreen Kimura
(1992), support the conclusion that sex-related cognitive differences result from these
brain differences. These cognitive differences also depend in part on the continuing circulation
of the sex hormones. The evidence:
1. The results of spatial and verbal tests given to females and males in many different
settings and cultures show that males tend to excel in the spatial tasks and females
in the verbal ones.
2. The results of similar tests given to female subjects in the course of the menstrual
cycle show fluctuations in test scores with various phases of the cycle. During the
phase in which the female sex hormones estradiol (metabolized from estrogen)
and progesterone are at their lowest levels, women do comparatively better on spatial
tasks, whereas, during the phase in which levels of these hormones are high,
women do comparatively better on verbal tasks.
3. Tests comparing premenopausal and postmenopausal women, women in various
stages of pregnancy, and females and males with varying levels of circulating hormones
all provide some evidence that hormones affect cognitive function.
These sex-hormone–related differences in cognitive function are not huge. A great
deal of overlap in performance scores exists between males and females.Yet statistically
the differences seem reliable. Similar influences of sex hormones on behavior are found
in other species. The example of the rooster described earlier shows the effects of
testosterone on that animal’s behavior. Findings from a number of studies demonstrate
that motor skills in female humans and other animals improve at estrus, a time when
progesterone levels are high.
Stress Hormones
Life is stressful. “Stress” is a term borrowed from engineering to describe a process in
which an agent exerts a force on an object. Applied to humans and other animals, a
stressor is a stimulus that challenges the body’s homeostasis and triggers arousal.
Stress responses are not only physiological, but also behavioral, and include both
arousal and attempts to reduce stress. A stress response can outlast a stress-inducing
incident and may even occur in the absence an obvious stressor. Living with constant
stress can be debilitating.
Surprisingly, the body’s response is the same whether the stressor is exciting, sad,
or frightening. Robert Sapolsky (1992) uses the vivid image of a hungry lion chasing
down a zebra to illustrate the stress response. The chase elicits very different reactions
in the two animals, but their physiological stress responses are exactly the same.
The stress response begins when the body is subjected to a stressor, and especially
when the brain perceives a stressor and responds with arousal. The response consists
of two separate sequences, one fast and the other slow.
260 ! CHAPTER 7
To learn more about hormones and
the body’s hormonal response to stress,
visit the Chapter 7 Web links on the Brain
and Behavior Web site (www.worth
publishers.com/kolb).
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HOW DO DRUGS AND HORMONES INFLUENCE THE BRAIN AND BEHAVIOR? ! 261
The left side of Figure 7-20 shows the fast response. The sympathetic division is activated
to prepare the body and its organs for “fight or flight,” and the parasympathetic
division for “rest and digest” is turned off (see Figure 2-29). In addition, the sympathetic
division stimulates the medulla on the interior of the adrenal gland to release epinephrine.
The epinephrine surge (often called the adrenaline surge after epinephrine’s
original name) prepares the body for a sudden burst of activity. Among its many functions,
epinephrine stimulates cell metabolism so that the body’s cells are ready for action.
The hormone controlling the slow response is the steroid cortisol, a glucocorticoid
released from the outer layer (cortex) of the adrenal gland, as shown on the right side
of Figure 7-20. The cortisol pathway is activated more slowly, taking from minutes to
hours. Cortisol has a wide range of functions, which include turning off all bodily systems
not immediately required to deal with a stressor. For example, cortisol turns off insulin
so that the liver starts releasing glucose, thus temporarily producing an increase in
energy supply. It also shuts down reproductive functions and inhibits the production of
growth hormone. In this way, the body’s energy supplies can be concentrated on dealing
with the stress.
Ending a Stress Response
Normally, stress responses are brief. The body mobilizes its resources, deals with the
challenge physiologically and behaviorally, and then shuts down the stress response.
Just as the brain is responsible for turning on the stress reaction, it is also responsible
for turning it off. Consider what can happen if the stress response is not shut down:
The body continues to mobilize energy at the cost of energy storage.
Proteins are used up, resulting in muscle wasting and fatigue.
Growth hormone is inhibited, and so the body cannot grow.
The gastrointestinal system remains shut down, reducing the intake and processing
of food to replace used resources.
Fast-acting pathway Slow-acting pathway
Adrenal
Adrenal cortex
medulla
Spinal
cord
Hypothalamus
Pituitary
gland
CRHHR
ACTH
Adrenal
glands
To brain
To endocrine
glands
To body
cells
Kidneys
Epinephrine activates
the body‘s cells,
endocrine glands, and
the brain.
4
In the fight-or-flight
response, the
hypothalamus sends a
neural message
through the spinal
cord.
1
The sympathetic
division of the
autonomic nervous
system is activated to
stimulate the medulla
of the adrenal gland.
2
The adrenal medulla
releases epinephrine
into the circulatory
system.
3 To brain
To endocrine
glands
To body
cells
Cortisol
Epinephrine
Cortisol activates
the body's cells,
endocrine glands,
and the brain.
4
The pituitary
gland releases
ACTH, which acts
on the cortex of
the adrenal gland.
2
1
The adrenal cortex
releases cortisol
into the
circulatory system.
3
In the brain, the
hypothalamus
releases CRH into
the pituitary gland.
Figure 7-20
Activating a Stress Response Two
pathways to the adrenal gland control
the body’s response to stress. The
fast-acting pathway primes the body
immediately for fight or flight. The slowacting
pathway both mobilizes the
body’s resources to confront a stressor
and repairs stress-related damage.
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Reproductive functions are inhibited.
The immune system is suppressed, contributing to the possibility of infection or
disease.
Sapolsky (2003) argued that the hippocampus plays an important role in turning
off the stress response. The hippocampus contains a high density of cortisol receptors,
and it has axons that project to the hypothalamus. Consequently, the hippocampus is
well suited to detecting cortisol in the blood and instructing the hypothalamus to reduce
blood-cortisol levels.
There may, however, be a more insidious relation between the hippocampus and
blood-cortisol levels. Sapolsky and his coworkers observed wild-born vervet monkeys
that had become agricultural pests in Kenya and had therefore been trapped and caged.
They found that some of the monkeys became sick and died of a syndrome that appeared
to be related to stress. Those that died seemed to have been subordinate animals
housed with particularly aggressive, dominant monkeys.
Autopsies showed high rates of gastric ulcers, enlarged adrenal glands, and pronounced
hippocampal degeneration that was especially noticeable in the CA3 region
of the hippocampus. The hippocampal damage may have been due to prolonged high
cortisol levels produced by the unremitting stress of being caged with the aggressive
monkeys.
Cortisol levels are usually regulated by the hippocampus, but, if these levels remain
elevated because a stress-inducing situation continues, the high cortisol levels eventually
damage the hippocampus. The damaged hippocampus is then unable to do its
work of reducing the level of cortisol. Thus, a vicious cycle is set up in which the hippocampus
undergoes progressive degeneration and cortisol levels are not controlled.
Remember that domoic acid, the agent in mussel poisoning, damages the hippocampus
because it mimics the effects of high levels of the neurotransmitter glutamate.
Prolonged high cortisol levels may damage the hippocampus by mimicking the
excitotoxicity of domoic acid. By stimulating some hippocampal cells, cortisol causes
them to release glutamate. If this stimulation is excessive, the sustained release of glutamate
may be toxic to other hippocampal cells.
The cycle of prolonged stress, elevated cortisol levels, and damage to the hippocampus
is illustrated in Figure 7-21. Because stress-response circuits in monkeys are
very similar to those in humans, the possibility exists that excessive stress in humans
also can lead to damaged hippocampal neurons. Because the hippocampus is thought
to play a role in memory, stress-induced damage to the hippocampus is postulated to
result in impaired memory as well as in posttraumatic stress disorder (PTSD). Posttraumatic
stress disorder is characterized by physiological arousal symptoms related to
recurring memories and dreams related to a traumatic event—for months or years
after the event. People with PTSD feel as if they are reexperiencing the trauma, and the
accompanying physiological arousal enhances their belief of impending danger.
Research has not led to a clear-cut answer concerning whether the cumulative
effects of stress damage the human hippocampus. For example, research on women
who were sexually abused in childhood and were diagnosed as suffering from posttraumatic
stress disorder yields some reports of no changes in memory or in hippocampal
volume, as measured with brain-imaging techniques, compared with other
reports of memory impairments and reductions in hippocampal volume (Liberson &
Phan, 2003). That such different results can be obtained in what appear to be similar
studies can be explained in a number of ways.
First, how much damage to the hippocampus must occur to produce a stress syndrome
is not certain. Second, brain-imaging techniques may not be sensitive to subtle
changes in hippocampal cell function or moderate cell loss. Third, large individual and
environmental differences influence how people respond to stress. Finally, preexisting
262 ! CHAPTER 7
off cortisol secretion
Decreased ability to shut
Destruction of
hippocampal neurons
Fewer
hippocampal
neurons
More
cortisol
secretion
Prolonged
stress
Figure 7-21
Vicious Cycle Unrelieved stress
promotes an excessive release of cortisol
that causes damage to neurons in the
hippocampus. The damaged neurons are
unable to detect cortisol and therefore
cannot signal the adrenal gland to stop
producing it. The result is a feedback
loop in which the enhanced secretion of
cortisol further damages hippocampal
neurons.
Posttraumatic stress disorder
(PTSD). Syndrome characterized by
physiological arousal symptoms related to
recurring memories and dreams related to
a traumatic event—for months or years
after the event.
Craig Lovell/Corbis
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injury to the hippocampus or other brain regions could influence the probability of developing
posttraumatic stress disorder (Gilbertson et al., 2002).
Humans are long lived and have many life experiences that complicate simple extrapolations
from a single stressful event. Nevertheless, changes to the brain induced
by prolonged stress complicate the treatment of stress-related disorders and suggest
that it is important to treat stress so that brain and body injury do not occur.
SUMMARY
How do psychoactive drugs work? Psychoactive drugs—substances that alter mood,
thought, or behavior—produce their effects by acting on receptors or on chemical
processes in the nervous system, especially on processes of neural transmission at
synapses. They act either as agonists to stimulate neuronal activity or as antagonists to
depress it. Psychopharmacology is the study of drug effects on the brain and behavior.
How does a drug enter the body, reach its target, and leave the body? Drugs, chemicals
taken to bring about some desired change in the body, are administered by mouth, by
inhalation, by absorption through the skin, and by injection. To reach a target in the
nervous system, a drug must pass a through numerous barriers posed by digestion, dilution,
the blood–brain barrier, and cell membranes. Drugs are diluted by body fluids
as they pass through successive barriers,metabolized in the body, and excreted through
sweat glands and in feces, urine, breath, and breast milk.
How do people respond to drugs? A drug does not have a uniform action on every person.
Physical differences—in body weight, sex, age, or genetic background—influence
the effects of a given drug on a given person, as do behaviors, such as learning, and environmental
context.
How are psychoactive drugs classified? Psychoactive drugs are classified into seven
groups according to their major behavioral effects, as sedative hypnotics and antianxiety
agents, antipsychotic agents, antidepressants,mood stabilizers, narcotic analgesics,
psychomotor stimulants, and stimulants that have psychedelic and hallucinogenic effects.
Each group contains natural or synthetic drugs or both, and they may produce
their actions in different ways.
How does the repeated use of drugs and their use in different contexts affect behavior? A
common misperception about drugs is that their actions are specific and consistent. But
the body and brain rapidly become tolerant to many drugs, and so the dose must be increased
to produce a constant effect. Alternatively, people may become sensitized to a
drug, in which case the same dose produces increasingly greater effects. Learning also
plays an important role in a person’s behavior under the influence of a drug.
In Review .
Hormones are hierarchically controlled by sensory experiences, the brain, the pituitary
gland, and the endocrine glands that produce and secrete them through the bloodstream
to targets throughout the body. Hormones are of two types, steroid and peptide, and can
be classified into three groups: (1) homeostatic hormones regulate body nutrients and
metabolic processes; (2) gonadal hormones regulate sexual behavior, pregnancy, and child
bearing; and (3) stress hormones regulate the body’s responses to challenging events. Because
these hormones often have such widespread targets, traveling through the bloodstream
is an effective way to deliver their chemical messages.
HOW DO DRUGS AND HORMONES INFLUENCE THE BRAIN AND BEHAVIOR? ! 263
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Why do people become addicted to drugs? Addiction develops in a number of stages
as a result of repeated drug taking. Initially, drug taking produces pleasure, or liking,
but, with repeated use, it becomes conditioned to associated objects, events, and places.
Eventually, those conditioned cues acquire incentive salience, causing the drug user to
seek them out, which leads to more drug taking. The subjective experience associated
with prominent cues and drug seeking promotes craving for the drug. As addiction
proceeds, the subjective experience of liking decreases while that of wanting increases.
Does the effect of a drug depend on the drug-taking situation? The influence of drugs
on behavior varies widely with the situation and as a person learns appropriate drugrelated
behaviors. Some drugs, such as alcohol, can produce behavioral myopia such
that a person is primarily influenced by prominent cues in the environment. These cues
may encourage the person to act in ways in which he or she would not normally behave.
Why doesn’t everyone abuse drugs? Considering how many people use tobacco, drink
alcohol, use recreational drugs, or abuse prescription drugs, it is probably rare to find
someone who has not used a drug when it was available. Nevertheless, some people do
seem vulnerable to drug use and addiction. Individual differences in genetics could be influential,
but drug availability and peer influences are likely more influential.Because the
neural mechanisms that are implicated in addiction are the same neural systems responsible
for wanting and liking more generally, anyone is likely to be a potential drug abuser.
Can the repeated use of drugs produce brain damage? Excessive use of alcohol can be
associated with damage to the thalamus and hypothalamus, but the cause of the damage
is poor nutrition rather than the direct actions of alcohol. Cocaine can harm brain
circulation, producing brain damage by reduced blood flow or by bleeding into neural
tissue. The drug “ecstasy,” or MDMA, can result in the loss of fine axon collaterals of
serotonin neurons and in the associated impairments in cognitive function. Psycedelic
drugs such as marijuana and LSD can be associated with psychotic behavior, but
whether this behavior is due to the direct effects of the drugs or to the aggravation of
preexisting conditions is not clear.
What are hormones? Steroid and peptide hormones are produced by endocrine glands
and circulate in the bloodstream to affect a wide variety of targets.Hormones are under
the hierarchical control of sensory events, the brain, the pituitary gland, and the endocrine
glands, which all interact to regulate hormone levels. Homeostatic hormones
regulate the balance of sugars, proteins, carbohydrates, salts, and other substances in the
body. Sex hormones regulate the physical features and behaviors associated with reproduction
and the care of offspring. Stress hormones regulate the body’s ability to cope
with arousing and challenging situations. Failures to turn stress responses off after a
stressor has passed can contribute to susceptibility to posttraumatic stress disorder and
other psychological and physical diseases.
KEY TERMS
addiction, p. 248
agonist, p. 231
alcohol myopia, p. 251
amphetamine, p. 242
antagonist, p. 231
antianxiety agent, p. 234
barbiturate, p. 234
cross-tolerance, p. 234
disinhibition theory,
p. 251
dopamine hypothesis of
schizophrenia, p. 237
endorphin, p. 241
fetal alcohol syndrome
(FAS), p. 237
glucocorticoid, p. 258
gonadal (sex) hormone,
p. 257
homeostasis, p. 257
incentive salience, p. 249
incentive-sensitization
theory, p. 249
major tranquilizer, p. 237
monoamine oxidase
(MAO) inhibitor,
p. 238
narcotic analgesic, p. 239
organizational hypothesis,
p. 259
peptide hormone, p. 257
264 ! CHAPTER 7
neuroscience interact ive
There are many resources available for
expanding your learning online:
www.worthpublishers.com/kolb
Try the Chapter 7 quizzes and
flashcards to test your mastery of the
chapter material. You’ll also be able to
link to other sites that will reinforce
what you’ve learned.
www.nofas.org
Link to this site to learn more about
fetal alcohol syndrome.
www.niaaa.nih.gov
Investigate the state of the research on
alcohol abuse at this branch of the
National Institutes of Health.
On your Foundations CD-ROM, the
module on Neural Communication
provides important review on the basics
of synaptic communication.
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REVIEW QUESTIONS
1. What problems are encountered in an effort to make a psychoactive drug a
“magic bullet” targeting the CNS?
2. Describe how the blood–brain barrier works.
3. Describe the seven categories of drugs.
4. Distinguish between the dependency hypothesis and the wanting-and-liking
theory of drug addiction.
5. Distinguish between the disinhibition, time-out, and alcohol-myopia
explanations of behavior under the effects of drugs.
6. Describe the hierarchical control of hormones.
7. Describe some proposed effects of prolonged stress responses on the body and
brain.
FOR FURTHER THOUGHT
A traditional view is that drugs cause people to behave in certain ways. Discuss
contemporary views of how drugs can influence our behavior.
Because many drugs work by affecting the function of synapses, the effect that they
produce must be similar to some naturally produced behavior. Discuss this idea in
relation to a drug of your choice.
RECOMMENDED READING
Becker, J. B., Breedlove, S. M., & Crews, D. (2002). Behavioral endocrinology. Cambridge,
MA: MIT Press. A book consisting of a number of chapters on hormones, each written
by an expert.
Cooper, J. R., Bloom, F. E., & Roth, R. H. (1996). The biochemical basis of neuropharmacology.
New York: Oxford University Press. A summary of how synapses respond to drugs.
Consists of a general description of how synapses work and summarizes the structure
and function of a number of different neurochemical synapses.
Feldman, R. S., Meyer, J. S., & Quenzer, L. F. (1997). Principles of neuropsychopharmacology.
Sunderland, MA: Sinauer. A comprehensive but advanced book about how various
drugs affect the nervous system. An outstanding reference on contemporary
neuropsychopharmacology.
Julien, R. M. (2001). A primer of drug action. New York:Worth Publishers. As the name
suggests, this book is an extremely readable introduction to how drugs affect the
nervous system and produce changes in behavior, mood, and cognitive function.
Sapolsky, R.M. (1994).Why zebras don’t get ulcers. New York:W. H. Freeman and Company.
A readable popular summary of everything you would like to know about stress. The
theme of the book is that stress affects the brain and contributes to a great many medical
conditions—including heart disease, depression, sexual and reproductive problems, and
hormonal disorders—to aging, and to death; finally, of course, it affects zebras.
posttraumatic stress
disorder (PTSD), p. 262
psychedelic drug, p. 242
psychoactive drug, p. 226
psychomotor activation,
p. 248
psychopharmacology, p. 226
second-generation
antidepressant, p. 238
selective serotonin reuptake
inhibitor (SSRI), p. 238
steroid hormone, p. 257
substance abuse, p. 248
tolerance, p. 234
tricyclic antidepressant,
p. 238
withdrawal symptoms,
p. 248
HOW DO DRUGS AND HORMONES INFLUENCE THE BRAIN AND BEHAVIOR? ! 265
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C H A P T E R8
How Do We Sense, Perceive,
and See the World?
Focus on Disorders: Migraines and a Case
of Blindsight
The Nature of Sensation and
Perception
Focus on New Research: Testing Vision in
Nonhuman Subjects
Sensory Experience and Sensory Reality
Analyzing Sensory Information
Anatomy of the Visual System
Light: The Stimulus for Vision
Structure of the Eye
Focus on Disorders: Optical Errors of Refraction
and Visual Illuminance
Photoreceptors
Retinal-Neuron Types
Visual Pathways
Dorsal and Ventral Visual Streams
Location in the Visual World
Coding Location in the Retina
Location in the LGN and Cortical Region V1
The Visual Corpus Callosum
Neural Activity
Seeing Shape
Seeing Color
Neural Activity in the Dorsal Stream
The Visual Brain in Action
Injury to the Visual Pathway Leading to the Cortex
Injury to the “What” Pathway
Focus on Disorders: Carbon Monoxide Poisoning
Injury to the “How” Pathway
266 ! Left: Carolina Biological Supply/Phototake. Middle: MacDuff Everton/Image
Bank. Right: WDCN/Univ. College London/Photo Researchers.
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his visual aura, which began as a spot of flashing (scintillating)
light and then slowly enlarged. Like D. B., Lashley had
no sight in the scintillating area; and, as that area enlarged,
Lashley could detect lines of different orientations in it.
Findings from blood-flow studies reveal that, during
such an aura, a reduction of blood flow in the posterior occipital
cortex spreads at a rate of about 2 millimeters per
minute. The aura may gradually expand to fill an entire side
of the person’s field of vision but rarely, if ever, crosses over
to the opposite visual field. At its maximum, the person can
see nothing on that side of the world. Vision then returns,
although most people feel dizzy and often nauseated for a
while.
Although D. B. and Lashley had visual auras, auras
may also be auditory or tactile; in some cases, they may result
in an inability to move or to talk. After the aura passes,
most people suffer a severe headache that results from a dilation
of cerebral blood vessels. The headache is usually on
one side of the head, just as the aura is on one side of the
field of vision. Left untreated, these migraine headaches
may last for hours or even days.
D. B.’s attacks continued at intervals of about 6 weeks for
10 years. After one attack, he did not totally regain his vision
but was left with a small blind spot, or scotoma, illustrated in
the accompanying series of photographs. In some attacks,
D. B. also began to experience occasional loss of skin sensation
along the left side of his body. Like his visual symptoms,
these tactile auras disappeared after the headache was gone.
When D. B. was 26 years old, a neurologist found that a
collection of abnormal blood vessels at the back of his right
Migraines and a Case of Blindsight
Focus on Disorders
B orn in a small English town in 1940, D. B.’s childhood
was uneventful medically until he began to experience
recurring headaches at about age 14. Before each
headache, D. B. received a warning in the form of a visual
aura: the sensation of an oval-shaped area containing a
flashing light appeared just to the left of center in his field
of vision. In the next few minutes, the oval enlarged, and,
after about 15 min, the flashing light vanished and D. B.
was blind in the region of the oval.
D. B. described the oval as an opaque white area surrounded
by a rim of color. A headache on the right side of
his head followed. The headache could persist for as long
as 48 hours, but usually D. B. fell asleep before that much
time elapsed. When he awakened, the headache was gone
and his vision was normal again.
D. B., a well-studied patient in visual
neuroscience, and Karl Lashley, a pioneer
of research in this field, both suffered severe
migraines. The term migraine (derived
from a Greek word meaning “half of
the skull”) refers to recurrent headaches
that are usually localized to one side of
the head. Migraines vary in severity, frequency, and duration
and are often accompanied by nausea and vomiting.
Migraine is perhaps the most common of all neurological
disorders, afflicting some 5 to 20 percent of the population
at some time in their lives.
D. B. and Karl Lashley suffered from classic migraine,
common to many sufferers, which is preceded by an aura that
usually lasts from 20 to 40 min. Lashley carefully described
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In the development of a migraine scotoma as described by Karl
Lashley, a person looking at the small “x” (shown in white in the
photograph at the far left) first sees a small patch of lines.
Information in the world is not visible at that location. The
striped area continues to grow outward, leaving an opaque area
(scotoma) where the stripes had been. Within 15 to 20 minutes,
the visual field is almost completely blocked by the scotoma.
Normal vision returns shortly thereafter.
Novastock/Stock
Connection/PictureQuest
X = Fixation point
X X X X X
Karl Lashley
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occipital lobe was causing the migraine attacks. (In case you
suffer from migraines, we hasten to point out that this cause
is unusual.) By the time D. B. was 30, the migraines became
more severe and began to interfere with his family and social
life, as well as his job.
Because no drug treatment was effective, D. B. had the
malformed blood vessels surgically removed in 1973. The
operation relieved his pain and generally improved his life,
but a part of his right occipital lobe was deprived of blood
and died. As a result, D. B. became blind in the left half of his
visual field; that is, as he looks at the world through either
eye, he is unable to see anything to the left of the midline.
What applies to D. B. applies to everyone. You are consciously aware of only
part of the visual information that your brain is processing. This selectivity
is an important working principle behind human sensation and perception.
Weizkrantz was able to detect it in the visual system because of D. B.’s injury.
Vision is not unique in this regard.We are also unaware of much of the processing
that takes place in other sensory pathways for hearing, balance and touch, taste, and
smell. But vision is the focus of this chapter. The ability to lose conscious visual perception
while retaining unconscious vision leads to this chapter’s major question: How
do we “see” the world?
The function of the visual system is to convert light energy into neural activity that
has meaning for us. In this chapter, we begin an exploration of how this conversion
takes place with a general summary of sensation and perception—what it really means
to experience the sensory information transmitted by our environment. In an overview
of the visual system’s anatomy, we then consider the anatomical structure of the eyes,
the connections between the eyes and the brain, and the sections of the brain that
process visual information.
Turning next to the experience of sight, we focus on how neurons respond to visual
input, enabling the brain to perceive different features, such as color and shape. “Testing
Vision in Nonhuman Species” on p. 270 describes one technique that researchers have
developed to study how the brain perceives movement. At the chapter’s end, we explore
the culmination of vision—to understand what we see: How do we infuse light energy
with meaning, to grasp the meaning of written words or to see the beauty in a painting?
THE NATURE OF SENSATION AND PERCEPTION
As we look at the world, we naturally assume that what we see is what is really “out
there.” Cameras and videos reinforce this impression, seeming to re-create the very
same visual world that we experience first hand. But our version of the world, whether
D. B. came to the attention of Lawrence Weizkrantz, a
world-renowned visual neuroscientist at Oxford University,
who made a remarkable discovery about D. B.’s blindness.
Although D. B. could not identify objects in his blind area,
he could very accurately “guess” if a light had blinked on
there. He could even say where the light that he did not
“see” was located.
Apparently, even though D. B. could not consciously
perceive a light in his blind region, his brain knew when a
light had blinked and where it had appeared. This phenomenon
is referred to as blindsight. D. B.’s brain, in other
words, knew more than he was consciously aware of.
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we see it directly or view it reproduced, is always a creation of the brain.What we see
is not an objective reproduction of what is “out there” but rather a subjective construction
of reality that the brain manufactures.
With this in mind, we can make a distinction between sensation and perception.
Sensation is the registration of physical stimuli from the environment by the sensory
organs, whereas perception is the interpretation of sensations by the brain. Our version
of reality is our perception of the sensory world.
Sensory Experience and Sensory Reality
Compared with humans, dogs have very limited color vision. Compared with dogs, humans
have an olfactory system that smells in black and white.Dogs smell in technicolor.
Which sensory system, dog or human, truly represents the world? Neither.Human
brains and dog brains create species-specific sensations. Each is merely one version of
“reality” among many. These sensory experiences are not genuine reproductions of the
world; rather, they exist only in the mind of the perceiver.
In fact, the version of the world that we experience is not even constant in our own
minds.As dusk falls, for example,our color perception shifts so that red now appears black
even as green remains green.You can observe this color shift in the petals of a red rose and
its green leaves.As light fails, the red rose becomes blackish,but the green leaves stay green.
It is not that red has suddenly vanished from the external world. Rather, it is that
your visual system can no longer create this color as light levels drop. But add light—
say, by shining a flashlight on the rose—and the petals will immediately look red again.
Visual artists from illustrators to filmmakers exploit such properties of visual perception
in their work.
The mind creates not just the visual world but the world of all the senses. Consider
hearing. There is an old philosophical question about whether a tree falling in the forest
makes a sound if no one is there to hear it. The answer is no. A falling tree makes
sound waves but no sound.
Sound as we perceive it does not exist without a brain to create it. The only reason
that we experience sound is that the information from the ear goes to a region of the
brain that converts the neural activity into what we then perceive to be sound. The
brain might just as well convert that neural activity into some other subjective sensation.
Imagine the ear being connected to the visual system. The sound of the tree falling
would become a visual experience rather than an auditory one, because the visual system
would not know that the information came from the ear.
It is hard to imagine just what the noise of a tree falling would “look” like, but we
would not experience sound. Sound is the product of the particular auditory processing
system that we possess.Without that system, there is no sound as we know it. Some
people have the capacity, known as synesthesia, to join sensory experiences across
modalities. To such a person, a particular sound will also produce a color or taste, as
we detail in Chapter 14.
If the sensory world is merely a creation of the brain, it follows that different brains
might create different sensory experiences, even among members of the same species.
To demonstrate, consider the color red.We perceive red because certain cells in our eyes
are activated by certain wavelengths of light that we call red or green. (How this works
will be explained shortly.) If we did not have these cells, we could not experience red.
In fact, about 5 percent of all human males lack the cells. They are therefore red–green
color-blind and cannot tell these two colors apart.
Color blindness is just one extreme of normal human variation in color perception.
More subtle variations also exist. For instance, Joris Winderickx and her colleagues
HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 269
Fritz Goro, LIFE Magazine, © 1971 Time Warner, Inc.
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270 ! CHAPTER 8
(1992) asked men who were not red–green color-blind to mix red and green lights together
to match a series of yellow lights (in the mixing of colors of light, red and green
make yellow). The men varied in the amounts of red versus green that they used to
match the different yellows, but these variations were consistent for each man. Some of
the men required relatively more red to match the yellows, others required relatively
more green.We could say that the second group, compared with the first, had a slightly
rosier view of the world to begin with.
Winderickx found two forms of the receptor cell that detects red; about 60 percent
of men have one form, 40 percent have the other. The difference between these two
forms is small but significant and results from a small difference in the gene that encodes
the red-detecting receptor. The Winderickx study provided the first evidence that
normal variation in our mental world is traceable to normal variation in our genes.
Analyzing Sensory Information
D. B., who was not consciously aware of the presence of a light in his blind area yet
could indicate where the light was, illustrates another point about sensory experiences.
Clearly, the brain must process visual information in multiple ways. Some processing
allows us to consciously analyze visual stimuli, whereas other information processing
happens unconsciously.
Testing Vision in Nonhuman Subjects
Focus on New Research
A challenge in studying sensory and perceptual systems in
nonhumans is to determine their capacities without the benefit
of verbal communication. Thus, if we wish to know what
a cat or dog or rat sees, we cannot simply show them an eye
chart and have them recite the letters. Rather, we have to figure
out a way to “speak” the animal’s language.
One way to ask animals about their perceptual capacities
is to use reward. For example, animals can be trained to
seek rewards that are associated with certain visual stimuli
and not with others, but this training may take weeks and is
not likely to work with young animals that do not yet have
the cognitive capacities to learn such reward-based tasks.
These drawbacks can be problematic because researchers
often want quick answers to questions related to sensory capacities,
and developmental neuroscientists would like to
track the development of sensory capacities.
Glen Prusky and Rob Douglas have been designing tests
to circumvent these problems. In one test, they take advantage
of the optomotor (eye movements generated to stabilize
moving information on the retina) responses that all animals
show spontaneously from a young age. If a moving grating
passes in front of you, it is very difficult to prevent your eyes
from following the moving vertical lines. In fact, both humans
and nonhumans track the lines not only with the eyes
(A) In a three-dimensional optomotor testing apparatus, a mouse
is placed on a platform positioned in the middle of an arena
created by a quadrangle of computer monitors. Line gratings
drawn on the screens are extended vertically with floor and ceiling
mirrors. A video camera monitors the animal’s behavior from
above. (B) The mouse is surrounded by line gratings and allowed
to move freely on the platform. Adapted from Prusky and Douglas (2004).
Computer
monitor
Mirror
Mirror
Camera
(A) Side view (B) Top view
Platform
Computer monitor
Mirror
Computer monitor
Computer monitor
Computer monitor
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HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 271
To prove to yourself that your brain operates in both ways, imagine yourself seated
at a desk writing an essay. As you work, you engage in many behaviors that require vision.
You read books and write notes, you type on a computer, and you reach for and
drink from a mug of coffee.
What exactly are you doing when you make these visually guided movements? What
happens when you reach for your pen or your coffee mug? Before reading further, reach
for objects of different sizes and shapes around you
and observe what you do. First, your eyes orient to
the object. Then, as your hand moves toward it,
your fingers form the appropriate shape long before
they get to the object. When you reach for a
pen, your thumb and index finger assume a position
as if to pinch the pen. When you reach for a
mug, your hand is oriented vertically so that your
fingers can grasp the handle.
These movements are illustrated in Figure
8-1A. You did not consciously think about this
finger-and-hand positioning. It just happened.
Reaching for the pen or the mug was conscious, but
the shaping of your hand for the particular object
was not. Although both movements are guided by
but also by moving the head. If the thickness of the lines is
made smaller and smaller, there will be a point at which we
can no longer perceive the individual lines, and the optomotor
response stops.
Thus, we can measure an animal’s visual acuity, the
equivalent of asking people to read smaller and smaller
print, by varying the size of the moving lines. This response
is natural and requires no training. Indeed, scientists have
known for more than 50 years that, if an animal is placed inside
a cylinder that has stripes and the cylinder is then rotated,
the animal will show the optomotor response.
Such tests have proved difficult to administer, however,
because the investigator needs many cylinders, each with different-
width lines, and it is difficult to change the cylinders
quickly. Prusky and Douglas (2004) solved this problem by
constructing a virtual three-dimensional cylinder as shown in
the illustration.
Four flat-screen computer monitors are arranged to form
a quadrangle. The animal is placed on a small platform in the
center of the quadrangle, and a small camera tracks its behavior.
A line grating is generated by computer and appears to be
moving around the subject. The subject responds by tracking
the movement with its head and neck. Because the moving
grating is computer generated, the width of the lines can be
changed instantly. This feature makes it possible to determine
the precise point at which the animal no longer perceives the
lines, because the animal stops tracking at this point.
There is one other clever feature of this task. As the animal
moves around on the platform, the distance between its
eyes and computer grating will vary. This feature is important
because, if the animal moves closer, lines that were not visible
may now be seen. The trick is to make the lines smaller
if the animal moves toward them and bigger if it moves away.
With the use of coordinates of head location obtained from
the camera, the precise position of the animal can be calculated
by the computer and the virtual world changes. (To see
this feature in action, go to www.CerebralMechanics.com
and try it for yourself.)
The Prusky and Douglas task thus provides a quick way
for an animal and investigator to communicate. Furthermore,
rodent infants can be tested as soon as their eyes are
open, at about 2 weeks of age. This type of test could be used
for human infants as well, especially if there is reason to believe
that an infant has visual problems that need treatment.
(A)
(B)
Figure 8-1
Visual Perception Although you
may consciously decide to reach for an
object such as a pen or a mug (A), your
hand forms the appropriate posture
automatically, without your conscious
awareness. The mug can be separated
into two distinct visual representations
(B), one for shape and another for
color. Note that the color pattern is
fuzzy, whereas the shape is sharp but
appears only in shades of gray. These
representations are meant to mimic
the types of analysis that take place in
two different brain regions as visual
information about the mug is being
processed. The mug does not actually
exist in the brain as we perceive it.
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272 ! CHAPTER 8
visual information, different regions of the brain and different kinds of processing are
required.
There is more. Consider your coffee mug. It has a shape and it has a color pattern.
Yet you are not consciously aware of each of these attributes separately, as depicted
in Figure 8-1B. Instead, you perceive the patterned mug to be a single object. It may
therefore surprise you to learn that your brain produces this unified perception after
analyzing color separately from shape, each analysis in a different neural location.Consequently,
people can have brain damage that allows them to see the color of an object
but to have no idea of what the object is, because its shape is indecipherable.
Conversely, a person with another sort of brain damage might see the shape of
an object clearly but have no clue to its color. The brain essentially dissects the object,
analyzes the various parts separately, and then produces what appears to be a unified
perception of the whole. Yet there is no “picture” of the entire object in one place in
the brain. How, then, do we perceive a single object if we have only multiple mental
versions of it with which to work? You may recall from Chapter 2 that we referred to
this conundrum as the binding problem. We will return to this fascinating question
later.
ANATOMY OF THE VISUAL SYSTEM
Vision is our primary sensory experience. Far more of the human brain is dedicated to
vision than to any of our other senses. Understanding the organization of the visual
system is therefore key to understanding human brain function. To build this understanding,
we begin by following the routes that visual information takes to the brain
and within it. This exercise is a bit like traveling a road to discover where it goes. The
first step is to consider what the visual system analyzes—namely, light.
Light: The Stimulus for Vision
Simply put, light is electromagnetic energy that we see. This energy comes either directly
from a source, such as a lamp or the sun, that produces it or indirectly after having
been reflected off one or more objects. In either case, light energy travels from the
outside world, through the pupil, and into the eye, where it strikes a light-sensitive surface
on the back of the eye called the retina. From this stimulation of receptors on the
retina, we start the process of creating a visual world.
In Review .
We identified two key points about sensation and perception. First, our perceptions of the
world are entirely a creation of the brain. Different species and, to a lesser extent, different
individual members of a species have different perceptions of what the world is really
like. Neither is right or wrong, but both are imaginary. Second, the brain does not analyze
sensory information as though it were uniform. Rather, sensory information entering the
brain is dissected and passed to specialized regions that analyze particular characteristics.
We only have the impression that we perceive a unified sensory world. This binding problem
is one of the puzzles of how the brain works. Before returning to that puzzle, we must
first identify how the visual system breaks down visual stimuli.
Retina. Light-sensitive surface at the
back of the eye consisting of neurons and
photoreceptor cells.
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HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 273
A useful way to represent light is as a continuously moving wave. Not all light
waves are the same length, however. Figure 8-2 shows that, within the rather narrow
range of electromagnetic energy visible to humans, the wavelength varies from about
400 nanometers (violet) to 700 nanometers (red). (A nanometer, abbreviated nm, is
one-billionth of a meter.)
The range of visible light is constrained not by the properties of light waves but
rather by the properties of our visual receptors. If our receptors could detect light in
the ultraviolet or infrared range, we would see additional colors. In fact, bees detect
light in both the visible and the ultraviolet range and so have a broader range of color
perception than we do.
Structure of the Eye
How do the cells of the retina absorb light energy and initiate the processes leading to
vision? To answer this question, we first consider the structure of the eye as a whole so
that you can understand how it is designed to capture and focus light. Only then do we
consider the photoreceptor cells.
The functionally distinct parts of the eye are shown in Figure 8-3. They include the
sclera, the white part that forms the eyeball; the cornea, the eye’s clear outer covering;
Visit the area on the eye in the
module on the Visual System on your CD.
Rotate the three-dimensional model to
better understand the anatomy of the eye
and the structure of the retina.
400 500 600 700
10–4
Gamma rays
Wavelength (nm)
Shorter waves
Visible light
Longer waves
10–3 10–2 10–1 102 103 104 1 10 105 106 107 108 109 1010 1011 1012 1013 1014
X rays Ultraviolet Infrared Microwaves Radio waves
Figure 8-2
Visible Light The part of the
electromagnetic spectrum visible to the
human eye is restricted to a mere sliver
of wavelengths.
Sclera
Retinal surface as seen
with an ophthalmoscope
Retina
Fovea
Blind spot
(optic disc)
Blind spot
Blood vessels
Optic
nerve
Cornea
Iris
Pupil Lens
Lenses
Fovea
Figure 8-3
Visual Basics The cornea and lens
of the eye, like the lens of a camera,
focus light rays to project a backward,
inverted image on the receptive
surface—namely, the retina and film,
respectively. The optic nerve conveys
information from the eye to the brain.
The fovea is the region of best vision
and is characterized by the densest
distribution of photoreceptor cells. The
region in the eye where the blood
vessels enter and the axons of the
ganglion cells leave, called the optic
disc, has no receptors and thus forms a
blind spot. Note that there are few
blood vessels around the fovea in the
photograph of the retina at far right.
Upper left: Lien/Nibauer Photography Inc./
Liaison International
Above: Ralph Eagle/Photo Researchers
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the iris, which opens and closes to allow more or less light
in; the lens, which focuses light; and the retina, where light
energy initiates neural activity. As light enters the eye, it is
bent first by the cornea, travels through the hole in the iris
called the pupil, and is then bent again by the lens. The curvature
of the cornea is fixed, and so the bending of light waves
there is fixed, whereas small muscles adjust the curvature of
the lens.
The shape of the lens adjusts to bend the light to greater
or lesser degrees. This ability allows near and far images to be
focused on the retina.When images are not properly focused,
we require a corrective lens, as discussed in “Optical Errors of
Refraction and Visual Illuminance.”
Figure 8-4 includes a photograph of the retina, which
is composed of photoreceptors beneath a layer of neurons
connected to them. Although the neurons lie in front of
the photoreceptor cells, they do not prevent incoming light
from being absorbed by those receptors, because the neurons
are transparent and the photoreceptors are extremely
sensitive to light. (The neurons in the retina are insensitive
to light and so are unaffected by the light passing through
them.)
Together, the photoreceptor cells and the neurons of the
retina perform some amazing functions. They translate light
into action potentials, discriminate wavelengths so that we
can distinguish colors, and work in a range of light intensities
from very bright to very dim. These cells afford visual
precision sufficient for us to see a human hair lying on the page of this book from a
distance of 18 inches.
As in a camera, the image of objects projected onto the retina is upside down and
backward. This flip-flopped orientation poses no problem for the brain. Remember
that the brain is creating the outside world, and so it does not really care how the image
is oriented initially. In fact, the brain can make adjustments regardless of the orientation
of the images that it receives.
In fact, if you were to put on glasses that invert visual images and kept those glasses
on for several days, the world would first appear upside down but then would suddenly
appear right side up again because your brain would correct the distortion (Held,
1968). Curiously, when you removed the glasses, the world would temporarily seem
upside down once more, because your brain at first would be unaware that you had
tricked it another time. Eventually, though, your brain would solve this puzzle, too, and
the world would flip back in the right orientation.
THE BLIND SPOT
Try this experiment. Stand with your head over a tabletop and hold a pencil in your
hand. Close one eye. Stare at the edge of the tabletop nearest you. Now hold the pencil
in a horizontal position and move it along the edge of the table, with the eraser on
the table. Beginning at a point approximately below your nose, move the pencil slowly
along the table in the direction of the open eye.
When you have moved the pencil about 6 inches, the eraser will vanish. You have
found your blind spot, a small area of the retina that is also known as the optic disc. As
shown on the far right in Figure 8-3, the optic disc is the area where blood vessels enter
and exit the eye and where fibers leading from retinal neurons form the optic nerve that
274 ! CHAPTER 8
Rod-free area
(cones are most
dense in this area)
Fovea
Light
Retina
Bipolar Cone Rod
cell
Ganglion
cell
Optic
nerve
Fovea
Blind spot. Region of the retina where
axons forming the optic nerve leave the
eye and where blood vessels enter and
leave; this region has no photoreceptors
and is thus “blind.”
Figure 8-4
Central Focus This cross
section through the retina
shows the depression at
the fovea—also shown in
the scanning electron
micrograph at left—where
receptor cells are packed
most densely and where
our vision is clearest.
Professor P. Motta, University of La Sapienza,
Rome/Science Photo Library/Photo Researchers
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HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 275
Optical Errors of Refraction and Visual Illuminance
Focus on Disorders
The eye, like a camera, works correctly only when sufficient
light passes through the lens and is focused on the receptor
surface—the retina of the eye or the film in
the camera. Too little light entering the eye
or the camera produces a problem of visual
illuminance: it is hard to see any image at
all. If the focal point of the light is slightly in
front of the receptor surface or slightly behind
it, a refractive error causes objects to
appear blurry.
Refractive errors in the eye are of two
basic types. Most common in young people
(afflicting about 50 percent of the population)
is myopia (nearsightedness), an inability
to bring distant objects into clear focus.
Myopia is most commonly caused by the
normally round eyeball being elongated instead.
Myopia can also be caused by excessive
curvature of the front of the cornea. In
either case, the focal point of light falls short of the retina.
In hyperopia (farsightedness), a less common refractive
error in which people are unable to focus on near objects,
the focal point of light falls beyond the retina. Whereas the
myopic eyeball may be too long, the hyperoptic eyeball
may be too short. Farsightedness may also result because
the lens is too flat and does not adequately refract light. As
people age, the lens loses its elasticity and consequently becomes
unable to refract light from nearby objects correctly.
This form of hyperopia is called presbyopia
(old sightedness). Presbyopia is so common
that it is rare to find people older than 50
who do not need glasses to see up close, especially
for reading. Fortunately, this error
and other errors of refraction can be cured
by corrective lenses.
An additional complication to the
aging eye cannot be cured by corrective
lenses. As we age, the eye’s lens and cornea
allow less light through, and so less light
strikes the retina—a problem of visual illuminance.
Don Kline (1994) estimated that,
between ages 20 and 40, there is a drop of
50 percent in visual illuminance in dim
lighting and a further drop of 50 percent
over every 20 additional years. As a result,
it becomes increasingly difficult to see in dim light, especially
at night.
Corrective lenses do not compensate for this reduced
visual illuminance; the only solution is to increase lighting.
Night vision is especially problematic. Not surprisingly, statistics
show a marked drop in the number of people driving
at night in each successive decade after age 40.
These photographs represent the drop in visual illuminance that occurs between age 20 (left) and age 60 (right).
Don Kline
Don Kline
Myopia
Hyperopia
Normal
Retina
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goes to the brain. There are therefore no photoreceptors
in this part of the retina, and so you cannot see
with it. Figure 8-5 enables you to demonstrate your
own blind spot.
Fortunately, your visual system solves the blindspot
problem by locating the optic disc in a different
location in each of your eyes. The optic disc is lateral
to the fovea in each eye, which means that it is left of
the fovea in the left eye and right of the fovea in the
right eye. Because the visual world of the two eyes
overlaps, the blind spot of the left eye can be seen by
the right eye and visa versa.
Thus, using both eyes together, you can see the
whole visual world. People with blindness in one eye
have a greater problem, however, because the sightless
eye cannot compensate for the blind spot in the functioning eye. Still, the visual
system compensates for the blind spot in several other ways, and so people who are
blind in one eye have no sense of a hole in their field of vision.
The optic disc that produces a blind spot is of particular importance in neurology.
It allows neurologists to indirectly view the condition of the optic nerve that lies behind
it while providing a window onto events within the brain.
If there is an increase in intracranial pressure, such as occurs with a tumor or brain
abscess (infection), the optic disc swells, leading to a condition known as papilloedema
(swollen disc). The swelling occurs in part because, like all neural tissue, the optic nerve
is surrounded by cerebrospinal fluid. Pressure inside the cranium can displace this fluid
around the optic nerve, causing swelling at the optic disc.
Another reason for papilloedema is inflammation of the optic nerve itself, a condition
known as optic neuritis. Whatever the cause, a person with a swollen optic disc
usually loses vision owing to pressure on the optic nerve. If the swelling is due to optic
neuritis, probably the most common neurological visual disorder, the prognosis for recovery
is good.
THE FOVEA
Now try another experiment. Focus on the print at the left edge of this page. The words
will be clearly legible. Now, while holding your eyes still, try to read the words on the
right side of the page. It will be very difficult and likely impossible, even though you
can see that words are there.
The lesson is that our vision is better in the center of the visual field than at the
margins, or periphery. This difference is partly due to the fact that photoreceptors are
more densely packed at the center of the retina, in a region known as the fovea. Figure
8-4 shows that the surface of the retina is depressed at the fovea. This depression is
formed because many of the fibers of the optic nerve skirt the fovea to facilitate light
access to its receptors.
Photoreceptors
The retina’s photoreceptor cells convert light energy first into chemical energy and then
into neural activity.When light strikes a photoreceptor, it triggers a series of chemical
reactions that lead to a change in membrane potential. This change in turn leads to a
change in the release of neurotransmitter onto nearby neurons.
276 ! CHAPTER 8
Figure 8-5
Find Your Blind Spot Hold this book
30 centimeters (about 12 inches) away
from your face. Shut your left eye and
look at the cross with your right eye.
Slowly bring the page toward you until
the red dot disappears from the center
of the yellow disc and is replaced by a
yellow surface. The red spot is now in
your blind spot and not visible. Your
brain replaces the area with the
surrounding yellow to fill in the image.
Turn the book upside down to test your
left eye.
Fovea. Region at the center of the retina
that is specialized for high acuity; its
receptive fields are at the center of the
eye’s visual field.
Rod. Photoreceptor specialized for
functioning at low light levels.
Cone. Photoreceptor specialized for
color and high visual acuity.
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HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 277
Rods and cones, the two types of photoreceptors, differ in many ways. As you can
see in Figure 8-6, they are structurally different. Rods are longer than cones and cylindrically
shaped at one end, whereas cones have a tapered end. Rods, which are more
numerous than cones, are sensitive to low levels of brightness (luminance), especially
in dim light, and are used mainly for night vision. Cones do not respond to dim light,
but they are highly responsive in bright light. Cones mediate both color vision and our
ability to see fine detail.
Rods and cones are not evenly distributed over the retina. The fovea has only
cones, but their density drops dramatically at either side of the fovea. For this reason,
our vision is not so sharp at the edges of the visual field, as demonstrated earlier.
A final difference between rods and cones is in their light-absorbing pigments. Although
both rods and cones have pigments that absorb light, all rods have the same
pigment, whereas cones have three different pigment types. Any given cone has one of
these three cone pigments. The four different pigments, one in the rods and three in
the cones, form the basis of our vision.
The three types of cone pigments absorb light over a range of frequencies, but their
maximum absorptions are at about 419, 531, and 559 nm, respectively. The small range
of wavelengths to which each cone pigment is maximally responsive is shown in Figure
8-7. Cones that contain these pigments are called “blue,” “green,” and “red,” respectively,
loosely referring to colors in their range of peak sensitivity.
Note, however, that, if you were to look at lights with wavelengths of 419, 531, and
559 nm, they would not appear blue, green, and red but rather violet, blue green, and
yellow green, as you can see on the background spectrum in Figure 8-7. Remember,
though, that you are looking at the lights with all three of your cone types and that each
cone pigment is responsive to light across a range of frequencies, not just to its frequency
of maximum absorption. So the terms blue, green, and red
cones are not that far off the mark. Perhaps it would be more accurate
to describe these three cone types as responsive to short, middle,
and long visible wavelengths, referring to the relative length of
light waves at which their sensitivities peak.
Not only does the presence of three different cone receptors contribute
to our perception of color, so does the relative number and
distribution of cone types across the retina. As Figure 8-8 shows,
the three cone types are distributed more or less randomly across
the retina, making our ability to perceive different colors fairly constant
across the visual field. Although there are approximately equal
Fovea
Cone
Rod
Inner
segment
Synaptic
terminal
Outer
segment
Rods are more numerous than cones
and are more sensitive to dim light.
They are mainly used for night vision.
Cones are responsive to bright light.
They are responsible for color vision
and our ability to see fine detail.
Retina
Light
Figure 8-6
Photoreceptor Cells Both rods and
cones are tubelike structures, as the
scanning electron micrograph at the far
right shows, but they differ, especially
in the outer segment, which contains
the light-absorbing visual pigment.
Functionally, rods are especially sensitive
to broad-spectrum luminance, and cones
are sensitive to particular wavelengths
of light.
400 450
Wavelength (nm)
Peak sensitivity
500 550 600 650
25
50
75
Maximum response (%)
100
Cone
419
Rod
496
Cone
531
Cone
559
Figure 8-7
Range and Peak Sensitivity Our
actual perception of color corresponds
to the summed activity of the three
types of cones, each type most sensitive
to a narrow range of the spectrum. Note
that rods, represented by the white
curve, also have a preference for a range
of wavelengths centered on 496 nm, but
the rods do not contribute to our color
perception; their activity is not summed
with the cones in the color system.
Omikron/Photo Researchers
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278 ! CHAPTER 8
numbers of red and green cones, there are fewer blue cones, which means
that we are not as sensitive to wavelengths in the blue part of the visible
spectrum.
Other species that have color vision similar to that of humans
also have three types of cones, with three color pigments. But, because
of slight variations in these pigments, the exact frequencies of maximum
absorption differ among different species. For humans, the exact
frequencies are not identical with the numbers given earlier, which
were an average across mammals. They are actually 426 and 530 nm
for the blue and green cones, respectively, and 552 or 557 nm for the
red cone. There are two peak sensitivity levels given for red because humans,
as stated earlier, have two variants of the red cone. The difference in these two red
cones appears minuscule, but recall that it does make a functional difference in color
perception.
This functional difference between the two human variants of red cone becomes
especially apparent in some women. The gene for the red cone is carried on the X
chromosome. Because males have only one X chromosome, they have only one of
these genes and so only one type of red cone. The situation is more complicated for
women. Although most women have only one type of red cone, some have both, with
the result that they are more sensitive than the rest of us to color differences at the red
end of the spectrum. Their color receptors create a world with a richer range of red
experiences. However, these women also have to contend with peculiar-seeming color
coordination by others.
Retinal Neuron Types
Figure 8-9 shows that the photoreceptors in the retina are connected to two layers of
retinal neurons. In the procession from the rods and cones toward the brain, the first
layer contains three types of cells: bipolar cells, horizontal cells, and amacrine cells. Two
cell types in the first neural layer are essentially
linkage cells. The horizontal cells link photoreceptors
with bipolar cells, whereas the amacrine
cells link bipolar cells with cells of the second
neural layer, the retinal ganglion cells. The
axons of the ganglion cells collect in a bundle at
the optic disc and leave the eye to form the optic
nerve.
Retinal ganglion cells are not all the same in
regard to the brain cells to which they connect.
They fall into two major categories, which in the
primate retina are called M and P cells. The designations M and P derive from the distinctly
different populations of cells in the visual thalamus to which these two classes
of ganglion cells send their axons.
As shown in Figure 8-10, one of these populations consists of magnocellular cells
(hence M), whereas the other consists of parvocellular cells (hence P). M cells, which
are larger (magno means “large” in Latin), receive their input primarily from rods and
so are sensitive to light but not to color. P cells, which are smaller (parvo means “small”
in Latin), receive their input primarily from cones and so are sensitive to color.
M cells are found throughout the retina, including the periphery, where we
are sensitive to movement but not to color or fine details. P cells are found largely in
Cones Rod
Figure 8-8
Retinal Receptors The retinal
receptors form a mosaic of rods and
three types of cones. This diagram
represents the distribution near the
fovea, where the cones outnumber the
rods. There are fewer blue cones than
red and green cones.
Horizontal Cone Rod
cell
Bipolar
cell
Amacrine
cell
Ganglion
cell
Axons of
ganglion cells
Optic
nerve
Light
Retina
Retinal ganglion cells. Neural cells of
the retina that give rise to the optic nerve.
Magnocellular (M) cell. Large-celled
visual-system neuron that is sensitive to
moving stimuli.
Parvocellular (P) cell. Small-celled
visual-system neuron that is sensitive to
form and color differences.
Figure 8-9
Retinal Cells The enlargement of the
retina at the right shows the positions of
the four types of neurons in the retina:
bipolar, horizontal, amacrine, and
ganglion cells. Notice that light must
pass through both neuron layers to
reach the photoreceptors.
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HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 279
the region of the fovea, where we are sensitive to color and fine details. A distinction
between these two categories of ganglion cells is maintained throughout the visual
pathways, as you will see in the next section, where we follow the ganglion cell axons
into the brain.
Visual Pathways
Imagine leaving your house and finding yourself on an unfamiliar road. Because the
road is not on any map, the only way to find out where it goes is to follow it. You soon
discover that the road divides in two, and so you must follow each branch sequentially
to figure out its end point. Suppose you learn that one branch goes to a city,
whereas the other goes to a national park. By knowing the end point of each branch,
you can conclude something about their respective functions—that one branch
carries people to work, whereas the other carries them to play, for
example.
The same strategy can be used to follow the paths of the visual
system. The retinal ganglion cells form the optic nerve, which
is the road into the brain. This road travels to several places, each
with a different function. By finding out where the branches go,
we can begin to guess what the brain is doing with the visual input
and how the brain creates our visual world.
Let us begin with the optic nerves, one exiting from each eye.
As you know, they are formed by the axons of ganglion cells leaving
the retina. Just before entering the brain, the optic nerves
partly cross, forming the optic chiasm (from the Greek letter v).
About half the fibers from each eye cross in such a way that
the left half of each optic nerve goes to the left side of the brain,
whereas the right halves go to the brain’s right side, as diagrammed
in Figure 8-11. The medial path of each retina, the nasal retina,
crosses to the opposite side. The lateral path, the temporal retina,
goes straight back on the same side. Because the light that falls on
the right half of the retina actually comes from the left side of the
Magnocellular
layers
Parvocellular
layers
Thalamus
LGN
Optic
nerve
1
2
3
4
5
6
Figure 8-10
Visual Thalamus The optic nerves
connect with the lateral geniculate
nucleus (LGN) of the thalamus. The LGN
has six layers: two magnocellular layers
that receive input mainly from rods and
four parvocellular layers that receive
input mainly from cones.
Optic chiasm. Junction of the optic
nerves from each eye at which the axons
from the nasal (inside) halves of the retinas
cross to the opposite side of the brain.
David H. Hubel
Eye
Optic nerve
Nasal retina
Temporal retina
Optic chiasm
Optic tract
Lateral
geniculate
nucleus
Optic
radiations
Primary visual
cortex (region V1)
Visual field
Figure 8-11
Crossing the Optic Chiasm This
horizontal slice through the brain shows
the visual pathway from each eye to
the primary visual cortex of each
hemisphere. Information from the blue
side of the visual field goes to the two
left halves of the retinas and ends up in
the left hemisphere. Information from
the red side of the visual field hits the
right halves of the retinas and travels to
the right side of the brain.
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visual field, information from the left visual field goes to
the brain’s right hemisphere, whereas information from
the right visual field goes to the left hemisphere. Thus,
half of each retina’s visual field is represented on each side
of the brain.
Having entered the brain, the axons of the ganglion
cells separate, forming two distinct pathways, charted
in Figure 8-12. All the axons of the P ganglion cells
and some of the M ganglion cells form a pathway called
the geniculostriate system. This pathway goes from the
retina to the lateral geniculate nucleus (LGN) of the thalamus
and then to layer IV of the primary visual cortex,
which is in the occipital lobe.
As Figure 8-13 shows, the primary visual cortex appears to have a broad stripe
across it in layer IV and so is known as striate cortex. The term geniculostriate therefore
means a bridge between the thalamus (geniculate) and the striate cortex. From the
striate cortex, the axon pathway now splits, with one route going to vision-related regions
of the parietal lobe and another route going to vision-related regions of the temporal
lobe.
The second pathway leading from the eye is formed by the axons of the remaining
M ganglion cells. These cells send their axons to the superior colliculus (located in the
tectum of the midbrain; see Chapter 2). The superior colliculus sends connections to
a region of the thalamus known as the pulvinar. This pathway is therefore known as
the tectopulvinar system because it goes from the eye through the tectum to the pulvinar
(see Figure 8-12). The pulvinar then sends connections to the parietal and temporal
lobe.
To summarize, two principal pathways extend into the visual brain—namely, the
geniculostriate and tectopulvinar systems. Each pathway eventually travels either to the
parietal or the temporal lobe. Our next task is to determine the respective roles of the
parietal lobe and the temporal lobe in creating our visual world.
Dorsal and Ventral Visual Streams
Identification of the temporal- and parietal-lobe visual pathways led researchers
on a search for the possible functions of each. One way to examine these functions
is to ask why evolution would produce two different destinations for the pathways in
the brain. The answer is that each route must create visual knowledge for a different
purpose.
David Milner and Mel Goodale (1995) proposed that these two purposes are to identify
what a stimulus is (the “what” function) and to use visual information to control
movement (the “how” function). Many authors have emphasized the role of the latter
280 ! CHAPTER 8
Brain
Lateral
geniculate
nucleus
Other
visual
cortical
areas
Superior
colliculus
Visual
information
Geniculostriate system
Tectopulvinar system
Striate
cortex
Eye
Optic nerve
Pulvinar
Figure 8-12
Flow of Visual Information into the Brain The optic
nerve has two principal branches: (1) the geniculostriate
system through the LGN in the thalamus to the primary
visual cortex and (2) the tectopulvinar system through the
superior colliculus of the tectum to the pulvinar region of
the thalamus and thus to the temporal and parietal lobes.
Parietal lobe Striate
cortex
Occipital
lobe
Temporal
lobe
Figure 8-13
Striate Cortex The primary
visual cortex is referred to as
striate cortex because it
appears to have striations
(stripes) when stained with
either a cell-body stain (left)
or a myelin stain (right) in
these sections from a rhesus
monkey brain.
Superior
colliculus
Geniculostriate system. Projections
from the retina to the lateral geniculate
nucleus to the visual cortex.
Striate cortex. Primary visual cortex in
the occipital lobe; its striped appearance
when stained gives it this name.
Tectopulvinar system. Projections
from the retina to the superior colliculus
to the pulvinar (thalamus) to the parietal
and temporal visual areas.
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pathway as a “where” function. The problem is that “where”
is a property of “what”a stimulus is as well as a cue for “how”
to control movement to a place. We therefore will use the
“what–how” distinction suggested by Milner and Goodale.
This “what” versus “how” distinction came from an
analysis of where visual information goes when it leaves the
striate cortex. Figure 8-14 shows the two distinct visual
pathways that originate in the striate cortex, one progressing to the temporal lobe and
the other to the parietal lobe. The pathway to the temporal lobe has become known as
the ventral stream, whereas the pathway to the parietal lobe has become known as the
dorsal stream.
To understand how these two streams function, we need to return to the details of
how the visual input from the eyes contributes to them. Both the geniculostriate and
the tectopulvinar systems contribute to the dorsal and ventral streams.
GENICULOSTRIATE PATHWAY
The retinal ganglion-cell fibers from the two eyes distribute their connections to the
two lateral geniculate nuclei (left and right) of the thalamus in what at first glance appears
to be an unusual arrangement.As seen in Figure 8-11, the fibers from the left half
of each retina go to the left LGN, whereas those from the right half of each retina go
to the right LGN. But the fibers from each eye do not go to exactly the same place in
the LGN.
Each LGN has six layers, and the projections from the two eyes go to different
layers, as illustrated in anatomical context in Figure 8-10 and alone in Figure 8-15. Layers
2, 3, and 5 receive fibers from the ipsilateral eye (i.e., the eye
on the same side), whereas layers 1, 4, and 6 receive fibers from
the contralateral eye (i.e., the eye on the opposite side). This
arrangement provides for combining the information from the
two eyes and for segregating the information from the P and M
ganglion cells.
Axons from the P cells go only to layers 3 through 6 (referred
to as the parvocellular layers), whereas axons from the
M cells go only to layers 1 and 2 (referred to as the magnocellular
layers). Because the P ganglion cells are responsive to
color and fine detail, layers 3 through 6 of the LGN must be
processing information about color and form. In contrast, the
M cells mostly process information about movement, and so
layers 1 and 2 must deal with movement.
Before we continue, you should be aware that just as there
are six layers of the LGN (numbered 1 through 6), there are
also six layers of the striate cortex (numbered I through VI).
That there happen to be six layers in each of these locations is
an accident of evolution found in all primate brains. Let us
now see where these LGN cells send their connections in the
visual cortex.
You learned in Chapter 2 that layer IV is the main afferent
(incoming) layer of the cortex. Layer IV of the visual cortex has
several sublayers, two of which are known as IVCa and IVCb.
Layers 1 through 4 of the LGN go to IVCb, and LGN layers 5 and 6 go to IVCa. As a
result, a distinction between the P and M functions continues in the cortex.
As illustrated in Figure 8-16, input from the two eyes also remains separated
in the cortex but through a different mechanism. The input from the ipsilaterally
HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 281
Ventral stream Occipital
lobe
Striate
cortex (region V1)
Temporal
lobe
Dorsal stream Parietal
lobe
Figure 8-14
Visual Streaming Visual information
travels from the occipital visual areas to
the parietal and temporal lobes, forming
the dorsal and ventral streams,
respectively.
David Milner Mel Goodale
Right eye
(ipsilateral)
Temporal
projection
Nasal
projection
Left eye
(contralateral)
Layers of LGN
Left LGN Right LGN
1
2
4 3
6 5
Information from the
ipsilateral side goes to
layers 2, 3, and 5.
Layers 3 through 6 receive input
from the parvocellular pathway.
Layers 1 and 2 receive input from
the magnocellular pathway.
Information from the
contralateral side goes
to layers 1, 4, and 6.
Information travels from the right
side of each retina to the right LGN.
Figure 8-15
Geniculostriate Pathway
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282 ! CHAPTER 8
connected LGN cells (that is, layers 2, 3, and 5) and the
input from the contralaterally connected LGN cells (layers
1, 4, and 6) go to adjacent strips of cortex. These
strips, which are about 0.5 millimeter across, are known
as cortical columns.We return to the concept of cortical
columns shortly.
In summary, the P and M ganglion cells of the retina
send separate pathways to the thalamus, and this segregation
remains in the striate cortex. The left and right eyes
also send separate pathways to the thalamus, and these pathways, too, remain segregated
in the striate cortex.
TECTOPULVINAR PATHWAY
As already noted, the tectopulviar pathway is formed by the axons of the remaining M
ganglion cells. These cells send their axons to the superior colliculus in the midbrain’s
tectum, which functions to detect the location of stimuli and to shift the eyes toward
stimuli. The superior colliculus sends connections to the region of the thalamus known
as the pulvinar.
The pulvinar has two main divisions: medial and lateral. The medial pulvinar
sends connections to the parietal lobe, whereas the lateral pulvinar sends connections
to the temporal lobe. One type of information that these connections are conveying
is related to “where,” which, as noted earlier, is important in both “what” and “how”
functions.
The “where” function of the tectopulvinar system is useful in understanding blindsight
in D. B.His geniculostriate system was disrupted but his tectopulvinar system was
not, thus allowing him to identify the location of stimuli that he could not identify. Let
us now look at how visual information proceeds from the striate cortex through the
rest of the occipital lobe to the dorsal and ventral streams.
OCCIPITAL CORTEX
As shown in Figure 8-17, the occipital lobe is composed of at least six different visual
regions, known as V1, V2, V3, V3A, V4, and V5. Region V1 is the striate cortex, which,
as already mentioned, is sometimes also referred to as the primary visual cortex. The
remaining visual areas of the occipital lobe are called the extrastriate cortex or secondary
visual cortex. Because each of these occipital regions has a unique cellular structure
(cytoarchitecture) and has unique inputs and outputs, we can infer that each must
be doing something different from the others.
You already know that a remarkable feature of region V1 is its distinct layers,which
extend throughout V1. These seemingly homogeneous layers are deceiving, however.
When Margaret Wong-Riley and her colleagues (1993) stained the cortex for the enzyme
cytochrome oxidase, which has a role in cell metabolism, they were surprised to
Cortical column. Cortical organization
that represents a functional unit six
cortical layers deep and approximately
0.5 mm square and that is perpendicular
to the cortical surface.
Primary visual cortex (V1). Striate
cortex that receives input from the lateral
geniculate nucleus.
Extrastriate (secondary) cortex.
Visual cortical areas outside the striate
cortex.
Blob. Region in the visual cortex that
contains color-sensitive neurons, as
revealed by staining for cytochrome
oxidase.
I
II
III
IVC
IVC
V
VI
Cortical visual area
Lateral geniculate
nucleus
Ocular dominance columns
1
2
3
4
5
6
Left
eye
Left
eye
Right
eye
Horizontal section
of striate cortex
Figure 8-16
Maintaining Separate Visual Input
(Left) Information from the two eyes is
segregated by layers in the lateral
geniculate nucleus, and the lateral
geniculate nucleus maintains this
segregation in its projections to the
visual cortex. Information from each eye
travels to adjacent columns in cortical
layer IV. (Right) A horizontal plane
through V1 shows a zebralike effect of
alternating ocular-dominance columns
in the cortex. Photograph from “Functional
Architecture of Macaque Monkey Visual
Cortex,” by D. H. Hubel and T. N. Weisel, 1977,
Proceedings of the Royal Society of London B,
198, Figure 23.
On your CD, find the primary visual
cortex area in the Visual System module
to see the visual connections to the
occipital cortex. Notice in particular how
the cortex is layered in this region and
how this layering parallels that seen in
the LGN.
Link to the area on the optic chiasm
in the module on the Visual System on
your CD to investigate the visual
pathways to the LGN.
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HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 283
find an unexpected heterogeneity in region V1. So they sectioned
the V1 layers in such a way that each cortical layer was in one
plane of section,much like peeling off the layers of an onion and
laying them flat on a table. The surface of each flattened layer can
then be viewed from above.
As Figure 8-18 illustrates, the heterogeneous cytochrome
staining now appeared as random blobs in the layers of V1. In
fact, these darkened regions have become known as blobs, and the less-dark regions
separating them have become known as interblobs. Blobs and interblobs serve different
functions. Neurons in the blobs take part in color perception, whereas neurons in
the interblobs participate in form and motion perception. So, within region V1, input
that arrives in the parvo- and magnocellular pathways of the geniculostriate system is
segregated into three separate types of information: color, form, and movement.
This information is then sent to region V2, which lies next to region V1. Here the
color, form, and movement inputs remain segregated.This segregation can again be seen
through the pattern of cytochrome oxidase staining, but the staining pattern is different
from that in region V1. Figure 8-19 shows that region V2 has a pattern of thick and thin
stripes that are intermixed with pale zones. The thick stripes receive input from the
V1
V1
V4
V3
V3A
V2
V5
V2
V2
V3
V3A
V2
V3
V3A
V1 = Primary visual cortex
V2–V5 = Extrastriate cortex
V3
V3A
V4
(A) Medial view of
functional areas
(B) Lateral view of
functional areas
Figure 8-17
Visual Regions of the Occipital Lobe
Thin
Thick
Blobs
Interblobs
Pale
V2
V1
Stripes
Figure 8-18
Heterogeneous Layering The blobs in
region V1 and the stripes in region V2
are illustrated in this drawing of a
flattened section through the visual
cortex. The blobs and stripes can be
visualized by using a special stain for
cytochrome oxidase, which is a marker
for mitochondria.
Extrastriate
cortex
Interblob regions
Ventral
stream
Striate
cortex (V1)
Temporal
lobe (TE)
Parietal
lobe (PG)
Extrastriate
cortex (V2)
V3A (form)
V5 (motion)
V3 (dynamic form)
V4 (color form)
Dorsal stream
Ventral stream
Form Movement
Parietal lobe
Temporal lobe
Blobs
(color)
Thick
Thin
Extrastriate
cortex
Dorsal
stream
Lateral
geniculate
nucleus
Figure 8-19
Charting the Dorsal and Ventral Streams The dorsal stream, which controls visual action, begins
in region V1 and flows through region V2 to the other occipital areas and finally to the parietal
cortex, ending in an area of the parietal lobe referred to as PG. The ventral stream, which controls
object recognition, begins in region V1 and flows through region V2 to the other occipital areas
and finally to the temporal cortex, ending in an area of the temporal lobe referred to as TE. The
flow of information from the subregions of V1 (blobs and interblobs) is to the thick, thin, and pale
zones of V2. Information in the thin and pale zones goes to regions V3 and V4 to form the ventral
stream. That in the thick and pale zones goes to regions V3A and V5 to form the dorsal stream.
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284 ! CHAPTER 8
movement-sensitive neurons in region V1; the thin stripes receive input from V1’s colorsensitive
neurons; and the pale zones receive input from V1’s form-sensitive neurons.
As diagrammed in Figure 8-19, the visual pathways proceed from region V2 to the
other occipital regions and then to the parietal and temporal lobes, forming the dorsal
and ventral streams. Although many parietal and temporal regions take part, the major
regions are region G in the parietal lobe (thus called region PG) and region E in the
temporal lobe (thus called region TE).
Within the dorsal and ventral streams, the function of the visual pathways becomes
far more complex than a simple record of color, form, and movement.Rather, the color,
form, and movement information is put together to produce a rich, unified visual
world made up of complex objects, such as faces and paintings, and complex visuomotor
skills, such as catching a ball. The functions of the dorsal and ventral streams
are therefore complex, but they can be thought of as consisting of “how” functions and
“what” functions.“How” is action to be visually guided toward objects, whereas “what”
identifies what an object is.
LOCATION IN THE VISUAL WORLD
One aspect of visual information that we have not yet considered is location. As we
move around, going from place to place, we encounter objects in specific locations. Indeed,
if we had no sense of location, the world would be a bewildering mass of visual
information. Our next task, then, is to look at how the brain constructs a spatial map
from this complex array of visual input.
The coding of location begins in the retina and is maintained throughout all the
visual pathways. To understand how this spatial coding is accomplished, you need to
imagine your visual world as seen by your two eyes. Imagine the large red and blue rectangles
in Figure 8-20 as a wall. Focus your gaze on the black cross in the middle of
the wall.
All of the wall that you can see without moving your head is your visual field. The
visual field can be divided into two halves, the left and right visual fields, by drawing a
vertical line down the middle of the black cross. Now recall from Figure 8-11 that the
left half of each retina looks at the right side of the visual field, whereas the right half
of each retina looks at the visual field’s left side. This means that input from the right
In Review .
Vision begins when photoreceptors in the retina at the back of the eye convert light energy
into neural activity in neighboring ganglion cells, the axons of which form the optic
nerve leading to the brain. P ganglion cells receive input mostly from cones and carry information
about color and fine detail, whereas M ganglion cells receive input mostly from
rods and carry information about light but not color. Visual input takes two routes into the
brain. The geniculostriate pathway travels through the LGN of the thalamus to layer IV of
the striate cortex in the occipital lobe. The tectopulvinar pathway is from the tectum of the
midbrain to the pulvinar of the thalamus and then to visual cortical areas. Both pathways
contribute to the dorsal and ventral visual streams that project to the parietal and temporal
lobes, respectively. The dorsal stream to the parietal lobe processes the visual guidance
of movements (the how), whereas the ventral stream to the temporal lobe processes the
visual perception of objects (the what).
Visual field. Region of the visual world
that is seen by the eyes.
Receptive field. Region of the visual
world that stimulates a receptor cell or
neuron.
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HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 285
visual field goes to the left hemisphere, whereas
input from the left visual field goes to the right
hemisphere.
Therefore the brain can easily determine
whether visual information is located to the left
or right of center. If input goes to the left hemisphere,
the source must be in the right visual field;
if input goes to the right hemisphere, the source
must be in the left visual field. This arrangement
tells you nothing about the precise location of an
object in the left or right side of the visual field,
however.To understand how precise spatial localization
is accomplished, we must return to the
retinal ganglion cells.
Coding Location in the Retina
Look again at Figure 8-9 and you can see that each retinal ganglion cell receives input
through bipolar cells from several photoreceptors. In the 1950s, Stephen Kuffler, a pioneer
in studying the physiology of the visual system, made an important discovery
about how photoreceptors and ganglion cells are linked. By shining small spots of light
on the receptors, he found that each ganglion cell responds to stimulation on just
a small circular patch of the retina. This patch became known as the ganglion cell’s
receptive field.
A ganglion cell’s receptive field is therefore the region of the retina on which it is
possible to influence that cell’s firing. Stated differently, the receptive field represents
the outer world as seen by a single cell. Each ganglion cell sees only a small bit of the
world, much as you would if you looked through a narrow cardboard tube. The visual
field is composed of thousands of such receptive fields.
Now let us consider how receptive fields enable the visual system to interpret the
location of objects. Imagine that the retina is flattened like a piece of paper. When a
tiny light is shone on different parts of the retina, different ganglion cells respond. For
example, when a light is shone on the top-left corner of the flattened retina, a particular
ganglion cell responds because that light is in its receptive field. Similarly, when a
light is shone on the top-right corner, a different ganglion cell responds.
By using this information, we can identify the location of a light on the retina by
knowing which ganglion cell is activated.We can also interpret the location of the light
in the outside world because we know where the light must come from to hit a particular
place on the retina. For example, light from above hits the bottom of the retina
after passing through the eye’s lens, whereas light from below hits the top of the retina.
(Refer to Figure 8-3 to see why this is so.) Information at the top of the visual field will
stimulate ganglion cells on the bottom of the retina, whereas information at the bottom
of the field will stimulate ganglion cells on the top of the retina.
Location in the LGN and Cortical Region V1
Now consider the connection from the ganglion cells to the lateral geniculate nucleus.
In contrast with the retina, the LGN is not a flat sheet; rather, it is a three-dimensional
structure in the brain.We can compare it to a stack of cards, with each card representing
a layer of cells.
Left visual field Right visual field Figure 8-20
Visual Field Demonstration As you
focus on the cross at the center of the
figure, the information at the left of
this focal point forms the left visual
field (red) and travels to the right
hemisphere. The information to the
right of the focal point forms the
right visual field (blue) and travels to
the left hemisphere. The visual field
can be broken horizontally as well so
that information above the focal
point is in the upper visual field and
that below the focal point is in the
lower visual field.
On your CD, find the area on the
optic chiasm in the module on the Visual
System to better understand the concept
of visual fields.
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Figure 8-21 shows how the connections from the retina to the LGN can represent
location. A retinal ganglion cell that responds to light in the top-left corner of the
retina connects to the left side of the first card.A retinal ganglion cell that responds to light
in the bottom-right corner of the retina connects to the right side of the last card. In this
way, the location of left–right and top–bottom information is maintained in the LGN.
Like the ganglion cells, each of the LGN cells has a receptive field, which is the region
of the retina that influences its activity. If two adjacent retinal ganglion cells
synapse on a single LGN cell, the receptive field of that LGN cell will be the sum of the
two ganglion cells’ receptive fields. As a result, the receptive fields of LGN cells can be
bigger than those of retinal ganglion cells.
The LGN projection to the striate cortex (region V1)
also maintains spatial information.As each LGN cell, representing
a particular place, projects to region V1, a topographic
representation, or topographic map, is produced in
the cortex. As illustrated in Figure 8-22, this representation
is essentially a map of the visual world.
The central part of the visual field is represented at the
back of the brain, whereas the periphery is represented
more anteriorly. The upper part of the visual field is represented
at the bottom of region V1, the lower part at the top
of V1. The other regions of the visual cortex (such as V3, V4,
and V5) also have topographical maps similar to that of V1.
Thus the V1 neurons must project to the other regions in an
orderly manner, just as the LGN neurons project to region
V1 in an orderly way.
Within each visual cortical area, each neuron has a receptive
field corresponding to the part of the retina to which
the neuron is connected. As a rule of thumb, the cells in the
cortex have much larger receptive fields than those of retinal
ganglion cells. This increase in receptive-field size means
that the receptive field of a cortical neuron must be composed
of the receptive fields of many retinal ganglion cells,
as illustrated in Figure 8-23.
There is one additional wrinkle to the organization of
topographic maps. Jerison’s principle of proper mass, which
286 ! CHAPTER 8
Topographic map. A neural
representation of the external world.
Retina
LGN
LGN
Figure 8-21
Receptive Field Projection The information
from a receptive field retains its spatial relation
when it is sent to the lateral geniculate nucleus
(LGN). In this example, information at the top
of the visual field goes to the top of the LGN
and information from the bottom of the visual
field goes to the bottom of the LGN. Similarly,
information from the left or right goes to the
left or right of the LGN, respectively.
Right visual cortex
Left visual field (projecting
to right visual cortex)
Fovea
The central part of
the visual field…
1
The peripheral areas of
the visual field are
located more anteriorly.
3
…is represented at
the back of the brain.
2
The top part of the visual field
is represented in the lower
part of the occipital lobe.
4
Periphery
Figure 8-22
Topographic Organization of the
Visual Cortex (V1) In the right
occipital lobe, the area of left central
vision (the fovea) is represented at the
back of the brain, whereas the more
peripheral visual areas are represented
more anteriorly. The fovea also occupies
a disproportionately large part of the
cortex, which is why visual acuity is best
in the central part of the visual field.
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we applied to overall brain size in Chapter 1, states that the amount of neural tissue responsible
for a particular function is equivalent to the amount of neural processing required
for that function. Jerison’s principle can be extended to regions within the brain as
well. The visual cortex provides some good examples.
You can see in Figure 8-22 that not all parts of the visual field are equally represented
in region V1. The small, central part of the visual field that is seen by the fovea
is represented by a larger area in the cortex than the visual field’s periphery, even
though the periphery is a much larger part of the visual field. In accord with Jerison’s
principle, we would predict more processing of foveal information in region V1 than
of peripheral information. This prediction makes intuitive sense because we can see
more clearly in the center of the visual field than at the periphery. In other words, sensory
areas that have more cortical representation provide a more detailed creation of
the external world.
The Visual Corpus Callosum
The creation of topographic maps based on the receptive fields of neurons is an effective
way for the brain to code the location of objects. But, if the left visual field is represented
in the right cerebral hemisphere and the right visual field is represented in the
left cerebral hemisphere, how are the two halves of the visual field ultimately bound together
in a unified representation of the world? After all, we have the subjective impression
not of two independent visual fields, but rather of a single, continuous field
of vision. The answer to how this unity is accomplished lies in the corpus callosum,
which binds the two sides of the visual field at the midline.
Until the 1950s, the function of the corpus callosum was largely a mystery. Physicians
had occasionally cut it to control severe epilepsy, as described in “Epilepsy”on page
000, or to reach a very deep tumor, but patients did not appear to be much affected by
this surgery.The corpus callosum clearly linked the
two hemispheres of the brain, but exactly which
parts were connected was not yet known.
We now realize that the corpus callosum connects
only certain brain structures.Whereas much
of the frontal lobes have callosal connections, the
occipital lobes have almost none, as shown in Figure
8-24. If you think about it, there is no reason
for a neuron in the visual cortex that is “looking at”
one place in the visual field to be concerned with
what another neuron in the opposite hemisphere is
“looking at” in another part of the visual field.
Cells that lie along the midline of the visual
field are an exception, however. These cells would
HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 287
On the CD, find the area on the
higher-order visual cortex in the module
on the Visual System to investigate the
location and anatomy of the LGN.
The receptive fields
of many retinal
ganglion cells…
…combine to form
the receptive field
of a single LGN cell.
The receptive fields of many
LGN cells combine to form the
receptive field of a single V1 cell.
Figure 8-23
Receptive Field Hierarchy The
receptive fields of region V1 neurons
are constructed from those of lateral
geniculate (LGN) cells, which, in turn, are
constructed from those of ganglion cells.
The receptive field of a single ganglion
cell is small. In this example, the
receptive fields of the LGN cells are the
summation of the fields of four ganglion
cells. The receptive field of the V1 cell is
the sum of the four LGN cells.
Corpus callosum
Parietal
lobe
Temporal
lobe
Frontal
lobe
Occipital
lobe
…whereas the
occipital lobes
have almost no
connections.
Most of the two
frontal lobes
have corpus
callosum
connections,...
Figure 8-24
Callosal Connections The
darker areas indicate regions of
the cortex of a rhesus monkey
that receive projections from the
opposite hemisphere by means of
the corpus callosum. Most of the
occipital lobe has no such
connections.
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288 ! CHAPTER 8
be “looking at” adjacent places in the field of vision, one slightly to the left of center
and one slightly to the right. If connections existed between such cells, we could zip the
two visual fields together by combining their receptive fields to cross at the midline,
which is exactly what happens.Cortical cells with receptive fields that lie along the midline
of your field of vision are connected to one another through the corpus callosum
so that their receptive fields overlap the midline. The two fields thus become one.
NEURAL ACTIVITY
The pathways of the visual system are made up of individual neurons. By studying how
these cells behave when their receptive fields are stimulated, we can begin to understand
how the brain processes different features of the visual world beyond just the locations
of light. To illustrate, we examine how neurons from the retina to the temporal
cortex respond to shapes and colors.We then briefly consider how neurons in the dorsal
stream behave.
Seeing Shape
Imagine that we have placed a microelectrode near a neuron somewhere in the visual
pathway from retina to cortex and are using that electrode to record changes in
the neuron’s firing rate. This neuron occasionally fires spontaneously, producing action
potentials with each discharge. Let us assume that the neuron discharges, on
the average, once every 0.08 second. Each action potential is brief, on the order of 1
millisecond.
If we plot action potentials spanning a second, we see only spikes in the record because
the action potentials are so brief. (Refer to Figure 4-12 for an illustration of this
effect.) Figure 8-25A is a single-cell recording in which there are 12 spikes in the span
of 1 second. If the firing rate of this cell increases, we will see more spikes (Figure 8-
25B). If the firing rate decreases, we will see fewer spikes (Figure 8-25C). The increase
in firing represents excitation of the cell, whereas the decrease represents inhibition.
Excitation and inhibition, as you know, are the principal mechanisms of information
transfer in the nervous system.
Now suppose we present a stimulus to the neuron by illuminating its receptive field
in the retina, perhaps by shining a light stimulus on a blank screen within the cell’s visual
field.We might place before the eye a straight line positioned at a 45° angle. The cell
In Review .
The brain can determine the location of a particular stimulus because each neuron of the
visual system connects to only a small part of the retina, known as that neuron’s receptive
field. Each receptive field, in turn, receives input from only a small part of the visual field,
and so which part of the retina is stimulated effectively detects exactly where the light
source is positioned in the environment. This location-detecting method is maintained at
different levels in the visual system, from the ganglion cells of the retina to the neurons of
the LGN in the thalamus to the neurons of the primary visual cortex. Inputs to different
parts of cortical region V1 from different parts of the retina essentially form a topographic
map of the visual world within the brain. Cells with receptive fields that lie along the midline
of the field of vision are connected by the corpus callosum, binding the two sides of
the visual world together as one.
Go to the area on the primary visual
cortex in the module on the Visual System
on your CD to learn more about how
shape is perceived within the cortex.
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HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 289
could respond to this stimulus either by increasing
or decreasing its firing rate. In either case, we would
conclude that the cell is creating information about
the line.
Note that the same cell could show excitation
to one stimulus, inhibition to another stimulus,
and no reaction at all. For instance, the cell could
be excited by lines oriented 45° to the left and inhibited
by lines oriented 45° to the right. Similarly,
the cell could be excited by stimulation in one
part of its receptive field (such as the center) and
inhibited by stimulation in another part (such as
the periphery).
Finally,we might find that the cell’s response to
a particular stimulus is selective. Such a cell would
be telling us about the importance of the stimulus
to the animal. For instance, the cell might fire (be excited) when a stimulus is presented
with food but not fire (be inhibited) when the same stimulus is presented alone. In each
case, the cell is selectively sensitive to characteristics in the visual world.
Now we are ready to move from this hypothetical example to what visual neurons
actually do when they process information about shape. Neurons at each level of the
visual system have distinctly different characteristics and functions. Our goal is not to
look at each neuron type but rather to consider generally how some typical neurons at
each level differ from one another in their contributions to processing shape.We focus
on neurons in three areas: the ganglion-cell layer of the retina, the primary visual cortex,
and the temporal cortex.
PROCESSING IN RETINAL GANGLION CELLS
Cells in the retina do not actually see shapes. Shapes are constructed by processes in
the cortex from the information that ganglion cells pass on about events in their receptive
fields. Keep in mind that the receptive fields of ganglion cells are very small
dots. Each ganglion cell responds only to the presence or absence of light in its receptive
field, not to shape.
The receptive field of a ganglion cell has a concentric circle arrangement, as illustrated
in Figure 8-26A. A spot of light falling in the central circle of the receptive
(A) Baseline (12 per second)
0 0.25 0.50 0.75 1.0
Time (seconds)
(B) Excitation
0.50
0.50
0 0.25 0.75 1.0
0.25 0.75
Time (seconds)
(C) Inhibition
0 1.0
Time (seconds)
Figure 8-25
Recording Neural Stimulation
When visually responsive neurons
encounter a particular stimulus in
their visual fields, they may show
either excitation or inhibition.
(A) At the baseline firing rate of
a neuron, each action potential
is represented by a spike. In a
1-second time period, there
were 12 spikes. (B) Excitation is
indicated by an increase in firing
rate over baseline. (C) Inhibition is
indicated by a decrease in firing
rate under baseline.
(A) On-center cell’s
receptive field
ON
OFF
Light strikes
center
ON
OFF
Light stimulus in a part of the
visual field
Response of cell to stimulus at left
0 1 Excitation 2 3
Time (seconds)
Inhibition
Light strikes
surround
0 1 2 3
Time (seconds)
(B) Off-center cell’s
receptive field
ON
OFF
ON
OFF
Light strikes
center
0 1 Inhibition 2 3
Time (seconds)
Excitation
Light strikes
surround
0 1 2 3
Time (seconds)
Figure 8-26
On–Off Receptivity (A) In the
receptive field of a retinal ganglion cell
with an on-center and off-surround, a
spot of light placed on the center causes
excitation in the neuron, whereas a spot
of light in the surround causes inhibition.
When the light in the surround region is
turned off, firing rate increases briefly
(called an “offset” response). A light
shining in both the center and the
surround would produce a weak increase
in firing in the cell. (B) In the receptive
field of a retinal ganglion cell with an
off-center and on-surround, light in the
center produces inhibition, whereas light
on the surround produces excitation, and
light across the entire field produces
weak inhibition.
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290 ! CHAPTER 8
field excites some of these cells, whereas a spot of light falling in the surround
(periphery) of the receptive field inhibits the cell. A spot of light
falling across the entire receptive field causes a weak increase in the cell’s
rate of firing.
This type of neuron is called an on-center cell. Other ganglion cells,
called off-center cells, have the opposite arrangement, with light in the center
of the receptive field causing inhibition, light in the surround causing
excitation, and light across the entire field producing weak inhibition (Figure
8-26B). The on–off arrangement of ganglion-cell receptive fields makes
these cells especially responsive to very small spots of light.
This description of ganglion-cell receptive fields might mislead you
into thinking that they form a mosaic of discrete little circles on the retina
that do not overlap. In fact, neighboring retinal ganglion cells receive their
inputs from an overlapping set of receptors. As a result, their receptive fields
overlap, as illustrated in Figure 8-27. In this way, a small spot of light shining
on the retina is likely to produce activity in both on-center and off-center ganglion
cells.
How can on-center and off-center ganglion cells tell the brain anything about
shape? The answer is that a ganglion cell is able to tell the brain about the amount of
light hitting a certain spot on the retina compared with the average amount of light
falling on the surrounding retinal region. This comparison is known as luminance
contrast.
To understand how this mechanism tells the brain about shape, consider the hypothetical
population of on-center ganglion cells represented in Figure 8-28. Their receptive
fields are distributed across the retinal image of a light–dark edge. Some of the
ganglion cells have receptive fields in the dark area, others have receptive fields in the
light area, and still others have fields that straddle the edge
of the light.
The ganglion cells with receptive fields in the dark or
light areas are least affected because they experience either
no stimulation or stimulation of both the excitatory and
the inhibitory regions of their receptive fields. The ganglion
cells most affected by the stimulus are those lying
along the edge. Ganglion cell B is inhibited because the
light falls mostly on its inhibitory surround, and ganglion
cell D is excited because its entire excitatory center is stimulated
but only part of its inhibitory surround is.
Consequently, information transmitted from retinal
ganglion cells to the visual areas in the brain does not give
equal weight to all regions of the visual field. Rather, it emphasizes
regions containing differences in luminance. Areas
with differences in luminance are found along edges. So retinal ganglion cells are really
sending signals about edges, and edges are what form shapes.
PROCESSING IN THE PRIMARY VISUAL CORTEX
Now consider cells in region V1, the primary visual cortex, that receive their visual inputs
from LGN cells, which in turn receive theirs from retinal ganglion cells. Because
each V1 cell receives input from multiple retinal ganglion cells, the receptive fields of
the V1 neurons are much larger than those of retinal neurons. Consequently, the V1
cells respond to stimuli more complex than simply “light on” or “light off.” In particular,
these cells are maximally excited by bars of light oriented in a particular direction
rather than by spots of light. These cells are therefore called orientation detectors.
Receptive fields of
neighboring ganglion cells
Two overlapping
receptive fields
The receptive fields of
retinal ganglion cells
overlap extensively…
…and so any two adjacent
fields look at almost the
same part of the world.
Figure 8-27
Overlapping Receptive Fields
Cell
response rate
Light–dark edge
Spontaneous level of activity
On-center ganglion cells
Position
A
B
C D
E
Figure 8-28
Activity at the Margins Responses of
a hypothetical population of on-center
ganglion cells whose receptive fields
(A–E) are distributed across a light–dark
edge. The activity of the cells along the
edge is most affected relative to those
away from the edge. Adapted from
Neuroscience (p. 195), edited by D. Purves,
G. J. Augustine, D. Fitzpatrick, L. C. Katz, A.-S.
LaMantia, and J. O. McNamara, 1997, Sunderland,
MA: Sinauer.
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HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 291
Like the ganglion cells, some orientation detectors have an on–off arrangement in
their receptive fields, but the arrangement is rectangular rather than circular. Visual
cortex cells with this property are known as simple cells. Typical receptive fields for simple
cells in the primary visual cortex are shown in Figure 8-29.
Simple cells are not the only kind of orientation detector in the primary visual cortex;
several functionally distinct types of neurons populate region V1. For instance, complex
cells such as those in Figure 8-30 have receptive fields that are maximally excited by
bars of light moving in a particular direction through the visual field. A hypercomplex
cell, like a complex cell, is maximally responsive to moving bars but also has a strong inhibitory
area at one end of its receptive field. As illustrated in Figure 8-31, a bar of light
Visit the area on the eye in the Visual
System module of your CD to learn more
about on-center and off-center ganglion
cells.
OFF
OFF
OFF
ON
OFF
(A) Horizontally aligned preferred orientation
No stimulus
Simple cell's
receptive
field
Light
Light
Light
Light
(B) Oblique preferred orientation
No stimulus
OFF
OFF
ON
OFF
ON
OFF
OFF
ON
OFF
OFF
OFF
ON
ON
Baseline response
Strong response
No response
Baseline response
No response
Strong response
Figure 8-29
Typical Receptive Fields for Simple Visual Cortex Cells
Simple cells respond to a bar of light in a particular
orientation, such as horizontal (A) or oblique (B). The
position of the bar in the visual field is important, because
the cell either responds (ON) or does not respond (OFF) to
light in adjacent regions of the visual field.
Complex cell’s
receptive field
No stimulus
Stimulus at 45°
Stimulus at 45°
Baseline response
Strong response
Light
Strong response
Stimulus at 60° Weak response
Stimulus at 15° No response
Figure 8-30
Receptive Field of a Complex Cell in the Visual
Cortex Complex cells respond to bars of light that
move across their circular receptive fields at a particular
angle. Unlike a simple cell’s on–off response pattern, a
complex cell shows the same response throughout the
field, responding best when the bar is at a particular
orientation. Its response is reduced or does not occur
with the bar of light at other orientations.
Luminance contrast. The amount of
light reflected by an object relative to its
surroundings.
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292 ! CHAPTER 8
landing on the right side of the hypercomplex cell’s receptive field excites the cell, but,
if the bar lands on the inhibitory area to the left, the cell’s firing is inhibited.
Note that each class of V1 neurons responds to bars of light in some way, yet this
response results from input originating in retinal ganglion cells that respond maximally
not to bars but to spots of light. How does this conversion from responding to
spots to responding to bars take place? An example will help explain the process.
A thin bar of light falls on the retinal photoreceptors, striking the receptive fields
of perhaps dozens of retinal ganglion cells. The input to a V1 neuron comes from a
group of ganglion cells that happen to be aligned in a row, as in Figure 8-32. That V1
neuron will be activated (or inhibited) only when a bar of light hitting the retina strikes
that particular row of ganglion cells. If the bar of light is at a slightly different angle,
only some of the retinal ganglion cells in the row will be activated, and so the V1 neuron
will be excited only weakly.
Figure 8-32 illustrates the connection between light striking the retina in a certain
pattern and the activation of a simple cell in the primary visual cortex, one that responds
to a bar of light in a particular orientation. Using the same logic, we can also
diagram the retinal receptive fields of complex or hypercomplex V1 neurons. Try this
as an exercise yourself by adapting the format in Figure 8-32.
A characteristic of cortical structure is that the neurons are organized into functional
columns. Figure 8-33 shows such a column, a 0.5-millimeter-diameter strip of
OFF
OFF
Hypercomplex cell’s
receptive field
No stimulus
Strong response
Strong response
Weak response
No response
ON
ON
ON
Baseline response
OFF ON
ON
Figure 8-31
Receptive Field of a Hypercomplex
Cell A hypercomplex cell responds to a
bar of light in a particular orientation
(e.g., horizontal) anywhere in the
excitiatory (ON) part of its receptive field.
If the bar extends into the inhibitory area
(OFF), no response occurs.
V1 neuron
– –
– –
OFF
ON
+ +
+
+
+
+ +
OFF
ON
+
+
+
Strong response
Weak response
Each circle
represents the
receptive field of a
ganglion cell.
Stimulation of a subset of
on-center ganglion cells
excites a V1 neuron
through connections in
the LGN (not shown here).
Figure 8-32
V1 Receptivity A V1 cell responds to a row of ganglion cells in a particular
orientation on the retina. The bar of light strongly activates a row of
ganglion cells, each connected through the LGN to a V1 neuron. The activity
of this V1 neuron is most affected by a bar of light at a 45° angle.
Ocular-dominance column.
Functional column in the visual cortex
maximally responsive to information
coming from one eye.
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cortex that includes neurons and their connections. The pattern of connectivity in a
column is vertical: inputs arrive in layer IV and then connect with cells in the other
layers.
The neurons within a column have similar functions. For example, Figure 8-34A
shows that neurons within the same column respond to lines oriented in the same direction.
Adjacent columns house cells that are responsive to different line orientations.
Figure 8-34B shows the columns of input coming from each eye, discussed earlier,
called ocular-dominance columns. So the visual cortex has both orientation columns
housing neurons of similar sensitivity and ocular-dominance columns with input from
one eye or the other.
PROCESSING IN THE TEMPORAL CORTEX
Finally, in regard to seeing shapes, consider neurons along the ventral stream in region
E of the temporal lobe (see Figure 8-19). Rather than being responsive to spots
or bars of light, these TE neurons are maximally excited by complex visual stimuli,
such as faces or hands, and can be remarkably specific in their responsiveness. They
may be responsive to particular faces seen head-on, to faces viewed in profile, to the
posture of the head, or even to particular facial expressions.
How far does this specialized responsiveness extend? Would it be practical to have
visual neurons in the temporal cortex specialized to respond to every conceivable feature
I
II
III
IV
Input destined
for layer IV
Stellate
cells
V
VI
Output
Pyramidal
cell
Vertical
column
Visual
cortex
Figure 8-33
Neural Circuit in a Column in the Visual Cortex In this stereoscopic view, the sensory inputs
terminate on stellate cells in layer IV. These stellate cells synapse in layers III and V with pyramidal
cells in the same vertical column of tissue. Thus the flow of information is vertical. The axons of the
pyramidal cells leave the column to join with other columns or structures. Adapted from “The ‘Module-
Concept’ in Cerebral Architecture,” by J. Szentagothai, 1975, Brain Research, 95, p. 490.
I
II & III
IV
V
VI
R
L
L R
(A)
(B)
Adjacent columns house
neurons that are responsive
to slightly different line
orientations, forming an
array of 180°.
Ocular-dominance columns
receive input from the right
or left eye.
Every neuron in the same
column has the same
orientation bias.
Figure 8-34
Organization of Functional Columns in
the Primary Visual Cortex (A) Cells
with the same orientation preference
are found throughout a column.
Adjacent columns have orientation
preferences that are slightly different
from one another. (B) Ocular-dominance
columns are arranged at right angles to
the orientation columns, producing a
three-dimensional organization of the
visual cortex. The ocular-dominance
columns alternate from left (L) to right
(R) across the primary visual cortex, with
two such alternations illustrated here.
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of objects? Keiji Tanaka (1993) approached this question by presenting monkeys
with many three-dimensional representations of animals and plants to find
stimuli that are effective in activating particular neurons of the inferior temporal
cortex.
Having identified stimuli that were especially effective, such as faces or
hands, he then wondered which specific features of those stimuli are critical to
stimulating the neurons. Tanaka found that most neurons in area TE require
rather complex features for their activation. These features include a combination
of characteristics such as orientation, size, color, and texture. Furthermore,
neurons with similar, although slightly different, responsiveness to particular
features tend to cluster together in columns, as shown in Figure 8-35.
Apparently, then, an object is not represented by the activity of a single neuron.
Rather, objects are represented by the activity of many neurons with slightly
varying stimulus specificity that are grouped together in a column. This finding
is important because it provides an explanation for stimulus equivalence, recognizing
an object as remaining the same despite being viewed from different
orientations.
Think of how the representation of objects by multiple neurons in a column
can produce stimulus equivalence. If each neuron in the column module varies
slightly in regard to the features to which it responds but the effective stimuli largely
overlap, the effect of small changes in incoming visual images will be minimized and
we will continue to perceive an object as the same thing.
Another remarkable feature of neurons of the inferior temporal cortex in monkeys
is that their stimulus specificity is altered by experience. If monkeys are trained to discriminate
particular shapes to obtain a food reward, not only do they improve their
discriminatory ability, but neurons in the temporal lobe also modify their preferred
stimuli to fire maximally to some of the stimuli used in training. This result shows that
the temporal lobe’s role in visual processing is not determined genetically but is instead
subject to experience, even in adults.
We can speculate that this experience-dependent characteristic evolved because
it allows the visual system to adapt to different demands in a changing visual environment.
Think of how different the demands on your visual recognition abilities are
when you move from a dense forest to a treeless plain to a city street. The visual neurons
of your temporal cortex can adapt to these differences (Tanaka, 1993). In addition,
experience-dependent visual neurons ensure that people can identify visual stimuli
that were never encountered as the human brain evolved.
Note that the preferred stimuli of neurons in the primary visual cortex are not
modified by experience, which implies that the stimulus preferences of V1 neurons are
genetically programmed. In any case, the functions of the V1 neurons provide the
building blocks for the more complex and flexible characteristics of the inferior temporal
cortex neurons.
Seeing Color
Scientists have long wondered how people are able to see a world so rich in color. Recall
from Chapter 1 the hypothesis that color vision evolved in primates whose diets
require them to identify ripe fruits or to avoid predators or other dangers. Another explanation
has its roots in the Renaissance, when painters discovered that they could
obtain the entire range of colors in the visual world by mixing only three colors of paint
(red, blue, and yellow), the process of subtractive color mixing.
294 ! CHAPTER 8
I
II & III
IV
V
VI
Temporal
lobe
Neurons in the
temporal lobe
form columns
that respond to
categories of shapes.
Figure 8-35
Columnar Organization of Area TE
Neurons with similar but slightly
different pattern selectivity cluster in
vertical columns, perpendicular to the
cortical surface.
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HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 295
Although people at the time did not understand the basis of this three-color
(trichromatic) mixing, we now know that color mixing is a property of the cones in the
retina. The primary colors of light, unlike those used by painters, are red, blue, and
green. Light of different wavelengths stimulates the three different types of cone receptors
in different ways, and the ratio of the activity of these three receptor types creates
our impression of different colors.
TRICHROMATIC THEORY
To see how the process works, look back at Figure 8-7. Light at 500 nanometers on the
horizontal axis excites short-wavelength receptors to about 30 percent of their maximum,
medium-wavelength receptors to about 65 percent of their maximum, and longwavelength
receptors to about 40 percent of their maximum. In contrast, a light at
600 nanometers excites these receptors to about 0, 25, and 75 percent of maximum,
respectively.
According to the trichromatic theory, the color that we see—in this case, blue
green at 500 nm and orange at 600 nm—is determined by the relative responses of the
different cone types. If all three cone types are equally active, we see white.
The trichromatic theory predicts that, if we lack one type of cone receptor, we cannot
process as many colors as we can with all three types, which is exactly what happens
when a person is born with only two cone types. The colors that the person is
unable to create depend on which receptor type is missing.
The most common deficiency, as mentioned earlier in this chapter, is red–green
color blindness, which afflicts about 5 percent of males and 0.5 percent of females. It
is caused by the absence of either the medium-wavelength or the long-wavelength receptor.
If a person is missing two types of cones, he or she cannot see any color, as the
trichromatic theory also predicts.
Notice that the mere presence of cones in an animal’s retina does not mean that
the animal has color vision. It simply means that the animal has photoreceptors that
are particularly sensitive to light.Many animals lack color vision as we know it, but the
only animal with eyes known to have no cones at all is a fish, the skate.
As helpful as the trichromatic theory is in explaining color blindness, it cannot explain
everything about human color vision—for example, the sense that, rather than
three primary colors, there are actually four “basic” colors (red, green, yellow, and
blue). A curious property of these four colors is that they seem to be linked as two pairs
of opposites, a red-and-green pair and a yellow-and-blue pair. Why do we call these
paired colors opposites?
You can see why by staring at one or more of these colors and then looking at a
white surface. Try staring first at the red and blue box in Figure 8-36 for about a minute
and then at the white box next to it.When you shift your gaze to the white surface, you
Go to the area on the eye in the
module on the Visual System on your CD.
Review the process of color vision and
move the wavelength to different locations
so that you can note the receptor ratios
involved in processing them.
Trichromatic theory. Explanation of
color vision based on the coding of three
primary colors: red, green, and blue.
People with deficiencies in red–green color
perception have difficulty seeing the
numbers within the circles.
Figure 8-36
Demostrating Opposing Color Pairs
Stare at the rectangle on the left for
about 30 seconds. Then stare at the
white box. You will experience an
afterimage of green on the red side
and of yellow on the blue side.
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296 ! CHAPTER 8
will experience a color afterimage in the color opposites of red and blue—that is, green
and yellow. Conversely, if you stare at a green and yellow box and then shift to white,
you will see a red and blue afterimage. These observations are not easily explained by
the trichromatic theory.
OPPONENT-PROCESS THEORY
In 1874, Ewald Hering, a German physiologist, proposed an explanation of human color
vision that also accounts for color afterimages.He argued that color vision is mediated by
opponent processes in the retina. Remember that retinal ganglion cells have an on–off/
center–surround organization.That is, stimulation to the center of the neuron’s receptive
field is either excitatory (in some cells) or inhibitory (in other cells),whereas stimulation
to the periphery of the receptive field has the opposite effect (see Figure 8-26).
You can probably guess how this arrangement could be adapted to create color opponent-
process cells. If excitation is produced by one wavelength of light and inhibition
by another, cells would evolve that are excited by red and inhibited by green (or vice
versa), as would cells that are excited by blue and inhibited by yellow (or vice versa).
Red–green and blue–yellow would therefore be linked to each other as color opposites,
just as Hering’s opponent-process theory says.
In fact, about 60 percent of human retinal ganglion cells are color sensitive in this
way, with the center responsive to one wavelength and the surround to another. The
most common pairing, shown in Figure 8-37, is medium-wavelength (green) versus
Strong response
Weak response
Very strong response
(A) White light Baseline response
(B) Red light
(C) Green light
(C)Green light
(D) Red and
green light
(E) Green and No response
red light
Strong response
Figure 8-37
Opponent-Color Contrast Response
A red–green color-sensitive retinal
ganglion cell responds weakly to whitelight
illumination of its center and
surround (A) because red and green
cones absorb white light to similar
extents, and so their inputs cancel out.
The cell responds strongly to a spot of
red light in its center (B), as well as to
red’s paired wavelength, green, in the
surround. It is inhibited by a small spot of
green in its center (C). The cell responds
very strongly to simultaneous
illumination of the center with red and
the surround with green (D) and is
completely inhibited by the simultaneous
illumination of the center with green
and the surround with red (E).
Opponent-process theory.
Explanation of color vision that
emphasizes the importance of the
opposition of pairs of colors: red versus
green and blue versus yellow.
Color constancy. Phenomenon
whereby the perceived color of an object
tends to remain constant relative to other
colors, regardless of changes in
illumination.
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long-wavelength (red), but blue versus yellow cells also exist.Most likely, the
reason that opponent-process cells evolved is to enhance the relatively small
differences in spectral absorption of the three types of cones.
Cortical neurons in region V1 also respond to color in an opponentprocess
manner reminiscent of retinal ganglion cells. Recall that color inputs
in the primary visual cortex go to the blobs that appear in sections stained for
cytochrome oxidase (see Figure 8-18). These blobs are where the color-sensitive cells
are found.
Figure 8-38 illustrates how the color-sensitive cells in the blobs are organized relative
to the columns of orientation-sensitive cells and the ocular-dominance columns.
The color-sensitive cells in the blobs are inserted amid the orientation and oculardominance
columns. In this way, the primary visual cortex appears to be organized into
modules that include ocular-dominance and orientation columns as well as blobs. You
can think of it as being composed of several thousand modules, each analyzing color
and contour for a particular region of the visual world. This organization allows the
primary visual cortex to perform several functions concurrently.
How do neurons of the visual system beyond region V1 process color? You have already
learned that cells in region V4 respond to color, but, in contrast with the cells in
region V1, these V4 cells do not respond to particular wavelengths. Rather, they are responsive
to different perceived colors,with the center of the field being excited by a certain
color and the surround being inhibited.
Speculation swirls about the function of these V4 cells. One idea is that they are
important for color constancy, the property of color perception whereby colors appear
to remain the same relative to one another despite changes in light. For instance, if you
were to look at a bowl of fruit through light-green glasses, the fruit would take on a
greenish tinge, but bananas would still look yellow relative to red apples. If you removed
all the fruit except the bananas and looked at them through the tinted glasses,
the bananas would appear green because their color would not be relative to any other.
Monkeys with V4 lesions lose color constancy, even though they can discriminate different
wavelengths.
Neural Activity in the Dorsal Stream
A striking characteristic of many cells in the visual areas of the parietal cortex is that
they are virtually silent to visual stimulation when a person is under anesthesia. This
is true of neurons in the posterior parietal regions of the dorsal stream. In contrast,
cells in the temporal cortex do respond to visual stimulation even when a person is
anesthetized.
The silence on the part of posterior parietal cortex neurons under anesthesia
makes sense if their role is to process visual information for action. In the absence of
action when a person is unconscious, there is no need for processing. Hence the cells
are quiescent.
Cells in the dorsal stream are of many types, their details varying with the nature
of the movement in which a particular cell is taking part. One interesting category of
cells processes the visual appearance of an object to be grasped. For instance, if a monkey
is going to pick up an apple, these cells respond even when the monkey is only looking
at the apple. The cells do not respond when the monkey encounters the same apple
in a situation where no movement is to be made.
Curiously, these cells respond if the monkey merely watches another monkey
making movements to pick up the apple. Apparently, the cells have some sort of
HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 297
Ocular-dominance
columns
Hypercolumn
Orientation
columns
Color-sensitive
blobs
Striate cortex
R
L
L R
Figure 8-38
V1 Module This module of striate
cortex showing the orientation columns,
ocular-dominance columns, and colorsensitive
blobs is composed of two
hypercolumns. Each hypercolumn
consists of a full set (shown in red and
blue) of orientation columns spanning
180° of preferred angle as well as a pair
of blobs. All cells in the hypercolumn
share the same receptive field.
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298 ! CHAPTER 8
“understanding” of what is happening in the external world. But that understanding
is always related to action performed with respect to visually perceived objects. These
cells are what led David Milner and Mel Goodale (1995) to conclude that the dorsal
stream is a “how” visual system.
THE VISUAL BRAIN IN ACTION
Anatomical and physiological studies of brain systems leave one key question unanswered:
How do all the cells in these systems act together to produce a particular function?
One way to answer this question is to evaluate what happens when parts of the
visual system are dysfunctional.Then we can see how these parts contribute to the workings
of the whole.We will use this strategy to examine the neuropsychology of vision—
the study of the visual brain in action.
Injury to the Visual Pathway Leading
to the Cortex
Let us begin by seeing what happens when various parts of the visual pathway leading
from the eye to the cortex are injured. For instance, destruction of the retina or optic
nerve of one eye produces monocular blindness, the loss of sight in that eye. Partial destruction
of the retina or optic nerve produces a partial loss of sight in one eye, with
the loss restricted to the region of the visual field that has severed connections to the
brain.
Injuries to the visual pathway beyond the eye also produce blindness. For example,
complete cuts of the optic tract, the LGN, or region V1 of the cortex result in
homonymous hemianopia, which is blindness of one entire side of the visual field, as
In Review .
The brain perceives color, form, and motion on the basis of information provided by retinal
ganglion cells. Because luminance contrasts are located along the edges of shapes, ganglion
cells send inputs to the brain that are the starting points for shape analysis. Neurons
in the primary visual cortex then respond to more-complex properties of shapes, especially
bars of light oriented in a certain direction. A V1 neuron’s particular response pattern depends
on the spatial arrangement of the ganglion cells to which it is connected. Visual
analysis is completed in the temporal lobes, where neurons respond to complex visual
stimuli, such as faces. Color analysis also begins in the retina, when light strikes the cone
receptors connected to ganglion cells. According to the trichromatic theory, light of different
wavelengths stimulates the three different types of cones in different ways, and the
ratio of the activity of these three receptor types creates our impression of different colors.
Color vision is also mediated by opponent processes in the retina. Ganglion cells are excited
by one wavelength of light and inhibited by another, producing two pairs of what
seem to be color opposites, which accounts for red-versus-green and yellow-versus-blue
afterimages. In contrast with neurons in the ventral stream, the many types of neurons in
the dorsal stream’s parietal cortex all respond to visual information only when movement
by the individual is to take place.
Homonymous hemianopia. Blindness
of an entire left or right visual field.
Quadrantanopia. Blindness of one
quadrant of the visual field.
Scotoma. Small blind spot in the visual
field caused by a small lesion or
migraines of the visual cortex.
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HOW DO WE SENSE, PERCEIVE, AND SEE THE WORLD? ! 299
shown in Figure 8-39A.We encountered this syndrome at the beginning of the chapter
in the story of D. B., who had a lesion in region V1. Should a lesion in one of these
areas be partial, as is often the case, the result is quadrantanopia, destruction of only
a part of the visual field. This condition is illustrated in Figure 8-39B.
Figure 8-39C shows that small lesions in the occipital lobe often produce small
blind spots, or scotomas, in the visual field. Unlike the blind spots described at the
beginning of the chapter as symptomatic of migraine, brain-injured people are often
totally unaware of scotomas. For one reason, the eyes are usually moving.We make tiny,
involuntary eye movements, called nystagmus, almost constantly. Because of this usually
constant eye motion, a scotoma moves about the visual field, allowing the intact
regions of the brain to perceive all the information in that field. If the eyes are temporarily
held still, the visual system actually compensates for a scotoma through pattern
completion—filling in the hole so to speak—so that the people and objects in the
visual world are perceived as whole. The result is a seemingly normal set of perceptions.
The visual system may cover up a scotoma so successfully
that its presence can be demonstrated to the patient
only by “tricking” the visual system. This can be done
by placing an object entirely within the scotoma and,
without allowing the patient to shift gaze, asking what the
object is. If the patient reports seeing nothing, the examiner
moves the object out of the scotoma so that it suddenly
“appears” in the intact region of the visual field, thus
demonstrating the existence of a blind area.
This technique is similar to that illustrated in Figure
8-5 to demonstrate the presence of the blind spot that is
due to the optic disc.When a person is looking at an object
with only one eye, the brain compensates for the scotoma
in the same way as it does for the optic-disc blind
spot. As a result, the person does not notice the scotoma.
As you may have deduced by now, the type of blindness
that a person suffers gives clues about where in the
visual pathway the cause of the problem lies. If there is a
loss of vision in one eye only, the problem must be in that
eye or its optic nerve; if there is loss of vision in both eyes,
the problem is most likely in the brain.Many people have
difficulty understanding why a person with damage to
the visual cortex has difficulty with both eyes. They fail to
remember that it is the visual field, not the eye, that is
represented in the brain.
Beyond region V1, the nature of visual loss caused by
injury is considerably more complex. It is also very different
in the ventral and dorsal streams. We therefore
look at each of these pathways separately.
Injury to the “What” Pathway
While taking a shower, D. F., a 35-year-old woman, suffered
carbon monoxide poisoning from a faulty gas-fueled
water heater. The length of her exposure to the carbon
monoxide is unclear, but, when her roommate found her,
(A) Hemianopia Left visual field
Left visual
cortex
Right visual field
Injury
Injury
Injury
(C) Scotoma
(B) Quadrantanopia
Figure 8-39
Consequences of Lesions in Region V1
The shaded areas indicate the regions of
visual loss. (A) The effect of a complete
lesion of V1 in the left hemisphere is
hemianopia affecting the right visual
field. (B) A large lesion of the lower lip
of the calcarine fissure produces
quadrantanopia that affects most of the
upper-right visual quadrant. (C) A smaller
lesion of the lower lip of the calcarine
fissure results in a smaller scotoma.
Visit the area on the higher-order
visual cortex in the Visual System module
of your CD to watch video clips from
patients with damage to their visual
pathways.
Jim Pickerell/Stock Connection/PictureQuest
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the shower water was cold.Although carbon monoxide poisoning can cause several kinds
of neurological damage, as discussed in “Carbon Monoxide Poisoning,” the result in D. F.
was an extensive lesion of the lateral occipital region, including cortical tissue in the ventral
visual pathway.
The principal deficit that D. F. experienced was a severe inability to recognize objects,
real or drawn, which is known as visual-form agnosia (see Farah, 1990). (Agnosia
literally means “not knowing,” and so a person with an agnosia has essentially no
knowledge about some perceptual phenomenon.) A visual-form agnosia is an inability
to recognize visual forms, whereas a color agnosia (achromatotopsia) is an inability
to recognize colors, and a face agnosia (prosopagnosia) is an inability to recognize faces.
Not only was D. F. unable to recognize objects, especially line drawings of objects,
she could neither estimate their size or their orientation nor copy drawings of objects.
300 ! CHAPTER 8
Carbon Monoxide Poisoning
Focus on Disorders
Brain damage from carbon monoxide (CO) poisoning is usually
caused either by a faulty furnace or by motor vehicle exhaust
fumes. CO gas is absorbed by the blood, resulting in
swelling and bleeding of the lungs and anoxia (a loss of oxygen)
in the brain. The cerebral cortex, hippocampus, cerebellum,
and striatum are especially sensitive to CO-induced
anoxia.
A curious characteristic of carbon monoxide poisoning
is that only a small proportion of people who succumb to it
have permanent neurological symptoms, and, among those
who do have them, the symptoms are highly variable. The
most common symptoms are cortical blindness and various
forms of agnosia, as seen in D. F. In addition, many victims
suffer language difficulties.
The peculiarities of the language difficulties are shown
clearly in a young woman whose case was described by
Norman Geschwind. Geschwind studied this patient for 9
years after her accidental poisoning; she required complete
nursing care during this time. She never uttered spontaneous
speech and did not comprehend spoken language. Nonetheless,
she could repeat with perfect accuracy sentences
that had just been said to her.
She could also complete certain well-known phrases.
For example, if she heard “Roses are red,” she would say
“Roses are red, violets are blue, sugar is sweet, and so are
you.” Even odder was her ability to learn new songs. She did
not appear to understand the content of the songs; yet, with
only a few repetitions, she began to sing along with it and,
eventually, she could sing the song spontaneously, making
no errors in either words or melody.
Postmortem examination of this woman’s brain found
that, although she had extensive damage to the parietal and
temporal lobes, as shown in the accompanying diagram, her
speech areas were intact. Geschwind proposed that she
could not comprehend speech, because the words that she
heard did not arouse associations in other parts of her cortex.
She could, however, repeat sentences because the internal
connections of the speech regions were undamaged.
Geschwind did not comment on whether this woman suffered
from agnosia, but it seems likely that she did. The difficulty
would be in diagnosing agnosia in a person who is
unable to communicate.
Areas damaged by carbon monoxide poisoning are shown in red in
this postmortem diagram of the brain of Geschwind’s patient.
Frontal
lobe
Parietal
lobe
SpeachSpeech
Occipital
lobe
Temporal
lobe
Visual-form agnosia. Inability to
recognize objects or drawings of objects