Science Brain and Behavior contiuned 14

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HOW NEURONS INTEGRATE INFORMATION
A neuron is more than just an axon connected to microelectrodes by
some curious scientist who stimulates it with electrical current.A neuron
has an extensive dendritic tree covered with spines, and, through these
dendritic spines, it can have more than 50,000 connections to other
neurons. Nerve impulses traveling to each of these synapses from other
neurons bombard the receiving neuron with all manner of inputs. In addition,
a neuron has a cell body between its dendritic tree and its axon,
and this cell body, too, can receive connections from many other neurons.
How does the neuron integrate this enormous array of inputs into a nerve impulse?
In the 1960s, John C. Eccles and his students performed experiments that helped
to answer this question. Rather than recording from the giant axon of a squid, the researchers
recorded from the cell bodies of large motor neurons in the vertebrate spinal
cord. They did so by refining the stimulating and recording techniques developed for
the study of squid axons.
A spinal-cord motor neuron has an extensive dendritic tree with as many as 20
main branches that subdivide numerous times and are covered with dendritic spines.
Motor neurons receive input from multiple sources, including the skin, joints,muscles,
and brain, which is why they are ideal for studying how a neuron responds to diverse
inputs. Each motor neuron sends its axon directly to a muscle, as you would expect for
neurons that produce movement. “Myasthenia Gravis” on page 132 explains what happens
when muscle receptors lose their sensitivity to motor-neuron messages.
Excitatory and Inhibitory Postsynaptic Potentials
To study the activity of motor neurons, Eccles inserted a microelectrode into a vertebrate
spinal cord until the tip was located in or right beside a motor neuron’s cell body.
He then placed stimulating electrodes on the axons of sensory fibers entering the spinal
cord. By teasing apart the fibers of the incoming sensory nerves, he was able to
stimulate one fiber at a time.
Figure 4-18 diagrams the experimental setup that Eccles used.He found that
stimulating some of the fibers produced a depolarizing graded potential (reduced
the charge) on the membrane of the motor neuron to which these fibers
were connected. Eccles called these potentials excitatory postsynaptic potentials
(EPSPs). Because they reduce the charge on the membrane toward the
threshold level, they increase the probability that an action potential will
result.
In contrast, when Eccles stimulated other incoming sensory fibers,
he produced a hyperpolarizing graded potential (increased the charge)
on the receiving motor-neuron membrane. Eccles called these potentials
inhibitory postsynaptic potentials (IPSPs). Because they increase the
charge on the membrane away from the threshold level, they decrease the
probability that an action potential will result.
.
associated with an action potential is sufficiently large to stimulate adjacent parts of the
axon membrane to the threshold for propagating the action potential along the length of
an axon as a nerve impulse. Along a myelinated axon, a nerve impulse travels by saltatory
conduction, jumping from one node of Ranvier to the next and greatly increasing the
speed at which a nerve impulse travels.
HOW DO NEURONS TRANSMIT INFORMATION? ! 131
Excitatory postsynaptic potential
(EPSP). Brief depolarization of a neuron
membrane in response to stimulation,
making the neuron more likely to
produce an action potential.
Inhibitory postsynaptic potential
(IPSP). Brief hyperpolarization of a
neuron membrane in response to
stimulation, making the neuron less
likely to produce an action potential.
John C. Eccles
(1903–1997)
Figure 4-18
Eccles’s Experiment To demonstrate
how input onto neurons influences their
excitability, a recording is made from a
motor neuron while either an excitatory
(left) or an inhibitory (right) input is
delivered. Stimulation (S) of the
excitatory pathway produces a
membrane depolarization, or EPSP.
Stimulation of the inhibitory pathway
produces a membrane
hyperpolarization, or IPSP.
Stimulate
Excitatory
pathway
Inhibitory
pathway
Oscilloscope
Motor neuron
S S
EPSP IPSP
Stimulate
Time (ms)
Voltage (mv)
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Both EPSPs and IPSPs last only a few milliseconds, after which they decay and the
neuron’s resting potential is restored. EPSPs are associated with the opening of sodium
channels, which allows an influx of Na" ions. IPSPs are associated with the opening of
potassium channels, which allows an efflux of K" ions (or with the opening of chloride
channels, which allows an influx of Cl! ions).
132 ! CHAPTER 4
Myasthenia Gravis
Focus on Disorders
R. J. was 22 years old in 1941 when she noticed that her eyelid
drooped. She consulted her physician, but he was unable
to explain her condition or give her any help. Over the next
few years, she experienced some difficulty in swallowing,
general weakness in her limbs, and terrific fatigue.
Many of the symptoms would disappear for days and
then suddenly reappear. R. J. also noted that, if she got a
good night’s sleep, she felt better but, if she performed physical
work or became stressed, the symptoms got worse.
About 3 years after the symptoms first appeared she was diagnosed
with myasthenia gravis, a condition that affects the
communication between motor neurons and muscles.
A specialist suggested that R. J. undergo a new treatment
in which the thymus gland is removed. She underwent the
surgery and, within the next 5 years, all her symptoms gradually
disappeared. She has been symptom free for more than
60 years.
In myasthenia gravis, the receptors of muscles are insensitive
to the chemical messages passed from axon terminals.
Consequently, the muscles do not respond to commands
from motor neurons. Myasthenia gravis is rare, with a prevalence
of 14/100,000, and the disorder is more common in
women than in men.
The age of onset is usually in the 30s to 40s for women
and after age 50 for men. In about 10 percent of cases, the
condition is limited to the eye muscles, but, for the vast majority
of patients, the condition gets worse. At the time when
R. J. contracted the disease, about a third of myasthenia
gravis patients died from the disease or from complications
such as respiratory infections.
Why is removal of the thymus gland sometimes an effective
treatment? A gland of the immune system, the thymus
takes part in producing antibodies to foreign material and
viruses that enter the body. In myasthenia gravis, the thymus
may start to make antibodies to the end-plate receptors
on muscles. Blocked by these antibodies, the receptors can
no longer produce a normal response to acetylcholine, the
chemical transmitter at the muscle synapse; so Na" and K"
do not move through the end-plate pore and the muscle does
not receive the signal to contract. Disorders in which the immune
system makes antibodies to a person’s own body are
called autoimmune diseases.
Myasthenia gravis has now been modeled almost completely
in animals and has become a model for studying
other autoimmune diseases. A variety of contemporary treatments
besides removal of the thymus include thyroid removal
and drug treatments, such as those that increase the
release of acetylcholine at muscle receptors. As a result,
most myasthenia gravis patients today live out their normal
life spans.
This myasthenia gravis patient was asked to look up (photograph
1). Her eyelids quickly became fatigued and drooped (photographs
2 and 3). Photograph 4 shows her eyelids open normally after a
few minutes rest.
Courtesy of Y. Harati, M.D./Baylor
College of Medicine, Houston, Texas
1 2
3 4
On the Foundations CD, visit the
module on neural communication. In the
section on synaptic transmission, you can
view animations of EPSP and IPSP.
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Although the size of a graded potential is proportional to the intensity of the stimulation,
an action potential is not produced on the motor neuron’s cell-body membrane
even when an EPSP is strongly excitatory. The reason is simple: the cell-body
membrane of most neurons does not contain voltage-sensitive channels. The stimulation
must reach the axon hillock, the area of the cell where the axon begins. This area
is rich in voltage-sensitive channels.
Summation of Inputs
Remember that a motor neuron has thousands of dendritic spines, allowing for myriad
inputs to its membrane, both EPSPs and IPSPs.How do these incoming graded potentials
interact? For example, what happens if there are two EPSPs in succession? Does
it matter if the time between them is increased or decreased? And what is the result
when an EPSP and an IPSP arrive together? Answers to such questions provide an understanding
of how the thousands of inputs to a neuron might influence its activities.
If one excitatory pulse of stimulation is delivered and is followed some time later
by a second excitatory pulse, one EPSP is recorded and, after a delay, a second identical
EPSP is recorded, as shown at the top of Figure 4-19. These two EPSPs are independent
and do not interact. If the delay between them is shortened so that the two
occur in rapid succession, however, a single large EPSP is produced, as also shown in
Figure 4-19.
Here the two excitatory pulses are summated (added together to produce a larger
depolarization of the membrane than either would induce alone). This relation between
two EPSPs occurring closely together in time is called temporal summation.
The bottom half of Figure 4-19 illustrates that equivalent results are obtained with
IPSPs. Therefore, temporal summation is a property of both EPSPs and IPSPs.
Now let us use two recording electrodes to see the effects of spatial relations on the
summation of inputs.What happens when inputs to the cell body’s membrane are located
close together, and what happens when the inputs are spaced farther apart?
If two EPSPs occur at the same time but on widely separated parts of the membrane
(Figure 4-20A), they do not influence each other. If two EPSPs occurring close together in
HOW DO NEURONS TRANSMIT INFORMATION? ! 133
Temporal summation. Graded
potentials that occur at approximately the
same time on a membrane are summated.
IPSPs
S1 S2
Wide temporal spacing
S1S2
0
S1 S2
0
0
Close temporal spacing
Simultaneous stimuli
EPSPs
S1S2
S1 S2
0
S1 S2
Wide temporal spacing
Close temporal spacing
Simultaneous stimuli
Threshold
0
Threshold
0
Threshold
Figure 4-19
Temporal Summation (Top) Two
depolarizing pulses of stimulation (S1 and
S2) separated in time produce two EPSPs
similar in size. Pulses close together in
time partly summate. Simultaneous EPSPs
sum as one large EPSP. (Bottom) Two
hyperpolarizing pulses (S1 and S2) widely
separated in time produce two IPSPs
similar in size. Pulses in close temporal
proximity partly summate. Simultaneous
IPSPs sum as one large IPSP.
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time are also close together in location, however, they
add to form a larger EPSP (Figure 4-20B).This spatial
summation indicates that two separate inputs occurring
very close to each other in space summate. Similarly,
two IPSPs produced at the same time summate if
they occur at approximately the same place on the cellbody
membrane but not if they are widely separated.
Summation is thus a property of both EPSPs and
IPSPs in any combination. The interactions between
EPSPs and IPSPs are understandable when you consider
that it is the influx and efflux of ions that are
being summated. The influx of sodium ions accompanying
one EPSP is added to the influx of sodium
ions accompanying a second EPSP if the two occur
close together in time and space. If the two influxes
of sodium ions are remote in time or in space or in both, no summation is possible.
The same is true regarding effluxes of potassium ions. When they occur close together
in time and space, they summate;when they are far apart in either or both of these
ways, there is no summation. The patterns are identical for an EPSP and an IPSP. The influx
of sodium ions associated with the EPSP is added to the efflux of potassium ions associated
with the IPSP, and the difference between them is recorded as long as they are
spatially and temporally close together. If, on the other hand, they are widely separated in
time or in space or in both, they do not interact and there is no summation.
A neuron with thousands of inputs responds no differently from one with only a few
inputs. It democratically sums all inputs that are close together in time and space. The
cell-body membrane, therefore, always indicates the summed influences of multiple inputs.
Because of this temporal and spatial summation, a neuron can be said to analyze its
inputs before deciding what to do. The ultimate decision is made at the axon hillock.
The Axon Hillock
The axon hillock, shown emanating from the cell body in Figure 4-21, is rich in voltage-
sensitive channels. These channels, like those on the squid axon, open at a particular
membrane voltage. The actual threshold voltage varies with the type of neuron,
but, to keep things simple, we will stay with a threshold level of !50 mV.
To produce an action potential, the summed IPSPs and EPSPs on the cell-body
membrane must depolarize the membrane at the axon hillock to !50 mV. If that
threshold voltage is only briefly obtained, just one or a few action potentials may occur.
If the threshold level is maintained for a longer period, however, action potentials
will follow one another in rapid succession, just as quickly as the gates on the voltagesensitive
channels can recover. Each action potential is then repeatedly propagated to
produce a nerve impulse that travels down the length of the axon.
Do all graded potentials equally influence the voltage-sensitive channels at the
axon hillock? Not necessarily. Remember that neurons often have extensive dendritic
trees. EPSPs and IPSPs on the distant branches of dendrites may have less influence
than that of EPSPs and IPSPs that are closer to the axon hillock. Inputs close to the
axon hillock are usually much more dynamic in their influence than those occurring
some distance away, which usually have a modulating effect. As in all democracies,
some inputs have more say than others.
To summarize the relation between EPSPs, IPSPs, and action potentials, imagine a
brick standing on end a few inches away from a wall. It can be tilted back and forth
134 ! CHAPTER 4
0
S1
1
(A)
EPSPs produced at the same time, but
on separate parts of the membrane,
do not influence each other.
(B)
EPSPs produced at the same time,
and close together, add to form a
larger EPSP.
S1
S2
R1
0
1
S2 S1 + S2
0
1
R1 R2
S1 S2
Figure 4-20
Spatial Summation Illustrated here for
EPSPs, the process for IPSPs is equivalent.
Cell body
Axon
Nerve
impulse
Terminal
Axon
hillock
Action potential
IPSP
EPSP
…depolarize
membrane
at axon
hillock to
threshold
level, …
Summed EPSPs
and IPSPs on
dendritic tree
and cell
body…
…generating
an action
potential.
Figure 4-21
Triggering an Action Potential If
the summated EPSPs and IPSPs on the
dendritic tree and cell body of a neuron
change the membrane to threshold level
at the axon hillock, an action potential
travels down the axon membrane.
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over quite a wide range. If it is tilted too far in one direction, it falls against the wall,
whereas, if it is tilted too far in the other direction, it topples over completely. Movements
toward the wall are like IPSPs (inhibitory inputs). No matter how much these
inputs summate, the brick never falls. Movements away from the wall are like EPSPs
(excitatory inputs). If their sum reaches some threshold point, the brick topples over.
With sufficient excitation, then, the brick falls, which is analogous to generating an action
potential.
INTO THE NERVOUS SYSTEM AND BACK OUT
The nervous system allows us to respond to sensory stimuli by detecting them in the
environment and sending messages about them to the brain. The brain interprets the
information, triggering responses that contract muscles and cause movements of the
body. Until now, we have been dealing with only the middle of this process—how neurons
convey information to one another, integrate that information, and generate action
potentials.We have not explored the beginning and end of the journey.
To fill in those missing pieces, we now explain how a sensory stimulus initiates a
nerve impulse and how a nerve impulse produces a muscular contraction. You will
learn that ion channels are again important but that these channels are different from
those described so far. You will first see how they differ as we examine the production
of action potentials by sensory stimuli.
How Sensory Stimuli Produce Action Potentials
We receive information about the world through tactile sensations (body senses such
as touch and pain), auditory sensations (hearing), visual sensations (sight), and chemical
sensations (taste and olfaction). Each sensory modality has one or more separate
functions. For example, the body senses include touch, pressure, joint sense, pain, and
temperature. Receptors for audition and balance are modified touch receptors. The
visual system has receptors for light and for different colors. And taste and olfactory
senses are sensitive to many chemical compounds. Some of these receptors are organelles
attached to a sensory neuron’s dendrite,whereas other receptors are part of the
neuron’s membrane.
To process all these different kinds of sensory inputs requires a remarkable array
of different sensory receptors. But one thing that neurons related to these diverse
In Review .
Stimulation at synapses produces graded potentials on a neuron’s cell body and dendrites.
Graded potentials that decrease the charge on the cell membrane, moving it toward the
threshold level, are called excitatory postsynaptic potentials because they increase the likelihood
that an action potential will occur. Graded potentials that increase the charge on
the cell membrane, moving it away from the threshold level, are called inhibitory postsynaptic
potentials because they decrease the likelihood that an action potential will result.
EPSPs and IPSPs that occur close together in time and space are summated. In this way, a
neuron integrates information that it receives from other neurons. If summated inputs are
sufficiently excitatory to bring the axon hillock to a threshold level, an action potential is
triggered and then propagated as it travels along the cell’s axon as a nerve impulse.
HOW DO NEURONS TRANSMIT INFORMATION? ! 135
Visit the module on neural
communication on the Foundations CD.
In the section on neural integration you
can watch an animation showing the
process of spatial and temporal
summation.
Spatial summation. Graded potentials
that occur at approximately the same
location on a membrane are summated.
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receptors have in common is the presence of ion channels on their cell membranes.
When a sensation stimulates these ion channels, it initiates the chain of
events that produces a nerve impulse.
Touch provides an example. Each hair on the
human body is very sensitive to touch, allowing us
to detect an even very slight displacement. You can
demonstrate this sensitivity to yourself by selecting a
single hair on your arm and bending it. If you are patient
and precise in your experimentation, you will
discover that some hairs are sensitive to displacement
in one direction only, whereas others respond to displacement
in any direction. What enables this very
finely tuned sensitivity?
The dendrites of sensory neurons are specialized
to conduct nerve impulses, and one of these dendrites
is wrapped around the base of each hair on your body,
as shown in Figure 4-22.When a hair is mechanically
displaced, the dendrite encircling it is stretched, initiating
the opening of a series of stretch-sensitive
channels in the dendrite’s membrane. When these
channels open, they allow an influx of Na" ions sufficient
to depolarize the dendrite to its threshold level. At threshold, the voltage-sensitive
sodium and potassium channels open to initiate the nerve impulse.
Other kinds of sensory receptors have similar mechanisms for transforming the
energy of a sensory stimulus into nervous system activity. The receptors for hearing
and balance have hairs that, when displaced, likewise activate stretch-sensitive channels.
In the visual system, light particles strike chemicals in the receptors in the eye, and
the resulting chemical change activates ion channels in the membranes of relay neurons.
An odorous molecule in the air that lands on an olfactory receptor and fits itself
into a specially shaped compartment opens chemical-sensitive ion channels. When
tissue is damaged, injured cells release a chemical called bradykinin that activates
bradykinin-sensitive channels on a pain nerve.
In later chapters, we consider the details of how sensory receptors change, or transduce,
energy from the external world into action potentials. The point here is that, in
all our sensory systems, ion channels begin the process of information conduction.
How Nerve Impulses Produce Movement
What happens at the end of the neural journey? How, after sensory information has
traveled to the brain and been interpreted, is a behavioral response that includes the
contraction of muscles generated? Behavior, after all, is movement, and, for movement
to take place, muscles must contract. If motor neurons fail to work, movement becomes
impossible and muscles atrophy (see “Lou Gehrig’s Disease”).
You know that motor neurons send nerve impulses through their axons to muscles.
The motor-neuron axons, in turn, generate action potentials in muscle cells,which
are instrumental in making the muscle contract. So the question is, How does an action
potential on a motor-neuron axon produce an action potential on a muscle?
The axon of each motor neuron makes one or a few contacts (synapses) with its
target muscle, similar to those that neurons make with one another (Figure 4-23). The
part of the muscle membrane that is contacted by the axon terminal is a specialized
136 ! CHAPTER 4
Stretch-sensitive channel. Ion
channel on a tactile sensory neuron that
activates in response to stretching of the
membrane, initiating a nerve impulse.
Stretch-sensitive
channel
Current
flow
Extracellular
fluid
Intracellular fluid
Voltage-sensitive
channels
Na+
K+
Na+
Feather
Dendrite
of sensory
neuron
wrapped
around
hair
Hair
Displacement
of hair…
Nerve
impulse
…causes stretchsensitive
channels
on dendrite to
open, allowing an
influx of Na+.
This Na+ influx causes
voltage-sensitive Na+
and K+ channels to
open, producing a
nerve impulse.
Figure 4-22
Tactile Stimulation A hair’s touch
receptor activated by a feather results in
a nerve impulse heading to the brain.
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HOW DO NEURONS TRANSMIT INFORMATION? ! 137
Lou Gehrig’s Disease
Focus on Disorders
Baseball legend Lou Gehrig played for the New York Yankees
from 1923 until 1939. He was a member of numerous World
Series championship teams, set a host of individual records,
some of which still stand today, and was immensely popular
with fans, who knew him as the “Iron Man.” His record of
2130 consecutive games was untouched until 1990, when
Cal Ripkin, Jr., played his 2131st consecutive game.
In 1938, Gehrig started to lose his strength. In 1939, he
played only eight games and then retired from baseball.
Eldon Auker, a pitcher for the Detroit Tigers, described Lou’s
physical decline: “Lou seemed to be losing his power. His
walking and running appeared to slow. His swing was not as
strong as it had been in past years.”
Eldon was not describing the symptoms of normal aging
but rather the symptoms of amyotrophic lateral sclerosis
(ALS), a diagnosis shortly to be pronounced by Lou’s physician.
ALS was first described by Jean-Martin Charcot in
1869, but, after Lou Gehrig developed the condition, it was
commonly called Lou Gehrig’s disease. Gehrig died in 1941
at the age of 38.
ALS affects about 6 of every 100,000 people and strikes
most commonly between the ages of 50 and 75, although its
onset can be as early as the teenage years. About 10 percent
of victims have a family history of the disorder. The disease
begins with general weakness, at first in the throat or upper
chest and in the arms and legs. Gradually, walking becomes
difficult and falling common. The patient may lose use of the
hands and legs, have trouble swallowing, and have difficulty
speaking. The disease does not usually affect any sensory systems,
cognitive functions, bowel or bladder control, or even
sexual function. Death is often within 5 years of diagnosis.
ALS is due primarily to the death of motor neurons, which
connect the rest of the nervous system to muscles, allowing
movement. Neurons in the brain that connect primarily with
motor neurons also can be affected. The technical term, amyotrophic
lateral sclerosis, describes its consequences on both
muscles (amyotrophic means “muscle weakness”) and on the
spinal cord (lateral sclerosis means “hardening of the lateral
spinal cord”) where motor neurons are located.
Several theories have been advanced to explain why
motor neurons suddenly start to die in ALS victims. Perhaps
this cell death is caused by the atrophy of microtubules that
carry proteins down the motor-neuron axons, perhaps by a
buildup of toxic chemicals within the motor neurons, perhaps
by toxic chemicals released from other neurons. No
one knows for sure. Recent evidence suggests that ALS can
result from head trauma that activates the cell’s D NA to produce
signals that initiate the neuron’s death, a phenomenon
known as programmed cell death (Przedborski, 2004). At the
present time, there is no cure for ALS, although some newly
developed drugs appear to slow its progression and offer
some hope for Lou Gehrig jumping over Yankee teammate Joe DiMaggio’s bat. future treatments.
Baseball Hall of Fame Library, Cooperstown, N.Y.
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138 ! CHAPTER 4
End plate. On a muscle, the
receptor–ion complex that is
activated by the release of the
neurotransmitter acetylcholine from
the terminal of a motor neuron.
Acetylcholine (ACh). The first
neurotransmitter discovered in the
peripheral and central nervous
systems; activates skeletal muscles.
Transmitter-sensitive channel.
Receptor complex that has both
a receptor site for a chemical and a
pore through which ions can flow.
area called an end plate, shown in Figure 4-23A and
B. The axon terminal releases onto the end plate
a chemical transmitter called acetylcholine (ACh)
that activates skeletal muscles.
This transmitter does not enter the muscle but
rather attaches to transmitter-sensitive channels on
the end plate (Figure 4-23C). When these channels
open in response to ACh, they allow a flow of ions
across the muscle membrane sufficient to depolarize
it to the threshold for its action potential. At threshold,
adjacent voltage-sensitive channels open. They,
in turn, produce an action potential on the muscle
fiber, which is the basis for muscular contraction.
The transmitter-sensitive channels on muscle
end plates are somewhat different from the channels
on axons and dendrites. A single end-plate channel
is larger than two sodium and two potassium channels
on a neuron combined. When transmittersensitive
channels open, they allow both sodium
ions and potassium ions to flow through the same
pore. The number of channels that open depends on
the amount of transmitter released. Therefore, to
generate a sufficient depolarization on the end plate
to activate neighboring voltage-sensitive channels
requires the release of an appropriate amount of
acetylcholine.
A wide range of neural events can be explained
by the actions of membrane channels. Some channels
generate the transmembrane charge. Others mediate graded potentials. Still others
trigger the action potential. Sensory stimuli activate channels on neurons to initiate
a nerve impulse, and the nerve impulse eventually activates channels on motor neurons
to produce muscle contractions.
These various channels and their different functions probably evolved over a long
period of time in the same way that new species of animals and their behaviors evolve.
So far, not all the different channels that neural membranes possess have been described,
but you will learn about some additional channels in subsequent chapters.
In Review .
The way in which a sensory stimulus initiates a nerve impulse is surprisingly similar for all
our sensory systems. The membrane of a receptor cell contains a mechanism for transducing
sensory energy into changes in ion channels that, in turn, allow ion flow to alter the voltage
of the membrane to the point that voltage-sensitive channels open, initiating a nerve impulse.
Muscle contraction also depends on ion channels. The axon terminal of a motor neuron
releases the chemical transmitter acetylcholine onto the end plate of a muscle-cell
membrane. Transmitter-sensitive channels on the end plate open in response, and the subsequent
flow of ions depolarizes the muscle membrane to the threshold for its action potential.
This depolarization, in turn, activates neighboring voltage-sensitive channels, producing
an action potential on the muscle fiber, which brings about contraction of the muscle.
(A)
(B)
(C)
Na+
Acetylcholine
Muscle fiber
Current flow
Voltage-sensitive
channel
Transmitter-sensitive
channel
K+
Receptor Na+
site
End plate
Axon terminal
Motor nerve
Axon
Motor nerve
Muscle
fiber
Axon Motor end plate
Figure 4-23
Muscle Contraction
(A) In this microscopic view
of a motor-neuron axon
collaterals contacting muscle
end plates, the dark patches
are end plates and the axon
terminals are not visible.
(B) An axon terminal contacts
an end plate. (C) The neurotransmitter
acetylcholine
attaches to receptor sites on
transmitter-sensitive endplate
channels, opening
them. These large channels
allow the simultaneous influx
of sodium ions and efflux of
potassium ions, generating a
current sufficient to activate
voltage-sensitive channels
that trigger an action
potential on the muscle,
causing it to contract.
Courtesy of Kitty S. L. Tan
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STUDYING THE BRAIN’S ELECTRICAL ACTIVITY
Our description of how a sensory stimulus initiates a flow of information in the nervous
system that eventually results in some behavioral response should not mislead you
into thinking that neurons are active only when something in the environment triggers
them. The results of brain-wave recording studies show that electrical activity is always
going on in the brain. The nervous system is electrically active during vigorous exercise,
during rest, during daydreaming and sleep, and even under anesthesia. In each
case, moreover, it is active in a different way.
The various electrical patterns associated with different kinds of behaviors are sufficiently
distinctive to allow some fairly accurate assessments of what a person is doing
at any given time. The ability to read the brain’s electrical activity has not progressed
to the point at which researchers can tell what someone is thinking, but it is getting
close. Investigators can tell whether someone is awake or asleep and whether the brain
is working normally.
As a result, measures of brain activity have become very important for studying
brain function, for medical diagnosis, and for monitoring the effectiveness of therapies
used to treat brain disorders. Three major techniques for studying the brain’s electrical
activity are single-cell recording, which tracks action potentials, and electroencephalographic
recording and event-related potential recording, both of which record
graded potentials. In part, these techniques are used to record the electrical activity at
different parts of the neurons. The activity of those parts is influenced by specialized
ion channels.
Rapid-acting, voltage-dependent sodium channels are located on the axon hillock
and axon of most neurons, and so action potentials that depend on the presence of
these channels are best recorded at these parts of a neuron. The electrical behavior of
cell bodies and dendrites tends to be much more varied than that of axons, and electroencephalograms
and event-related potentials are recorded from these parts of the
neuron. Most dendrites do not have rapid voltage-dependent sodium channels and
so do not produce action potentials, but some do have them and thus produce action
potentials.
Single-Cell Recordings
While recording the activity of single neurons in the limbic region of the rat brain,
James Ranck (see Taube & Bassett, 2003) noticed that the action potentials of a single,
especially interesting neuron had a remarkable relation to the rat’s behavior, summarized
in Figure 4-24.Whenever the rat faced in a particular direction, the neuron vigorously
fired; that is, it generated action potentials. When the rat turned somewhat
away from this direction, the neuron fired more slowly. And, when the rat’s position
was opposite this neuron’s favored direction, the neuron did not fire at all.
Ranck called this type of neuron a head-direction cell. In studying it further, he
found that it displays still more remarkable behavior. If a rat is taken to another room,
the neuron maintains its directional selectivity. Even when the rat is picked up and
pointed in different directions, the neuron still behaves just as it does when the rat
turns by itself.
Who would have predicted that a neuron in the brain would behave in such a way?
This discovery serves as an excellent example of the power of single-cell recording techniques
to provide information about how different regions of the brain work.We humans
also may have head-direction cells to help us locate where we are in relation to
some reference point, such as home.We can keep track of both our active and our passive
movements to maintain a “sense of direction” no matter how many times we turn
HOW DO NEURONS TRANSMIT INFORMATION? ! 139
Figure 4-24
Single-Cell Recording Head-direction
cells help the rat determine its location
in space. Located in the limbic system,
these cells fire when the rat faces in a
given direction—in this case, the bottom
of the page. The firing rate of a single
cell decreases as the rat is rotated from
the cell’s preferred direction. Each of the
eight surrounding traces of neural
activity shows the cell’s relative rate of
firing when the rat faces in the direction
indicated by the corresponding arrow.
Head-direction cell. A neuron in the
hippocampus that discharges when an
animal faces in a particular direction.
CH04.qxd 1/28/05 10:02 AM Page 139

or are turned. The hippocampal formation, in which head-direction cells are found,
presumably regulates this sense of direction.
The technique of single-cell recording has come a long way in the decades since
Hodgkin and Huxley’s pioneering experiments on giant axons in squid. We can now
record the activity of single neurons in freely moving mammals by permanently implanting
microelectrodes into their brains. The massive amount of information obtained
during cell recordings is stored and analyzed on a computer. Nevertheless, the
basic recording procedure has not changed that much.
Small, insulated wire microelectrodes, with their uninsulated tips filed to a fine
point, are preferred to glass microelectrodes. An oscilloscope is still used to visualize
the behavior of the cell, but, in addition, the cell’s activity is played into a loudspeaker
so that cell firing can be heard as a beep or pop. The head-direction cell that Ranck
recorded went “beep beep” extremely rapidly when the rat pointed in the preferred direction,
and it was silent when the rat turned completely away.
Many hundreds of single-cell recording studies have been conducted to discover
the types of stimuli that cause neurons to fire. Neurons fire in response to stimuli as
simple as lights or tones and as complex as the face of a particular person or the sound
of a particular voice. Single neurons have also been found to have a wide range of firing
patterns. They may discharge in proportion to the intensity of a stimulus, fire
rhythmically with it, or fire when the stimulus starts or stops. Remarkably, single cells
also communicate by their silence. The cells in the pathway between the eye and the
brain, for example, have a very high discharge rate when an animal is in the dark.Many
of these cells decrease their rate of firing in response to light.
You will encounter other examples of the link between behavior and single-cell activity
in later chapters. It is impossible to fully understand how a region of the brain
works without understanding what the individual cells in that region are doing, and
this knowledge is acquired through single-cell recording techniques. Such studies must
usually be done with animals, because only in exceptional circumstances, such as brain
surgery or as a treatment for disease, is it possible to implant electrodes into the brain
of a person for the purposes of recording single-cell activity.
EEG Recordings
Recall your encounter with EEGs at this beginning of this chapter in connection with
epilepsy. In the early 1930s, Hans Berger discovered that electrical activity in the brain
could be recorded simply by placing electrodes onto the skull. Popularly known as
“brain waves,” recording this electrical activity produces an “electrical record from the
head,” or an electroencephalogram. EEGs reveal some remarkable features of the
brain’s electrical activity. The EEGs in Figure 4-25 illustrate three:
1. The living brain’s electrical activity is never silent even when a person is asleep or
anesthetized.
2. An EEG recorded from the cortex has a large number of patterns, some of which
are rhythmical.
3. The EEG changes as behavior changes.
When a person is aroused, excited, or even just alert, the EEG pattern has a low
amplitude (the height of the brain waves) and a fast frequency (the number of brain
waves per second), as shown in Figure 4-25A. This pattern is typical of an EEG taken
from anywhere on the skull of an alert subject, not only human subjects but other
animals, too. In contrast, when a person is calm and relaxing quietly, especially with
140 ! CHAPTER 4