Selasa, 05 April 2011

Science Brain and Behavior contiuned 23

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Spinal circuits can also produce more-complex reflexive movements. An example
is the stepping reflex. If body weight is supported while the feet are in contact with a
conveyor belt, the legs “walk” reflexively to keep up with the belt.
Each leg has its own neural circuit that allows it to step.When the limb is moved
backward on the conveyor belt, causing the foot to lose support, the limb reflexively
lifts off the belt and swings forward underneath the body. As the foot then touches the
surface of the belt again, tactile receptors initiate the reflex that causes the foot to push
against the surface and support the body’s weight. In this way, several spinal reflexes
work together to produce the complex movement of walking. Because this walking is
reflexive, even a newborn baby will display it when held in the correct position on a
conveyor belt.
One of the more complex reflexes that can be observed in other vertebrates is the
scratch reflex. Here, an animal reflexively scratches a part of its body in response to a
flapping the hands. Some may engage as well in aggressive
or self-injurious behavior. The severity of these symptoms
varies. Some are severely impaired, whereas others learn to
function quite well. Still others have exceptional abilities in
music, art, or mathematics.
As might be expected of a disorder with the range of
symptoms seen in autism, anatomical studies reveal abnormal
structures and cells in a number of brain regions, including
the limbic system and the cerebellum. Brain scans
indicate that the cerebellum may be smaller in people with
autism than in control subjects.
At birth, children with autism have relatively small
heads compared with normal children, but, over the first
year, 60 percent develop an excessive increase in head size,
largely owing to an increase in the volume of the neocortex
(Courchesne & Akshoomoff, 2003). Brain imaging also
shows that the sulci in the frontal lobes of children with
autism retain an immature organization (Levitt et al., 2003).
Together these findings suggest that the normal sculpturing
of the brain in early infancy, in which there is normally a loss
of cells, dendrites, and synapses to sculpture the adult brain,
is abnormal in autistism.
An indication of a genetic influence on developing
autism stems from the finding that both members of identical
twin pairs are more likely than are those of fraternal twin
pairs to develop the disorder. Patricia Roder (2000) suggested
that one cause may be an abnormality in the gene that
plays a central role in the development of the brainstem. She
found that an area of the brainstem in the caudal part of the
pons is small in people diagnosed autistic, as the accompanying
diagram shows. Several nuclei in this area, including
the nucleus that controls facial muscles, are either small or
missing, which may lead to subtle facial abnormalities such
as those shown in the photographs.
Evidence also reveals that a virus can trigger autism.
Women have an increased risk of giving birth to an autistic
child if they are exposed to rubella (German measles) in the
first trimester of pregnancy. Researchers also suspect that industrial
toxins can trigger autism, but the evidence remains
Although children with autism often are normal in appearance,
some physical anomalies characterize the disorder. The corners of
the mouth may be low compared with the upper lip, and the tops
of the ears may flop over (left). The ears may be a bit lower than
normal and have an almost square shape as well (right).
Scratch reflex. Automatic response in
which the hind limb reaches to remove a
stimulus from the surface of the body.
Scratch reflex
Photos courtesy of Susan L. Hyman
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Spinal-Cord Injury
Focus on Disorders
Each year, on average, about 11,000 people in the United
States and 1000 people in Canada suffer spinal-cord injury.
Often the spinal cord is completely severed, leaving
the victim with no sensation or movement from the site of
the cut downward. Although 12,000 people annually incurring
spinal-cord injury may seem like a large number, it
is small relative to the number in these two countries who
suffer other kinds of nervous system damage each year. Recall
from Chapter 1, for example, that complications related
to head trauma disable a reported 80,000 Americans in a
To increase public awareness about their condition and
promote research into possible treatments, some, like Christopher
Reeve, become activists. Canadian Rick Hansen, pictured
here, is especially active. He may even have been a role
model for Reeve.
Hansen, an athletic teenager, became a paraplegic as
the result of a lower thoracic spinal injury in 1975. Twelve
years later, to raise public awareness to the potential of
people with disabilities, Rick wheeled himself 40,000 kilometers
around the world, generating more than $24 million
for the Man in Motion Legacy Trust Fund. To date, the Fund
has contributed more than $100 million in support of spinalcord
research, rehabilitation, wheelchair sports, and publicawareness
Rick Hansen is currently executive director of the Rick
Hansen Institute at the University of British Columbia. The
Institute provides leadership and support for initiatives in the
field of disability research, with a special focus on spinalcord
Research to find treatments for spinal-cord damage is a
frustrating field. A severed spinal cord, like a severed electrical
cord, entails just a single cut that leaves the machinery
on both sides of it intact. If only the cut could somehow be
bridged, function might be restored. Reconnecting a severed
electrical cord is easy—just strip and reconnect the wires.
Restoring a severed spinal cord is not so easy.
Among the factors preventing nerve fibers from growing
across a cut in a spinal cord are the formation of scar tissue,
a lack of a blood supply, and the absence of appropriate
growth factors to stimulate neuron growth. Add to these factors
the fact that normal tissue at the edge of the cut actively
repels regrowth. Can these obstacles be overcome? From a
theoretical and experimental perspective, spinal-cord regeneration
and recovery do seem achievable.
The results of studies suggest that it may be possible to
induce neural fibers to grow across a spinal-cord cut. For instance,
if the spinal cord in chicks and other baby animals is
cut in the first 2 weeks of life, the spinal cord regrows and
apparently normal function returns. Presumably, if the mixture
of growth factors that enables this regeneration can be
identified and applied to the severed spinal cords of adults,
the same regrowth could result.
Also encouraging is the finding that, when a nerve fiber
in the peripheral nervous system is cut, it regrows no matter
how old the injured person is. Schwann cells that form the
severed axon’s myelin are thought to produce the chemical
environment that facilitates this regrowth. Results of experiments
in which Schwann cells are implanted into a cut
spinal cord have been positive, although no cure has as yet
been effected.
Other investigators, who built little bridges across a severed
spinal cord, also obtained some encouraging evidence
of regrowth. Rats that had been unable to move their legs regained
postural support and were able to step after receiving
Rick Hansen on the Man in Motion Tour in 1987. this treatment.
Courtesy of Nike/Rick Hansen Institute
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stimulus from the surface of the body. The complexity of the scratch reflex is revealed
in the accuracy of the movement.Without direction from the brain, the tip of a limb,
usually a hind limb, can be correctly directed to the part of the body that is irritated.
In humans and other animals with a severed spinal cord, spinal reflexes still function,
even though the spinal cord is cut off from communication with the brain. As a
result, the paralyzed limbs may display spontaneous movements or spasms. But the
brain can no longer guide the timing of these automatic movements. Consequently, reflexes
related to bladder and bowel control may need to be artificially stimulated by
If we compare how Kamala paints a picture with her trunk with how human artists
paint with their hands, the achievement of the same goal by such different behavioral
strategies may seem remarkable. But the use of different body parts for skilled movements
is widespread among animals. Dolphins and seals are adept at using their noses
to carry and manipulate objects, and many other animals, including domestic dogs, accomplish
the same end by using their mouths. Birds’ beaks are specially designed for
getting food, for building nests, and sometimes even for making and using tools.
Tails also are useful appendages. Some marsupials and some species of New World
primates use their tails to pick up and carry objects. Among horses, the lips are dexterous
enough to manipulate a single blade of grass of the type that a horse prefers
from a patch of vegetation. Although humans tend to rely primarily on their hands for
manipulating objects, they can still learn to handle things with other body parts, such
as the mouth or a foot, if they have to. Some people without arms become extremely
proficient at using a foot for writing or painting or even for driving.
What properties of the motor system allow such versatility in carrying out skilled
movements? In this section, you will find the answer to this question as we examine the
organization of the motor cortex and its descending pathways to the brainstem and
spinal cord, which in turn connects with the muscles of the body.
The Motor Cortex
In 1870, two Prussian physicians, Gustav Fritsch and Eduard Hitzig, electrically stimulated
the neocortex of an anesthetized dog and produced movements of the mouth,
limbs, and paws on the opposite side of the dog’s body. They provided the first direct evidence
that the neocortex controls movement.Later researchers confirmed the finding by
In Review .
The motor system is organized hierarchically. The forebrain, especially the frontal lobe, is
responsible for selecting plans of action, coordinating body parts to carry out those plans,
and executing precise movements. The brainstem, in contrast, is responsible for speciestypical
movements, for survival-related actions, and for posture and walking. In addition
to being a pathway between the brain and the rest of the body, the spinal cord is independently
responsible for reflexive movements. Although lower-level functions in this hierarchical
system can continue in the absence of higher-level ones, it is the higher levels
that provide voluntary control over movements. Consequently, when the brain is disconnected
from the spinal cord, movement can no longer be controlled at will.
On your CD, link to the area on the
organization of the motor system in the
module on Control of Movement for a
review of the organization of movement
and motor systems.
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Homunculus. Representation of the
human body in the sensory or motor
cortex; also any topographical
representation of the body by a neural
Topographic organization. Neural
spatial representation of the body or areas
of the sensory world perceived by a
sensory organ.
using a variety of animals as subjects, including
primates such as monkeys and apes.
On the basis of this research background,
beginning in the 1930s, Wilder Penfield used
electrical stimulation to map the cortices of conscious
human patients who were about to undergo
neurosurgery with the aim of using the
results to assist surgery (see Figure 9-18).He and
his colleagues confirmed that movements in humans
also are triggered mainly in response to
stimulation of the primary motor cortex.
Penfield summarized his results by drawing
cartoons of body parts to represent the areas of
the primary motor cortex that produce movement
in those parts.The result was a homunculus
(little person) that could be spread out across
the motor cortex, as illustrated in Figure 10-6.
Because the body is symmetrical, an equivalent
motor homunculus is represented in the cortex of
each hemisphere, and each mainly controls movement
in the opposite side of the body.Penfield also
identified another, smaller motor homunculus in
the dorsal premotor area of each frontal lobe, a region
sometimes referred to as the supplementary
motor cortex.
The most striking feature of the motor homunculus is the disproportionate relative
sizes of its body parts, shown in Figure 10-7, compared with the relative sizes of
actual parts of the human body. As you can see, the homunculus has very large hands
with an especially large thumb. Its lips and tongue are especially prominent as well. In
contrast, the trunk, arms, and legs, which constitute most of the area of a real body, are
much smaller in relative size. These distortions illustrate the fact that large parts of the
motor cortex regulate the hands, fingers, lips, and tongue, giving us precise motor control
over these body parts. Areas of the body over which we have much less motor control
have a much smaller representation in the motor cortex.
Another curious feature of the homunculus as laid out across the motor cortex is
that the body parts are arranged much differently from those of an actual body. The area
of the cortex that produces eye movements is located in front of the homunculus head
on the motor cortex, as shown in the upper drawing in Figure 10-6. The head is oriented
with the chin up and the forehead down, and the tongue is located below the forehead.
Such details aside, the homunculus shows at a glance that relatively larger areas of
the brain control the parts of the body that we use to make the most skilled movements.
It is thus a useful concept for understanding the topographic organization
(functional layout) of the primary motor cortex.
The discovery of the topographical representation of the motor cortex suggested
how movements might be produced. Information from other regions of the neocortex
could be sent to the motor homunculus, and neurons in the appropriate part of the
homunculus could then execute the movements called for. If finger movements are
needed, for example, messages can be sent to the finger area of the motor cortex, triggering
the required activity there. If this model of how the motor system works is correct,
damage to any part of the homunculus would result in loss of movement in the
corresponding part of the body.
Although the general idea underlying this model is correct, more-detailed mapping
of the motor cortex and more-detailed studies of the effects of damage to it
354 ! CHAPTER 10
Figure 10-7
Homunclular Man An artist’s
representation illustrates the
disproportionate areas of the sensory
and motor cortices that control different
parts of the body.
Movement of
body parts
Motor cortex
Electrical stimulation
of the motor cortex…
…elicits movements
of body parts
corresponding to the
map of the body.
Figure 10-6
Penfield’s Homunculus Movements
are topographically organized in the
motor cortex. Stimulation of the dorsal
medial regions of the cortex produces
movements in the lower limbs.
Stimulation in ventral regions of the
cortex produces movements in the upper
body, hands, and face.
The BritishMuseum, Natural History
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indicate that the picture is a bit more complex. When researchers investigated the
motor cortex in nonhuman primates, with the use of smaller electrodes than those
used by Penfield to examine his patients, they discovered as many as 10 motor homunculi
(Galea & Darian-Smith, 1994).As many as 4 representations of the body may
exist in the primary motor cortex, and a number of other representations may be
found in the premotor cortex.
What each of these different homunculi does is still unclear. Perhaps each is responsible
for a particular class of movements. Perhaps we select different parts of different
homunculi for different movements, as a piano player selects different keys on a
piano to play different cords.Whatever the functions turn out to be, they will have to
be described by future research.
Corticospinal Tracts
The main pathways from the motor cortex to the brainstem and spinal cord are called
the corticospinal tracts. (Recall from Chapter 2 that bundles of nerve fibers within the
central nervous system are called tracts; outside the CNS they are called nerves. The
term corticospinal indicates that these fiber bundles begin in the neocortex and terminate
in the spinal cord.) The axons of the corticospinal tracts originate mainly in layer
V pyramidal cells of the motor cortex. Axons also come from the premotor cortex and
the sensory cortex.
The axons from the motor cortex descend into the brainstem, sending
collaterals to a few brainstem nuclei and eventually emerging on the brainstem’s
ventral surface. There they form a large bump on each side of the
brainstem surface. These bumps, known as pyramids, give the corticospinal
tracts their alternate name, the pyramidal tracts.
At this point, most of the axons descending from the left hemisphere
cross over to the right side of the brainstem. Likewise,most of the axons descending
from the right hemisphere cross over to the left side of the brainstem.
The rest of the axons stay on their original sides.
This division produces two corticospinal tracts, one uncrossed and the
other crossed, entering each side of the spinal cord. Figure 10-8 illustrates
the division of tracts originating in the left-hemisphere cortex. The dual
tracts on each side of the brainstem then descend into the spinal cord, forming
the two spinal cord tracts.
In the cross section of the spinal cord in Figure 10-9, you can see the
location of the two tracts on each side. Those fibers that cross to the opposite
side of the brainstem descend the spinal cord in a lateral (side) position,
giving them the name lateral corticospinal tract. Those fibers that remain on
On your CD, go to the area on
the primary motor cortex in the module
on the Control of Movement for a
more detailed analysis of the motor
homunculus. Notice the exaggerated
body parts associated with fine motor
motor cortex
Spinal cord
corticospinal tract
Ventral corticospinal
tract moves muscles of
midline of the body.
Lateral corticospinal
tract moves limbs
and digits.
Figure 10-8
Corticospinal Tract Nerve fibers from each hemisphere (only the tract from the
left hemisphere is shown here) descend from the motor cortex to the brainstem,
where they produce a protrusion (a pyramid) on the ventral surface. There the tract
branches into the spinal cord. A lateral tract crosses the midline to the opposite side
of the spinal cord, and a ventral tract remains on the same side. Fibers in the lateral
tract are represented by the limbs and digits of the cortical homunculus and are
destined to move muscles of the limbs and digits. Fibers of the ventral tract are
represented by the midline of the homunculus and are destined to move muscles of
the midline of the body. Photograph of spinal cord reproduced from The Human Brain:
Dissections of the Real Brain, by T. H. Williams, N. Gluhbegovic, and J. Jew, on CD-ROM. Published by
Brain University, 2000.
Corticospinal tract. Bundle of nerve
fibers directly connecting the cerebral
cortex to the spinal cord, branching at the
brainstem into an opposite-side lateral
tract that informs movement of limbs and
digits and a same-side ventral tract that
informs movement of the trunk; also
called pyramidal tract.
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their original side of the brainstem continue down the
spinal cord in a ventral (front) position, giving them the
name ventral corticospinal tract. As we will see, the two tracts
eventually control different parts of the body.
Motor Neurons
The spinal-cord motor neurons that connect to muscles are
located in the ventrolateral part of the spinal cord and jut
out to form the spinal column’s ventral horns. There are two
kinds of neurons in the ventral horns. Interneurons lie just
medial to the motor neurons and project onto them. The
motor neurons send their axons to the muscles of the body.
The fibers from the corticospinal tracts make synaptic connections
with both the interneurons and the motor neurons,
but all nervous system commands to the muscles are
carried by the motor neurons.
Figure 10-9 shows that the more laterally located motor
neurons project to muscles that control the fingers and
hands, whereas intermediately located motor neurons project to muscles that control
the arms and shoulders. The most medially located motor neurons project to muscles
that control the trunk. Axons of the lateral corticospinal tract connect mainly with the
lateral interneurons and motor neurons, and axons of the ventral corticospinal tract
connect mainly to the medial interneurons and motor neurons. In other words, a homunculus
of the body is represented again in the spinal cord.
To picture how the motor homunculus in the cortex is related to the motor neuron
homunculus in the spinal cord, place your right index finger on top of your head
above the index-finger region of the motor homunculus on the left side of the brain
(see Figure 10-6). Following the axons of the cortical neurons downward, your route
takes you through the brainstem, across its midline, and down the right lateral corticospinal
The journey ends at the interneurons and motor neurons in the most lateral region
of the spinal cord’s right ventral horn—the horn on the opposite side of the nervous
system from which you began. If you next follow the axons of these motor neurons,
you will find that they synapse with muscles that move the index finger on that same
right-hand side of the body. (By the way, the neurons that your brain is using to carry
out this task are the same neurons whose pathway you are tracing.)
If you repeat the procedure by tracing the pathway from the trunk of the motor
homunculus on the left side of the brain, you will follow the same route through the
upper part of the brainstem. However, you will not cross over to the brainstem’s opposite
side. Instead, you will descend into the spinal cord on the left side, the same side
of the nervous system on which you began, eventually ending up in the most medially
located interneurons and motor neurons of the left side’s ventral horn. In addition,
some of these axons will also cross over to the other side of the spinal cord. Thus, if you
follow the axons of these motor neurons, you will end up at their synapses with muscles
that move the trunk on both sides of the body.
This exercise of the imagination should help you to remember the routes taken by
the axons of the motor system. The limb regions of the motor homunculus contribute
most of their fibers to the lateral corticospinal tract. Because these fibers have crossed
over to the opposite side of the brainstem, they activate motor neurons that move the
arm, hand, leg, and foot on the opposite side of the body.
356 ! CHAPTER 10
Trunk The interneurons and motor
neurons of the spinal cord are
envisioned as a homunculus
representing the muscles that
they innervate.
Interneurons project to motor
Motor neurons project to
muscles of the body.
Lateral corticospinal tract
synapses with interneurons and
motor neurons that innervate
muscles of the limbs and digits.
Ventral corticospinal tract
synapses with interneurons
and motor neurons that
innervate the trunk (midline of
the body).
Ventral horn
of spinal
Figure 10-9
Motor-Tract Organization
The interneurons and the motor
neurons of the ventral spinal
cord are topographically
arranged so that the more lateral
neurons innervate the more
distal parts of the limbs and the
more medial neurons innervate
the more proximal muscles of
the body.
On your CD, click on the area on
descending motor tracts in the module on
the Control of Movement for a visual
overview of the corticospinal tracts.
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In contrast, the trunk regions of the motor homunculus contribute their fibers to
the ventral corticospinal tract. These fibers do not cross over at the brainstem, although
some do cross over in the spinal cord. In short, the neurons of the motor homunculus
in the left-hemisphere cortex control the trunk on both sides and the limbs on the
body’s right side. Similarly, neurons of the motor homunculus in the right-hemisphere
cortex control the trunk on both sides of the body and the limbs on the body’s left side
(Kuypers, 1981). Thus, one hemisphere of the cortex controls the hands and fingers of
the opposite side of the body and the trunk on both sides of the body. About a quarter
of corticospinal neurons use glutamate as a neurotransmitter, another quarter use
aspartate, and about half use both. At present, the specific motor functions mediated
by these subpopulations of corticospinal neurons are unknown.
This description of motor-system pathways descending from the brain is highly
simplified. There are actually about 26 pathways, including the corticospinal tracts. The
other pathways carry instructions from the brainstem, such as information related to
posture and balance, and control the autonomic nervous system. For all these functions,
however, the motor neurons are the final common path.
Control of Muscles
The muscles with which spinal-cord motor neurons
synapse control movement of the body. For example,
the biceps and triceps of the upper arm control
movement of the lower arm. Limb muscles are
arranged in pairs, as shown in Figure 10-10. One
member of a pair, the extensor, moves (extends) the
limb away from the trunk. The other member of the
pair, the flexor,moves the limb toward the trunk.
Connections between the interneurons and
motor neurons of the spinal cord ensure that the
muscles work together so that, when one muscle
contracts, the other relaxes. Thus, the interneurons
and motor neurons of the spinal cord not only relay instructions from
the brain but also, through their connections, cooperatively organize the
movement of many muscles. As you know, the neurotransmitter at the
motor neuron–muscle junction is acetylcholine.
In Review .
The motor cortex is topographically organized as a homunculus in which parts of the body
that are capable of the most skilled movements (especially the mouth, fingers, and thumb)
are regulated by larger cortical regions. Instructions regarding movement travel from the
motor cortex through the corticospinal tracts to interneurons and motor neurons in the
ventral horn of the spinal cord. A large part of the corticospinal-tract fibers cross to the
opposite side of the spinal cord to form the lateral corticospinal tracts, and a smaller part
stay on the same side to form the ventral corticospinal tracts. The ventral corticospinal
tracts carry instructions for trunk movements, whereas the lateral corticospinal tracts carry
instructions for arm and finger movements. The axons of motor neurons in the spinal cord
then carry instructions to muscles.
Biceps (flexor muscle)
moves the lower arm
toward the body.
Acetylcholine is the
neurotransmitter at the
neuromuscular junction.
The spinal cord ventral horn
contains interneurons and
motor neurons.
Extensor motor neurons
and flexor motor neurons
project to muscles.
Spinal cord
Triceps (extensor muscle)
extends the lower arm
away from the body.
Figure 10-10
Coordinating Movement
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People everywhere perform skilled movements in remarkably similar ways. For instance,
most people who reach for a small paperclip on a desk do so with the hand rotated so
that the fingers are on the top and the thumb is on the bottom. They also use this pincer
grip to hold the clip—that is, they grasp it between the thumb and index finger. These
movements could be learned by watching other people, but we have no recollection of
having, as children, spent any time observing and mastering such movement patterns.
In fact, even before 4 months of age, babies begin practicing finger movements by
making them in the air; then they use the movements to touch themselves and their
clothes (Wallace & Whishaw, 2003). Between 8 and 11 months of age, babies spontaneously
begin to use the pincer grip to pick up tiny objects such as breadcrumbs.Most
other primates also make use of the pincer grasp. All the evidence therefore suggests
that, although we learn to make this skilled movement, the neurons and connections
that enable the movement are innate. Basic similarities in the neural connections of the
motor cortex and spinal cord are responsible for the basic patterns of movement that
are common to the particular species.
These innate movement patterns are synergies. In primates, the pincer grip is one
synergy and the power grasp is another. In this section, we describe how neurons produce
synergies.We also explore how the motor cortices of other species produce their
skilled movements, including the highly dexterous movements of an elephant’s trunk.
Investigating Neural Control of
Skilled Movements
In a study designed to investigate how the motor cortex controls movement, Edward
Evarts (1968) used the simple procedure illustrated in the Procedure section of Experiment
10-2. He trained a monkey to flex its wrist in order to move a bar to which different
weights could be attached. An electrode implanted in the wrist region of the
motor cortex recorded the activity of neurons there.
Evarts discovered that these neurons began to discharge even before the monkey
flexed its wrist, as shown in the Results section of Experiment 10-2. Apparently, they
take part in planning the movement as well as initiating it. The neurons also continued
to discharge as the wrist moved, confirming that they play a role in producing the
movement. Finally, the neurons discharged at a higher rate when the bar was loaded
with a weight. This finding shows that motor-cortex neurons increase the force of a
movement by increasing their rate of firing, and its duration, as stated in the experiment’s
Evarts’s findings also revealed that the motor cortex has a role in specifying the direction
of a movement. The neurons of the motor-cortex wrist area discharged when
the monkey flexed its wrist inward but not when the wrist was extended back to its
starting position. These on–off responses of the neurons, depending on whether the
flexor or extensor muscle is being used, are a simple way of coding the direction in
which the wrist is moving.
A generation later, Apostolos Georgopoulos and his coworkers (1999) used a
method similar to that of Evarts to further examine the coding of movement direction.
They trained monkeys to move a lever in different directions across the surface of a
table. Recording from single cells in the arm region of the motor cortex, they found that
each cell was maximally active when the monkey moved its arm in a particular direction.
Experiment 10-3 summarizes the results.As the monkey’s arm moves in directions
other than the one to which a particular cell maximally responds in the Procedure
358 ! CHAPTER 10
Synergy. Innate pattern of movement
coded by the motor cortex.
On your CD, visit the area on control
of movement in the module on the
Control of Movement for more detail on
the role of the central nervous system.
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section, the cell decreases its activity in proportion to the displacement from the “preferred”
direction, diagrammed in the Results section. For example, if a neuron discharges
maximally as the arm moves directly forward, its discharge will be halved if the
arm moves to one side, and discharge ceases altogether if the arm moves backward.
According to Georgopoulos and his coworkers, the motor cortex seems to calculate
both the direction and the distance of movements. Each neuron in a large population
of motor-cortex neurons could participate in producing a particular movement, just as
Question: How does the motor cortex take part in the control of movement?
The motor cortex takes part in planning
movement, executing movement, and adjusting
the force and duration of a movement.
Neural activity increases
before movement,
suggesting motor-cortex
participation in planning.
Neural activity continues
throughout movement,
suggesting motor-cortex
participation in
Neural activity increases over
no-weight condition,
suggesting that motor-cortex
neurons code force of
Electrode from motor-cortex
neurons to recording
Monkey flexes wrist
to rotate lever.
Attached weight can
be changed to vary
force of movement.
Pulley Lever
Results Response of motor-cortex neurons to wrist movement
Adapted from “Relation of Pyramidal Tract Activity to Force Exerted During
Voluntary Movement,” by E. V. Evarts, 1968, Journal of Neurophysiology,
31, p. 15.
Monkey moves lever
in different directions.
The firing of individual motor-cortex neurons is tuned to the
direction of a movement.
Question: What is the activity of a motor-cortex neuron during changes in
the direction of movement?

3 90° 270°
Electrode from
neurons to
Maximal discharge
as lever is moved
forward (180º)
Minimal discharge
as lever is moved
backward (0º)
Results Activity of a single motor-cortex neuron
Adapted from “On the Relations Between the Direction of Two-Dimensional Arm
Movements and Cell Discharge in Primate Motor Cortex,” by A. P. Georgopoulos,
J. F. Kalaska, R. Caminiti, and J. T. Massey, 1982, Journal of Neuroscience, 2, p. 1530.
CH10.qxd 1/6/05 3:20 PM Page 359

findings from other studies suggest. But the discharge rate of a particular neuron depends
on that movement’s direction.
Georgopoulos and Evarts emphasize somewhat different views about how the
motor cortex exerts control over movement. Both researchers believe that motor-cortex
neurons plan and execute movements, but they disagree about what those planning and
execution strategies entail. To better understand the difference between their hypotheses,
imagine that you are preparing to pitch a ball to a catcher.
Does your throw require calculating which muscles to use and how much force to
apply to each one? This position is that of Evarts. It is based on his findings about how
neurons of the motor cortex change their rates of discharge in response not only to
which muscle is needed (flexor or extensor, for instance) but also to how much force
is required to make a particular movement.
Alternatively, perhaps your throw to the catcher simply requires determining where
you want the ball to arrive. This position is that of Georgopoulos.He maintains that the
cortex needs to specify only the spatial target of a movement—that is, its basic direction.
Other brain structures, such as the brainstem and spinal cord, will look after the
details of the throw.
Both theories are probably correct. Possibly, a subset of neurons codes force and another
subset codes direction or, possibly, in some way cortical motor neurons can code
both force and direction at the same time. Exactly what the code entails is still not understood.
The “directional”hypothesis and the “force”hypothesis are both topics of current
debate in the study of how the motor cortex controls movement (Crowe et al., 2004).
What investigators do agree on is that there is not a simple point-to-point correspondence
between a part of the cortical topographic map and movement of a particular
part of the body—for example, between a finger representation and a finger
movement. Georgopoulos and his coworkers (1999) investigated the neural control of
movement by recording from neurons in the motor cortices of monkeys that had been
trained to make specific finger movements. They expected that,when a thumb or a certain
finger moves, only the area of the motor cortex that represents that particular digit
will be active.
But their expectations were not met.When one finger moved, not only were neurons
in that finger’s area of the motor cortex active but so were neurons in the cortical
areas of other fingers. Apparently, the entire hand’s representation in the motor cortex
participates even in simple acts, such as moving one finger. Although this finding may
seem surprising at first, it makes intuitive sense.
After all, to move one finger, some effort must be exerted to keep the other fingers
still or to move them out of the way. There must be connections between all participating
neurons to allow them to act in concert. These same connections would be necessary
for sequential movements of the fingers, such as those used in playing the piano
or painting a work of art. Furthermore, there are likely similar connections between
the fingers, the arm, and the body that allow more-complex movements entailing many
body segments to take place.
Control of Skilled Movements in
Nonhuman Species
Humans are far from the only species that makes skilled movements. Kamala the elephant
paints works of art with her trunk, and primates other than humans are very
skilled with their hands, as we are. How is the motor cortex in other species organized
to enable these skilled movement patterns?
360 ! CHAPTER 10
Baseball pitcher
winding up
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The results of studies of a wide range of animals show that their motor cortices are
organized to correspond to the skilled movements of their species. Just as in humans,
larger parts of the motor cortex regulate body parts that carry out these movements.
Figure 10-11 shows cartoons representing the human homunculus and comparable
drawings of four other animals—the rabbit, cat, monkey, and elephant.
As you can see, rabbits have a large motor-cortex representation for the head and
mouth, cats for the mouth and front claws, and monkeys for the hands, feet, and digits.
Although no one has mapped the motor cortex of an elephant, a disproportionately
large area of its motor cortex is likely dedicated to regulating the trunk.
How did these specialized representations of the motor cortex evolve? One possibility
is that they were adapted from the outside inward (Woolsey & Wann, 1976).
Chance mutations caused an adaptive increase in the number of muscles in a particular
part of the body, which led to more motor neurons in the spinal cord. Concurrent
with this increase in motor neurons, the area of the motor cortex controlling those
spinal-cord motor neurons increased. The larger motor-cortex representation, along
with an increased possibility of making connections between these cortical neurons,
led to an evolved capacity for making new and more-complex movements. That is, after
the motor cortex had expanded, evolutionary pressure could then select for subregions
to become specialized for new behaviors.
Let us apply this scenario to the development of the elephant’s trunk. First, chance
mutations led to the expansion of muscles in the elephant’s lip and nose and the spinalcord
motor neurons needed to move them. These developments were retained because
they were useful, perhaps because the trunk was stronger than in the elephant’s ancestors.
The area of the motor cortex coexpanded to represent the new muscles of the
trunk. The cortical area for the trunk motor cortex expanded and differentiated to enable
fine control of different trunk muscles that enabled selectively advantageous behaviors,
such as feeding on new food sources.
How Motor-Cortex Damage Affects
Skilled Movements
Scientists produced the first maps of the motor cortex in the 1930s. A number of researchers
got slightly different results when they repeated the mapping procedures on
the same subjects. These findings led to a debate.
Some scientists held that the map of the motor cortex was capable of changing—
that areas controlling particular body parts might not always stay in exactly the same
place and retain exactly the same dimensions. But other researchers felt that this view
was unlikely. They argued that, given the enormous specificity of topographic maps of
the motor cortex, these maps must surely be quite stable. If they appeared to change,
it must be because the large electrodes used for stimulating and recording from cortical
neurons must be producing inexact results.
As cortical-mapping procedures improved, however, and as smaller and smaller
electrodes were used, it became clear that motor maps can indeed change. They can
change as a result of sensory or motor learning (a topic to be explored in Chapter 13),
and they can change when part of the motor cortex is damaged, as the following example
A study by Randy Nudo and his coworkers (1996), summarized in the Procedure
section of Experiment 10-4, illustrates change in a map of the motor cortex
due to cortical damage. These researchers mapped the motor cortices of monkeys to
identify the hand and digit areas. They then surgically removed a small part of the
Rabbit Cat
Monkey Elephant
Figure 10-11
Motor-Control Cartoons The size of
the cortical area regulating a body part
in these motor-cortex representations
corresponds to the skill required
in moving that body part. The
representation for the elephant is
only surmised. Adapted from Principles of
Neural Science (3rd ed., p. 373), by E. R. Kandel,
J. H. Schwartz, and T. M. Jessel, 1991, New York:
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cortex that represents the digit area. After the surgery, the monkeys
used the affected hand much less, relying mainly on the good
Three months later, the researchers examined the monkeys.
They found that the animals were unable to produce many movements
of the lower arm, including the wrist, the hand, and the digits
surrounding the area with the lesion. They also discovered that
much of the area representing the hand and lower arm was gone
from the cortical map. The shoulder, upper arm, and elbow areas
had spread to take up what had formerly been space representing the
hand and digits. The Results section of Experiment 10-4 shows this
topographic change.
The experimenters wondered whether the change could have
been prevented had they forced the monkeys to use the affected arm.
To find out, they used the same procedure on other monkeys, except
that, during the postsurgery period, they made the animals rely on
the bad arm by binding the good arm in a sling.
Three months later, when the experimenters reexamined the
motor maps of these monkeys, they found that the hand and digit
area retained its large size, even though there was no neural activity
in the spot with the lesion. Nevertheless, the monkeys had gained
some function in the digits that had formerly been connected to the
damaged spot.Apparently, the remaining digit area of the cortex was
now controlling the movement of these fingers.
The property of the motor cortex that allows it to change as a
result of experience, as you know, is plasticity. Thus, plasticity in the
motor cortex underlies our ability to acquire new motor skills as well
as our ability to recover from brain injury. Most likely plasticity is
enabled by the formation of new connections among different parts
of the homunculus in the motor cortex.
The motor-cortex reorganization that Nudo and his colleagues
observed in monkeys probably explains some kinds of recovery from
brain damage observed in humans. For instance, Paul Bucy and his
coworkers (1964) studied a man whose corticospinal tract was surgically
cut on one side of his nervous system to stop involuntary
movement of his muscles.During the first 24 hours after the surgery,
the side of his body contralateral to the cut was completely flaccid,
and he was unable to make any movements on that side. (The impairment
was on the side of the body opposite that of the cut because
the corticospinal tract crossed to the other side just below the location
of the cut.)
Then, gradually, there was some recovery of function. By the 10th day after the surgery,
the patient could stand alone and walk with assistance. By the 24th day, he could
walk unaided.Within 7 months, he could move his feet, hands, fingers, and toes with
only slight impairment.
The explanation of this man’s remarkable recovery is twofold. First, when the man
died about 21/2 years later, an autopsy revealed that approximately 17 percent of the corticospinal
fibers were intact in the tract that had been cut. Apparently, the remaining
fibers were able to take over much of the function formerly served by the entire pathway.
Second, extensive reorganization likely took place in the map of the man’s motor
cortex, and so many cortical regions could use the fibers that had remained intact to
send messages to motor neurons in the spinal cord.
362 ! CHAPTER 10
Elbow and
Hand and
Question: What is the effect of rehabilitation on the cortical representation
of the forelimb after brain damage?
Rehabilitation prevents both a loss of movement in the
hand and a decrease in the hand’s cortical representation.
Elbow and
3 months postlesion
with rehabilitation
Elbow and
3 months postlesion
with no rehabilitation
Areas of motor
cortex that produce
digit, wrist, and
forearm movement.
Small lesion
is made with
electrical current.
Without rehabilitation, the
area regulating the hand
becomes smaller and the
area regulating the elbow
and shoulder becomes larger.
With rehabilitation,
the area regulating the
hand retains its large
cortical representation.
Hand and
Adapted from “Neural Substrates for the Effects of
Rehabilitative Training on Motor Recovery after
Ischemic Infarct,” by R. J. Nudo, B. M. Wise,
F. SiFuentes, and G. W. Milliken, 1996, Science,
272, p. 1793.
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The main evidence that the basal ganglia and the cerebellum perform motor functions
is that damage to either structure impairs movement. Both structures also have extensive
connections with the motor cortex, further suggesting their participation in movement.
After an overview of the anatomy of the basal ganglia and cerebellum, we look
at some of the symptoms that arise after they are damaged. Then we consider some
experiments that illustrate the roles that these structures might play in controlling
The Basal Ganglia and Movement Force
Our control over movement is remarkable.We can manipulate objects as light as a needle,
to sew, or swing objects as heavy as a baseball bat to drive a ball more than 100
yards. The brain areas that allow us to adjust the force of our movements in these ways
include the basal ganglia, a collection of nuclei within the forebrain that make connections
with the motor cortex and with the midbrain. As shown in Figure 10-12, a
prominent structure in the basal ganglia is the caudate putamen, a large cluster of nuclei
that extends as a “tail” into the temporal lobe, ending in the amygdala.
The basal ganglia receive inputs from two main sources:
1. All areas of the neocortex and limbic cortex, including the motor cortex, project
to the basal ganglia.
2. The nigrostriatial dopaminergic activating system projects to the basal ganglia
from the substantia nigra, a cluster of darkly pigmented cells in the midbrain.
Basal ganglia nuclei project back to both the motor cortex and the substantia nigra as
Two different, in many ways opposite, kinds of movement disorders result from
damage to the basal ganglia. If cells of the caudate putamen are damaged, unwanted
choreiform (writhing and twitching) movements result. For example, Huntington’s
chorea, in which cells of the caudate putamen are destroyed, is characterized by
involuntary and exaggerated movements (see “Huntington’s Chorea” on page 000).
Other examples of involuntary movements related to caudate putamen damage are the
In Review .
Basic innate patterns of movement common to a particular mammalian species are organized
in the motor cortex as synergies. The discharge patterns of motor-cortex neurons
suggest that these neurons take part in planning and initiating movements as well
as in carrying them out. Their discharge rate is related both to the force of muscle contraction
and to the direction of a movement. Individual motor-cortex neurons are maximally
responsive to movements in a particular direction. The topographic map of the
motor cortex in a particular species is related to the species’ body parts that are capable
of making the most skillful movements. The relation between neurons in the motor
cortex and the movement of specific muscles is plastic. Considerable change can
take place in the cortical motor map and in recovery of function after injury to the motor
Investigate the area on control of
movement in the module on Control of
Movement on your CD. Look for details
on what happens when there is damage
to these regions.
Tail of
caudate nucleus
Figure 10-12
Basal Ganglia Connections The
caudate putamen in the basal ganglia
connects to the amygdala through the
tail of the caudate nucleus. The basal
ganglia also makes reciprocal
connections with the substantia nigra,
receives input from most regions of the
cortex, and sends input into the frontal
lobes through the thalamus.
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364 ! CHAPTER 10
unwanted tics and vocalizations peculiar to Tourette’s syndrome, which is discussed in
“Tourette’s Syndrome.”
In addition to causing involuntary movements, or hyperkinetic symptoms, damage
to the basal ganglia can result in a loss of motor ability, or hypokinetic symptoms.
One hypokinetic disorder, Parkinson’s disease, has been considered in several preceding
chapters. It is caused by the loss of dopamine cells in the substantia nigra and
is characterized by an inability to produce normal movements. The two different
kinds of symptoms that arise subsequent to basal ganglia damage—hyperkinetic and
hypokinetic symptoms—suggest that a major function of these nuclei is to modulate
Steven Keele and Richard Ivry (1991) tried to relate the two opposing kinds of
basal ganglia symptoms by suggesting that the underlying function of the basal ganglia
is to generate the force required for each particular movement. According to this idea,
Tourette’s Syndrome
Focus on Disorders
The neurological disorder Tourette’s syndrome (TS) was first
described in 1885 by Georges Gilles de la Tourette, a young
French neurologist and friend of Sigmund Freud. Here is how
de la Tourette described the symptoms as they appeared in
Madame de D., one of his patients:
Madame de D., presently age 26, at the age of 7 was
afflicted by convulsive movements of the hands and
arms. These abnormal movements occurred above
all when the child tried to write, causing her to
crudely reproduce the letters she was trying to trace.
After each spasm, the movements of the hand became
more regular and better controlled until another
convulsive movement would again interrupt
her work. She was felt to be suffering from over-excitement
and mischief, and because the movements
became more and more frequent, she was subject to
reprimand and punishment. Soon it became clear
that these movements were indeed involuntary and
convulsive in nature. The movements involved the
shoulders, the neck, and the face, and resulted in
contortions and extraordinary grimaces. As the disease
progressed, and the spasms spread to involve
her voice and speech, the young lady made strange
screams and said words that made no sense (Friedhoff
& Chase, 1982).
The incidence of Tourette’s syndrome is fewer than 1 in
1000 people. It is found in all racial groups and seems to be
hereditary. The age range of onset is between 2 and 25 years.
The most frequent symptoms are involuntary tics and involuntary
complex movements, such as hitting, lunging, or
People with the syndrome may also suddenly emit cries
and other vocalizations or inexplicably utter words that do not
make sense in the context, including scatology and swearing.
Tourette’s syndrome is not associated with any other disorders,
although much milder cases of tics may be related to it.
Tourette’s syndrome is thought to be due to an abnormality
of the basal ganglia, especially the right-hemisphere basal
ganglia. It is one of the hyperkinetic disorders that can result
from basal ganglia dysfunction. Its symptoms can be controlled
with haloperidol, which blocks dopamine synapses in
the basal ganglia.
Many people with TS function quite well, coping successfully
with their symptoms. There are people with TS in all
walks of life, even surgeons who must perform delicate operations.
With the existence of the Tourette’s Society in
the past 20 years, public awareness of the disorder has increased.
Children with TS are now less likely to be diagnosed
as having a psychiatric condition, being hyperactive, or being
Hyperkinetic symptom. Symptom of
brain damage that results in excessive
involuntary movements, as seen in
Tourette’s syndrome.
Hypokinetic symptom. Symptom of
brain damage that results in a paucity of
movement, as seen in Parkinson’s disease.
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some types of basal ganglia damage cause errors of too much force
and so result in excessive movement, whereas other types of damage
cause errors of too little force and so result in insufficient movement.
Keele and Ivry tested their hypothesis by giving healthy subjects
as well as patients with various kinds of basal ganglia disorders a task
that tested their ability to exert appropriate amounts of force. The
subjects viewed a line on a television screen. By pushing a button with
varying amounts of force, they could produce a second line to match
the length of the first.
After a number of practice trials, the subjects were asked to press
the button with the appropriate amount of force even when the first
line was no longer visible as a guide. In contrast with control subjects,
patients with basal ganglia disorders were unable to reliably do so. The
force that they exerted was usually too little or too much, resulting in
a line too short or too long.
What neural pathways enable the basal ganglia to modulate the force of movements?
Basal ganglia circuits are quite complex, but one theory holds that two pathways
affect the activity of the motor cortex: an inhibitory pathway and an excitatory
pathway (Alexander & Crutcher, 1990). Both these pathways converge on an area of
the basal ganglia called the internal part of the globus pallidus (GPi), as charted in
Figure 10-13.
The GPi in turn projects into the the ventral thalamic nucleus, and the thalamus
projects to the motor cortex. The thalamic projection modulates the size or force of a
movement that the cortex produces and is influenced by the GPi. The GPi acts like the
volume dial on a radio because its output determines whether a movement will be
weak or strong.
The inputs to the GPi are shown in red and green in Figure 10-13 to illustrate how
they affect movement. If activity in the inhibitory pathway (red) is high relative to that
in the excitatory pathway (green), inhibition of the GPi will predominate, and the thalamus
will be free to excite the cortex, thus amplifying movement force. If, on the other
hand, activity in the excitatory pathway is high relative to that in the inhibitory pathway,
excitation of the GPi will predominate, and the thalamus will be inhibited, thus
reducing input to the cortex and decreasing the force of movements.
The idea that the GPi acts like a volume control over movement is currently receiving
a great deal of attention as the basis for one type of treatment for Parkinson’s
disease. If the GPi is surgically destroyed in Parkinson patients,muscular rigidity is reduced
and the ability to make normal movements is improved. Also consistent with
this “volume hypothesis,” recordings made from cells of the globus pallidus show that
they are excessively active in people with Parkinson’s disease.
The Cerebellum and Movement Skill
Musicians have a saying:“Miss a day of practice and you’re OK; miss two days and you
notice; miss three days and the world notices.” Apparently, some change must take
place in the brain when practice of a motor skill is neglected. The cerebellum may be
the part of the motor system that is affected.Whether the skill is playing a musical instrument,
pitching a baseball, or typing on a computer keyboard, the cerebellum is critical
for acquiring and maintaining motor skills.
The cerebellum, a large and conspicuous part of the motor system, sits atop the
brainstem, clearly visible just behind the cerebral cortex. The cerebellum is divided into
spinal cord
Globus pallidus
Globus pallidus
Figure 10-13
Regulating Movement Force Two
pathways in the basal ganglia modulate
cortically produced movements. On this
flowchart, the green pathways are
excitatory, and the red are inhibitory.
The indirect pathway has an excitatory
effect on the GPi, whereas the direct
pathway has an inhibitory effect. If
activity in the indirect pathway
dominates, the thalamus shuts down
and the cortex is unable to produce
movement. If direct-pathway activity
dominates, the thalamus can become
overactive, thus amplifying movement.
Adapted from “Functional Architecture of Basal
Ganglia Circuits: Neural Substrates of Parallel
Processing,” by R. E. Alexander and M. D.
Crutcher, 1990, Trends in Neuroscience, 13, p. 269.
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two hemispheres, as is the cerebral cortex. A small lobe, the flocculus, projects from its
ventral surface. Although smaller than the neocortex, the cerebellum has many more
gyri and sucli than the neocortex, and it contains about one-half of all the neurons in
the entire nervous system.
As Figure 10-14 shows, the cerebellum can be divided into several regions, each
specialized in a different aspect of motor control.At its base, the flocculus receives projections
from the middle-ear vestibular system, described later in the chapter, and takes
part in the control of balance.Many of its projections go to the spinal cord and to the
motor nuclei that control eye movements.
Just as the motor cortex has a homuncular organization and a number of homunculi,
the hemispheres of the cerebellum have at least two, as shown in Figure 10-14.
The most medial part of each homunculus controls the face and the midline of the
body. The more lateral parts are connected to areas of the motor cortex and are associated
with movements of the limbs, hands, feet, and digits. The pathways from the
hemispheres project to nuclei of the cerebellum, which in turn project to other brain
regions, including the motor cortex.
To summarize the cerebellum’s topographic organization, the midline of the homunculus
is represented in its central part, whereas the limbs and digits are represented
in the lateral parts. Tumors or damage to midline areas of the cerebellum disrupt balance,
eye movement, upright posture, and walking but do not substantially disrupt
other movements such as reaching, grasping, and using the fingers. For example, a person
with medial damage to the cerebellum may,when lying down, show few symptoms.
Damage to lateral parts of the cerebellum disrupts arm, hand, and finger movements
much more than movements of the body’s trunk.
Attempts to understand how the cerebellum controls movement have centered on
two major ideas: that the cerebellum (1) plays a role in the timing of movements and
(2) maintains movement accuracy. Keele and Ivry support the first idea. They suggest
that underlying impairment in disorders of the cerebellum is a loss of timing.
366 ! CHAPTER 10
Inferior surface of cerebellum
Digits Limbs
Face and
Medial part of cerebellar
hemispheres (movement of
body midline)
Floccular lobe
(eye movements and balance)
Lateral parts of cerebellar
hemispheres (movement of body
Figure 10-14
Cerebellar Homunculus The
cerebellar hemispheres control body
movements, and the flocculus controls
eye movements and balance. The
cerebellum is topographically organized:
its more medial parts represent the
midline of the body and its more lateral
parts represent the limbs and digits.
Photograph of cerebellum reproduced from The
Human Brain: Dissections of the Real Brain, by
T. H. Williams, N. Gluhbegovic, and J. Jew, on CDROM.
Published by Brain University, brainuniversity.
com 2000.
ED.: Pls. proof
CH10.qxd 1/6/05 3:20 PM Page 366

Keele and Ivry (1991) maintain that the cerebellum acts as a
clock or pacemaker to ensure that both movements and perceptions
are appropriately timed. In a motor test of timing, subjects were
asked to tap a finger to keep time with a metronome. After a number
of taps, the metronome was turned off and the subjects were to
maintain the beat. Those with damage to the cerebellum, especially
to the lateral cerebellum, were impaired on the task.
In a perceptual test of timing, subjects were presented with two
pairs of tones. The silent period between the first two tones was always
the same length, whereas the silent period between the second
two tones changed from trial to trial. The subjects had to judge
whether the second silent period was longer or shorter than the
first. Those with damage to the cerebellum were impaired on this
Apparently, the cerebellum can act like a clock to time perceptions
as well as movements. Not all researchers believe that the cerebellum’s
major contribution to controlling movements is only one
of timing, however. Tom Thach and his coworkers (1992) argued
that another role for the cerebellum is to help make the adjustments
needed to keep movements accurate.
The Thach team gathered evidence in support of this view by
having subjects throw darts at a target, as shown in the Procedure
section of Experiment 10-5. After a number of throws, which allowed
the subjects to become reasonably accurate, the subjects put
on glasses containing wedge-shaped prisms that displaced the apparent
location of the target to the left.Now when the subjects threw
a dart, it landed to the left of the intended target.
All subjects showed this initial distortion in aim. But then came
an important difference, graphed in the Results section of Experiment
10-5.When normal subjects saw the dart miss the mark, they
adjusted each successive throw until reasonable accuracy was restored.
In contrast, subjects with damage to the cerebellum could not
correct for this error. They kept missing the target far to the left time
after time.
Next the control subjects removed the prism glasses and threw
a few more darts. Again, another significant difference emerged. The
first dart thrown by each normal subject was much too far to the
right (owing to the previous adjustment that the subject had learned
to make), but soon each adjusted once again until his or her former
accuracy was regained.
In contrast, subjects with damage to the cerebellum showed no
aftereffects from having worn the prisms, as if they had never compensated
for the glasses to begin with. This experiment suggests that
many movements that we make—whether throwing a dart, hitting a
ball with a bat, writing neatly, or painting a work of art—depend on
moment-to-moment learning and adjustments that are made by the
To better understand how the cerebellum improves motor skills
by adjusting movements, imagine throwing a dart yourself. Suppose you aim at the
bull’s eye, throw the dart, and find that it misses the board completely. You then aim
again, this time adjusting your throw to correct for the original error. Notice that there
Normal subject
Distance from target
Distance from target
(to the left) (to the right) (to the left) (to the right)
Subject throws
dart at target
Prisms removed,
subject adapts
Subject wears
prisms that
divert gaze
Patient with damage to cerebellum
The normal subject adapts when wearing the prisms and
shows aftereffects when the prisms are removed. A patient
with damage to the cerebellum fails to correct throws while
wearing the prisms and shows no aftereffects when the
prisms are removed.
Question: Does the cerebellum help to make adjustments required to keep
movements accurate?
Initial throws With prisms Prisms removed
Initial throws With prisms Prisms removed
Adapted from “The Cerebellum and the Adaptive
Coordination of Movement,” by W. T. Thach, H. P.
Goodkin, and J. G. Keating, 1992, Annual Review of
Neuroscience, 15, p. 429.
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are actually two versions of your action: (1) the movement
that you intended to make and (2) the actual
movement as recorded by sensory receptors in your
arm and shoulder.
If the intended movement is successfully carried
out, you need make no correction on your next try.
But if you miss, an adjustment is called for. One way
in which the adjustment might be made is through the
feedback circuit shown in Figure 10-15.
The cortex sends instructions to the spinal cord to
throw a dart at the target. A copy of the same instructions
is sent to the cerebellum through the inferior olive
in the brainstem. When you then throw the dart, the
sensory receptors in your arm and shoulder code the
actual movement that you make and send a message
about it back to the cerebellum through the spinocerebellar
tract. This sensory pathway carries information
about movements that have been made from the spinal
cord to the cerebellum.
The cerebellum now has information about both
versions of the movement: what you intended to do
and what you actually did. The cerebellum can now calculate the error and tell the cortex
how to correct the movement.When you next throw a dart, you incorporate that
correction into your throw.
The motor system is responsible for producing movements, but movement would
quickly become impaired without sensation. The somatosensory system tells us what
the body is up to and what’s going on in the environment by providing information
about bodily sensations, such as touch, temperature, pain, position in space, and movement
of the joints.
In addition to helping us learn about the world, the somatosensory system allows
us to distinguish what the world does to us from what we do to it. For example, when
someone pushes you sideways, your somatosensory system tells you that you have been
pushed. If you lunge to the side yourself, your somatosensory system tells you that you
did the moving.
In Review .
The basal ganglia contribute to motor control by adjusting the force associated with each
movement. Consequently, damage to the basal ganglia results either in unwanted, involuntary
hyperkinetic movements (too much force being exerted) or in such hypokinetic
rigidity that movements are difficult to perform (too little force being exerted). The cerebellum
contributes to the control of movement by improving movement skill. One way in
which it may do so is by keeping track of the timing of movements. Another way is by
making adjustments in movements to maintain their accuracy. In the latter case, the cerebellum
compares an intended movement with an actual movement, calculates any necessary
corrections, and informs the cortex.
368 ! CHAPTER 10
reach spinal cord
Inferior olive
sends copy
of instructions
from actual
Corticospinal tracts
Figure 10-15
Intention, Action, and
Feedback A feedback circuit
allows the cerebellum to
correct movements to match
intention. By comparing the
message for the intended
movement with the movement
that was actually performed,
the cerebellum can send an
error message to the cortex to
improve the accuracy of a
subsequent movement.
Review the somatosensory system in
the brain-overview section in the Central
Nervous System module on your CD.
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We are exploring the somatosensory system and the motor system in the same
chapter because somatosensation has a closer relation to movement than the other
senses do. If we lose sight or hearing or even both, we can still move around, and the
same is true of other animals. Fish that inhabit deep, dark caves cannot see at all, yet
they are able to move about normally. Animals, such as the butterfly, that cannot hear
can still move very well. If an animal were to lose its body senses, however, its movements
would quickly become so impaired that it would not be able to survive. Some
aspects of somatosensation are absolutely essential to movement.
In considering the motor system, we started at the cortex and followed the motor
pathways out to the spinal cord. This efferent (outward) route makes sense because it
follows the direction in which instructions regarding movements flow. As we explore
the somatosensory system, we will proceed in the opposite direction, because afferent
sensory information flows inward from sensory receptors in various parts of the body
through sensory pathways to the cortex.
Somatosensation is unique among sensory systems. It is not localized in the head
as are vision, hearing, taste, and smell but rather is distributed throughout the entire
body. Somatosensory receptors are found in all parts of the body, and neurons from
these receptors carry information to the spinal cord.
Within the spinal cord, two somatosensory pathways project to the brain and,
eventually, to the somatosensory cortex. One part of the somatosensory system, however,
is confined to a single organ, the middle ear, which houses the vestibular system
that contributes to our sense of balance and head movement. Before we detail its workings,
we will investigate the anatomy of the somatosensory system and how it contributes
to movement.
Somatosensory Receptors and Perception
Our bodies are covered with sensory receptors. They include our skin and body hair
and are embedded in both surface layers and deeper layers of the skin and in muscles,
tendons, and joints. Some receptors consist simply of the surface of a sensory neuron
dendrite. Other receptors include a dendrite and other tissue, such as the dendrite attached
to a hair or covered by a special capsule or attached by a sheath of connective
tissue to adjacent tissue.
The density of sensory receptors, in the skin, muscles, tendons, and joints, varies
greatly in different parts of the body. The variation in density is one reason why different
parts of the body are more or less sensitive to stimulation. Body parts that are
very sensitive to touch or capable of fine movements—including the hands, feet, lips,
and eyes—have many more sensory receptors than other body parts do. Sensitivity to
different somatosensory stimuli is also a function of the kinds of receptors that are
found in a particular region.
Humans have two kinds of skin, hairy skin and glabrous skin, which is hairless
and exquisitely sensitive to a wide range of stimuli. Glabrous skin, which includes
the skin on the palms of the hands and feet, the lips, and the tongue, is much more
richly endowed with receptors than hairy skin is. The need for heightened sensitivity
in glabrous skin is due to the fact that it covers the body parts that we use to explore
The touch sensitivity of skin is often measured with a two-point sensitivity test.
This test consists of touching the skin with two sharp points simultaneously and observing
how close together the points can be placed while still being detected as two
points rather than one. On glabrous skin, we can detect the two points when they are
as close as 3 mm apart.
Two-point sensitivity
Glabrous skin. Skin that does not have
hair follicles but contains larger numbers
of sensory receptors than do other skin
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On hairy skin, two-point sensitivity is much weaker. The two points seem to
merge into one below a separation distance ranging from 2 to 5 cm, depending on exactly
which part of the body is tested. You can confirm these differences in sensitivity
on your own body by touching two sharp pencil points to a palm and to a forearm,
varying the distances that you hold the points apart. Be sure not to look as you touch
each surface.
Figure 10-16 illustrates a sampling of the various somatosensory receptors located
in the skin. There may be as many as 20 or more kinds of somatosensory receptors in
the human body, but they can all be classified into the three groupings in Figure 10-16,
depending on the type of perception that they enable. These three types of perception
and the receptors that mediate them are
nocioception, the perception of pain and temperature.Nocioceptors consist of free
nerve endings. When these endings are damaged or irritated, they secrete chemicals,
usually peptides, which stimulate the nerve to produce an action potential. The action
potential then conveys a message about pain or temperature to the central nervous
hapsis, the perception of objects that we grasp and manipulate or that contact the
body—that is, the perception of fine touch and pressure. Haptic receptors are found
both in superficial layers and in deep layers of the skin and are attached to body hairs
as well. A haptic receptor consists of a dendrite attached to a hair or to connective tissue
or a dendrite encased in a capsule of tissue.Mechanical stimulation of the hair, tissue,
or capsule activates special channels on the dendrite, which in turn initiate an
action potential. Differences in the tissue forming the capsule determine the kinds of
mechanical energy conducted through the haptic receptor to the nerve. For example,
pressure that squeezes the capsule of a Pacinian corpuscle is the necessary stimulus for
initiating an action potential.
370 ! CHAPTER 10
Hapsis (fine touch and pressure)
Meissner’s corpuscle (touch)
Pacinian corpuscle (flutter) Rapid
Ruffini corpuscle (vibration) Rapid
Merkel's receptor
(steady skin indentation)
Hair receptors (flutter or steady
skin indentation)
Free nerve endings for pain
(sharp pain and dull pain)
Free nerve endings for temperature
(heat or coldness)
Nocioception (pain and temperature) Adaptation
Damage to the dendrite or
to surrounding cells releases
chemicals that stimulate the
dendrite to produce action
Pressure on the various
types of tissue capsules
mechanically stimulates the
dendrites within them to
produce action potentials.
Proprioception (body awareness)
Muscle spindles (muscle stretch)
Golgi tendon organs (tendon stretch) Rapid
Joint receptors (joint movement) Rapid
Movements stretch the
receptors to mechanically
stimulate the dendrites
within them to produce
action potentials.
Figure 10-16
Somatosensory Receptors Perceptions
derived from the body senses of
nocioception, hapsis, and proprioception
depend on different receptors located in
different parts of the skin, muscles,
joints, and tendons.
Nocioception. Perception of pain and
Hapsis. Perceptual ability to discriminate
objects on the basis of touch.
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proprioception, the perception of the location and movement of the body. Proprioceptors,
which also are encapsulated nerve endings, are sensitive to the stretch of muscles
and tendons and the movement of joints. In the Golgi tendon organ shown at the
bottom of Figure 10-16, for instance, an action potential is triggered when the tendon
moves, stretching the receptor attached to it.
Somatosensory receptors are specialized to tell us two things about a sensory event:
when it occurs and whether it is still occurring. Information about when a stimulus occurs
is handled by rapidly adapting receptors. These receptors respond to the beginning
and the end of a stimulus and produce only brief bursts of action potentials. As
shown in Figure 10-16,Meissner’s corpuscles (which respond to touch), Pacinian corpuscles
(which respond to fluttering sensations), and Ruffini corpuscles (which respond
to vibration) are all rapidly adapting receptors.
In contrast, slowly adapting receptors detect whether a stimulus is still occurring.
These receptors continue to respond as long as a sensory event is present. For instance,
after you have put on an article of clothing and become accustomed to how it feels,
only slowly adapting receptors (such as Merkel’s receptors and hair receptors) remain
active. The difference between a rapidly adapting and a slowly adapting receptor is due
in part to the way in which each is stimulated and in part to the way in which ion channels
in the membrane of the dendrite respond to mechanical stimulation.
Dorsal-Root Ganglion Neurons
The dendrites that carry somatosensory information belong to neurons whose cell bodies
are located just outside the spinal cord in dorsal-root ganglia (see Figure 2-28). Their
axons enter the spinal cord. As illustrated in Figure 10-17, such a dorsal-root ganglion
neuron contains a single long dendrite, only the tip of which is responsive to sensory
stimulation. This dendrite is continuous with the somatosensory neuron’s axon.
Each segment of the spinal cord has one dorsal-root ganglion on each side containing
many dorsal-root ganglion neurons, each of which responds to a particular
kind of somatosensory information. In the spinal cord, the axons of dorsal-root ganglia
neurons may synapse with other neurons or continue to the brain or both.
Cell body
Somatosensory neuron
…have large, myelinated axons
whose receptors are located in
the skin, muscles, and tendons.
Spinal cord
Dorsal-root ganglion
neurons that carry
fine touch and
pressure information…
As the name implies, the
cell body is located in a
dorsal-root ganglion.
Fine touch and pressure axons
ascend in the ipsilateral spinal
cord, forming the dorsal
spinothalamic tract.
Figure 10-17
Haptic Dorsal-Root Ganglion Neuron
The dendrite and axon of this dorsalroot
ganglion neuron are contiguous
and carry sensory information from the
skin to the central nervous system. The
large myelinated dorsal-root axons travel
up the spinal cord to the brain in the
dorsal column, whereas the small axons
synapse with neurons whose axons cross
the spinal cord and ascend on the other
side (shown in Figure 10-18).
Proprioception. Perception of the
position and movement of the body,
limbs, and head.
Rapidly adapting receptor. Body
sensory receptor that responds briefly to
the onset of a stimulus on the body.
Slowly adapting receptor. Body
sensory receptor that responds as long as
a sensory stimulus is on the body.
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The axons of dorsal-root ganglion neurons vary in diameter and myelination.
These structural features are related to the kind of information carried by the neurons.
Proprioceptive (location and movement) information and haptic (touch and pressure)
information are carried by dorsal-root ganglion neurons that have large, well-myelinated
axons. Nocioceptive (pain and temperature) information is carried by dorsalroot
ganglion neurons that have smaller axons with little or no myelination.
Because of their size and myelination, the larger neurons carry information much
faster than the smaller neurons do. One explanation of why proprioceptive and haptic
neurons are designed to carry messages quickly is that their information requires rapid
responses. For instance, the nervous system must react to moment-to-moment changes
in posture and to the equally rapid sensory changes that take place as we explore an object
with our hands. In contrast, when the body is injured or cold, such rapid responding
is not as essential, because these forms of stimulation usually continue for
quite some time.
We can support the claim that sensory information is essential for movement by
describing what happens when dorsal-root ganglion cells do not function. A clue
comes from a visit to the dentist. If you have ever had a tooth “frozen” for dental work,
you have experienced the very strange effect of losing sensation on one side of your
face. Not only do you lose pain perception, you also seem to lose the ability to move
your facial muscles properly, making it awkward to talk, eat, and smile. So, even though
the anesthetic is blocking sensory nerves, your movement ability is affected as well.
In much the same way, damage to sensory nerves affects both sensory perceptions
and motor abilities. John Rothwell and his coworkers (1982) described a patient, G.O.,
who was deafferented (lost afferent sensory fibers) by a disease that destroyed sensory
dorsal-root ganglion neurons. G. O. had no somatosensory input from his hands. He
could not, for example, feel when his hand was holding something. However, G. O.
could still accurately produce a range of finger movements, and he could outline figures
in the air even with his eyes closed. He could also move his thumb accurately
through different distances and at different speeds, judge weights, and match forces by
using his thumb.
Nevertheless, his hands were relatively useless to him in daily life. Although G. O.
could drive his old car, he was unable to learn to drive a new one. He was also unable
to write, to fasten shirt buttons, or to hold a cup.
He could begin movements quite normally, but, as he proceeded, the movement
patterns gradually fell apart, ending in failure. Part of G. O.’s difficulties lay in maintaining
muscle force for any length of time.When he tried to carry a suitcase, he would
quickly drop it unless he continually looked down to confirm that it was there. Clearly,
although G. O. had damage only to his sensory neurons, he suffered severe motor disability
as well, including the inability to learn new motor skills.
Abnormalities in movement also result from more-selective
damage to neurons that carry proprioceptive information about
body location and movement. Neurologist Oliver Sacks (1998) gave
a dramatic example in his description of a patient, Christina, who
suffered damage to proprioceptive sensory fibers throughout her
body after taking megadoses of vitamin B6. Christina was left with
very little ability to control her movements and spent most of each day lying prone.
Here is how she describes what a loss of proprioception means:
“What I must do then,” she said slowly, “is use vision, use my eyes, in every situation
where I used—what do you call it?—proprioception before. I’ve already
noticed,” she added,musingly, “that I may lose my arms. I think they are
in one place, and I find they’re in another. This proprioception is like the eyes
372 ! CHAPTER 10
Deafferentation. Loss of incoming
sensory input usually due to damage to
sensory fibers; also loss of any afferent
input to a structure.
Oliver Sacks
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of the body, the way the body sees itself. And if it goes, as it’s gone with me,
it’s like the body’s blind. My body can’t see itself if it’s lost its eyes, right? So I
have to watch it—be its eyes.” (Sacks, 1998, p. 46)
Clearly, although Christina’s motor system is intact, she is almost completely immobilized
without a sense of where her body is in space and what her body is doing.
She tries to use her eyes to compensate for loss of proprioception, but visual monitoring
is less than satisfactory. Just imagine what it would be like to have to look at each
of your limbs in order to move them to appropriate locations, which explains why proprioception
is so essential for movement (Cole, 1995).
Somatosensory Pathways to the Brain
As the axons of somatosensory neurons enter the spinal cord, they divide, forming two
pathways to the brain. The haptic–proprioceptive axons ascend the spinal cord ipsilaterally
(on the same side of the body on which they enter), whereas nocioceptive fibers
synapse with neurons whose axons cross to the contralateral side of the spinal cord before
ascending to the brain. Figure 10-18 shows these two routes through the spinal
cord. The haptic–proprioceptive pathway is shown as a sold red line and the nocioceptive
pathway as a dashed red line.
The haptic–proprioceptive axons are located in the dorsal portion of the spinal cord
and form the dorsal spinothalamic tract. These axons synapse in the dorsal-column
nuclei located at the base of the brain.Axons of neurons
in the dorsal-column nuclei then cross over to the other
side of the brainstem and ascend through the brainstem
as part of a pathway called the medial lemniscus.
These axons synapse in the ventrolateral thalamus.
The neurons of the ventrolateral thalamus send most of
their axons to the somatosensory cortex, but some
axons go to the motor cortex. Thus, three neurons are
required to carry haptic–proprioceptive information to
the brain: dorsal-root ganglia neurons, dorsal-column
nuclei neurons, and thalamic neurons.
The nocioceptive axons, as already stated, take a
different route to the brain. They synapse with neurons
in the dorsal part of the spinal cord’s gray matter. These
neurons, in turn, send their axons to the ventral part of
the other side of the spinal cord, where they form the
ventral spinothalamic tract. This tract joins the medial
lemniscus in the brainstem to continue on to the
ventrolateral thalamus.
Some of the thalamic neurons receiving input from
axons of the ventral spinothalamic tract also send their
axons to the somatosensory cortex. So, again, three neurons
are required to convey nocioceptive information to
the brain: dorsal-root neurons, spinal-cord gray-matter
neurons, and ventrolateral thalamic neurons.
Notice that the haptic-proprioceptive and the
nocioceptive pathways enter the spinal cord together,
separate in the spinal cord, and join up again in the
brainstem. Thus, two separate pathways in the spinal
Dorsal-root ganglion Spinal cord
neurons respond to fine
touch and pressure; joint,
tendon, and muscle
change; and pain and
The dorsal-column nuclei
relay fine touch and
pressure sensations.
The ventral spinothalamic
tract receives input from
pain and temperature
neurons and then joins
the pathway called the
medial lemniscus.
The medial lemniscus
contains axons that carry
sensory information to the
ventrolateral thalamus.
The ventrolateral thalamus
relays sensory information
to the somatosensory cortex.
The primary somatosensory
cortex (areas 3-1-2) receives
somatosensory information.
Figure 10-18
Dual Somatosensory Pathways to the
Brain As neurons from the dorsal-root
ganglia enter the spinal cord, the
somatosensory pathways to the brain
Dorsal spinothalamic tract. Pathway
that carries fine-touch and pressure fibers.
Ventrolateral thalamus. Part of the
thalamus that carries information about
body senses to the somatosensory cortex.
Ventral spinothalamic tract. Pathway
from the spinal cord to the thalamus that
carries information about pain and
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374 ! CHAPTER 10
cord convey somatosensory information. Because of this arrangement, unilateral damage
in the spinal cord results in distinctive sensory losses to both sides of the body
below the site of injury.
As is illustrated in Figure 10-19, there is loss of hapsis and proprioception on the
side of the body on which the damage occurred and there is a loss of nocioception on
the opposite side of the body. Unilateral damage to the dorsal roots or in the brainstem
or the thalamus affects hapsis, proprioception, and nocioception equally, because these
parts of the pathways for hapsis and proprioception and that for nocioception lie in
close proximity.
Spinal Reflexes
Not only do somatosensory nerve fibers convey information to the cortex but they participate
in behaviors mediated by the spinal cord and brainstem as well. Spinal-cord somatosensory
axons, even those ascending in the dorsal columns, give off axon collaterals
that synapse with interneurons and motor neurons on both sides of the spinal cord. The
circuits made between sensory receptors and muscles through these connections mediate
spinal reflexes.
The simplest spinal reflex consists of a single synapse between a sensory neuron and
a motor neuron. Figure 10-20 illustrates such a monosynaptic reflex, the knee jerk that
affects the quadriceps muscle of the thigh,which is anchored to the leg bone by the patellar
tendon.When the lower leg hangs free and this tendon is tapped with a small hammer,
the quadriceps muscle is stretched, activating the stretch-sensitive sensory receptors embedded
in it.
The sensory receptors then send a signal to the spinal cord through sensory neurons
that synapse with motor neurons projecting back to the same thigh muscle. The
discharge from the motor neurons stimulates the muscle, causing it to contract to resist
the stretch. Because the tap is brief, the stimulation is over before the motor message ar-
Spinal cord
A tap on the patellar
tendon stretches the
quadriceps muscle.
The quadriceps contracts,
extending the lower leg.
The sensory nerve
responds to the
muscle stretch…
…by sending a signal to the spinal
cord, where it connects to a motor
neuron through a single synapse.
The motor neuron
stimulates the quadriceps
muscle to contract and
reduce the stretch.
damage to
spinal cord
…and loss of pain
and temperature
sensation on the
opposite side of
the body below
the cut.
Unilateral damage
causes loss of finetouch
and pressure
sensation on the
same side of the
body below the
Figure 10-19
Effects of Unilateral Injury Damage
to only one side of the spinal cord has
different effects on fine-touch and
pressure sensations compared with those
on pain and temperature sensations.
Figure 10-20
Monosynaptic Reflex
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rives; so the muscle contracts even though it is no longer stretched. This contraction
pulls the leg up, thereby producing the reflexive knee jerk.
This very simple reflex entails monosynaptic connections between single sensory
neurons and single motor neurons. Somatosensory axons from other receptors, especially
those of the skin, make much more complex connections with both interneurons
and motor neurons. These multisynaptic connections are responsible for morecomplex
spinal reflexes that include many muscles on both sides of the body.
Feeling and Treating Pain
One survey concerning complaints about pain reports that the average person will suffer
the equivalent of 10 years of pain in his or her lifetime. Another survey reports that
36 percent—more than a third—of patients visiting a physician’s office complain of
chronic pain. Pain symptoms may be related to arthritis, myalgias (muscle pains), migraine,
cancer, nocioceptive pain (due to irritation of pain receptors), or neuropathic
pain (due to irritation of pain nerves). People suffer pain as a result of acute injuries—
including sprains, broken bones, cuts, burns—and stiffness due to exercise. Women
may experience pain during menstruation, pregnancy, and childbirth.
People can also experience “central pain” in a part of their body that is not obviously
injured. One kind of central pain, phantom pain, seems to occur in a limb, but
the limb has been lost. People suffering pain would happily dispense with it. But pain
is necessary, because the occasional person born without pain receptors experiences
body deformities through failure to adjust posture and acute injuries through failure
to avoid harmful situations.
Pain is a perception that results from the synthesis of a number of kinds of sensory
information. There may be as many as eight different kinds of pain fibers, judging
from the peptides and other chemicals released by pain fibers when irritated or
damaged. Some of these chemicals irritate surrounding tissue, stimulating the tissue to
release other chemicals to stimulate blood flow and to stimulate the pain fibers themselves.
These reactions contribute to pain, redness, and swelling at the site of an injury.
In addition, haptic information contributes to the perception of pain. For example,
people can accurately report the location and characteristics of various kinds of
pain, but, in the absence of fine-touch and pressure information, pain is more difficult
to identify and localize.
As described earlier, the ventral spinothalamic tract is the main pain pathway to
the brain, but as many as four other pathways may carry pain information from the
spinal cord to the brain. These pathways are both crossed and uncrossed and project
to the reticular formation of the midbrain, where they may produce arousal, to the
amygdala, where they may produce emotional responses, and to the hypothalamus,
where they activate hormonal and cardiovascular responses. The fact of multiple pain
pathways in the spinal cord makes it difficult to treat chronic pain by selectively cutting
the ventrospinothalamic tract.
Circuits in the spinal cord also allow haptic–proprioceptive and nocioceptive pathways
to interact. Such interactions may be responsible for our very puzzling and variable
responses to pain. For example, people who are engaged in combat or intense
athletic competition may receive a serious injury to the body but start to feel the pain
only much later.
A friend of ours, F.V.,who was attacked by a grizzly bear while hiking, received 200
stitches to bind his wounds.When friends asked if it hurt to be bitten by a grizzly bear,
he surprisingly answered no, explaining, “I had read the week before about someone
On your CD, go to the area on the
spinal reflexes in the Control of
Movement module for more illustrations
of the spinal cord and the spinal reflexes.
Monosynaptic reflex. Reflex requiring
one synapse between sensory input and
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who was killed and eaten by a grizzly bear. So I was thinking that this
bear was going to eat me unless I got away. I did not have time for
pain. I was fighting for my life. It was not until the next day that I
started feeling pain and fear.”
Pain is puzzling in the variety of ways in which it can be lessened.
The primacy of our friend’s fear over his pain is related to the stress
that he was under. Failure to experience pain in a fight-or flightsituation
may be related to the activation of endogenous brain opioids
(see Chapter 5). Treatments for pain include opioid drugs (such
as morphine), acupuncture (which entails the rapid vibration of
needles embedded in the skin), and simply rubbing the area surrounding
the injury. To explain in part how pain can be suppressed in so many different
ways, Ronald Melzack and Patrick Wall (1965) proposed a “gate” theory of pain.
The essence of their idea is that activity due to haptic–proprioceptive stimulation
can reduce pain, whereas the absence of such stimulation can increase pain. They argued
that activity in the haptic–proprioceptive pathway can inhibit the pain pathway
in the spinal cord through axon collaterals to spinal-cord interneurons. These neurons
in turn inhibit pain neurons. For example, if the fine-touch and pressure pathway is active,
it will excite the interneuron, which will in turn inhibit the second-order neurons
in the pain and temperature pathway.
The action of this pain gate is charted in Figure 10-21.Notice that both the haptic–
proprioceptive fibers and the nocioceptive fibers synapse with the interneuron. Collaterals
from the haptic–proprioceptive pathway excite the interneuron, whereas collaterals
from the nocioceptive pathway inhibit the interneuron. The interneuron, in turn,
inhibits the neuron that relays pain information to the brain. Consequently, when the
haptic–proprioceptive pathway is active, the pain gate partly closes, reducing the sensation
of pain.
The gate theory can help explain how different treatments for pain work. For instance,
when you stub your toe, you feel pain because the pain pathway to the brain is
open. If you then rub the toe, activating the haptic–proprioceptive pathway, the flow
of information in the pain pathway is reduced because the pain gate partly closes,
which relieves the pain sensation.
Similarly, acupuncture may produce its pain-relieving effects because the vibrating
needles used in this treatment selectively activate haptic and proprioceptive fibers,
closing the pain gate. Interestingly, the interneurons in the pain gate may use opioid
peptides as a neurotransmitter. If so, the gate theory can also explain how endogenous
opoids reduce pain.
The gate theory even suggests an explanation for the “pins and needles” that we
feel after sitting too long in one position. Loss of oxygen from reduced blood flow may
first deactivate the large myelinated axons that carry touch and pressure information,
leaving the small unmyelinated fibers that carry pain and temperature messages unaffected.
As a result, “ungated” sensory information flows in the pain and temperature
pathway, leading to the pins-and-needles sensation.
Melzack and Wall propose that pain gates may be located in the brainstem and cortex
in addition to the spinal cord. These additional gates could help explain how other
approaches to pain relief work. For example, researchers have found that feelings of severe
pain can be lessened when people have a chance to shift their attention from the
pain to other stimuli. Dentists have long used this technique by giving their patients
something soothing to watch or listen to while undergoing painful work on their teeth.
This influence of attention on pain sensations may work through a cortical pain
gate. Electrical stimulation in a number of sites in the brainstem also can reduce pain,
perhaps by closing brainstem pain gates.Another way in which pain perceptions might
376 ! CHAPTER 10
Pain gate. Hypothetical neural circuit in
which activity in fine-touch and pressure
pathways diminishes the activity in pain
and temperature pathways.
Figure 10-21
A Pain Gate An interneuron in the
spinal cord receives excitatory input (plus
sign) from the fine-touch and pressure
pathway and inhibitor input (minus sign)
from the pain and temperature pathway.
The relative activity of the interneuron
then determines whether pain and
temperature information is sent to the
brain. Adapted from The Puzzle of Pain (p. 154),
by R. Melzack, 1973, New York: Basic Books.

Fine-touch and pressure
pathway to the brain
and pressure pathway
from body receptors
Pain and
temperature pathway
from body receptors
Pain and temperature
pathway to the brain
CH10.qxd 1/6/05 3:20 PM Page 376

be lessened is through descending pathways from the forebrain and the brainstem to
the spinal-cord pain gate.
The presence of relatively complex neural circuits in the spinal cord, such as the
pain gate, may be related both to the variable nature of pain and to some successful
treatments and some problems in treating pain. In response to noxious stimulation,
pain neurons in the spinal cord can undergo sensitization (see Experiment 5-3). In
other words, successive pain experience can produce an escalating response to a similar
noxious stimulus. Spinal-cord neurons thus learn to produce a larger pain signal.
One of the most successful treatments for pain is the injection of small amounts
of morphine under the dura of the spinal cord. This epidural anesthesia is mediated by
the action of morphine or other opioid drugs on pain neurons in the spinal cord. Although
morphine is a very useful treatment for pain, the effects of morphine lessen
with continued use. This form of habituation (see Experiment 5-2) may be related to
changes that take place on the receptors of pain neurons in the spinal cord and brain.
The brain can also influence the pain signal that is sent to it from the spinal cord.
Electrical stimulation in a region of the midbrain called the periaqueductal gray
matter (PAG) is surprisingly effective in suppressing pain. The cell bodies of these
neurons surround the cerebral aqueduct connecting the third and fourth ventricles
(see Figure 2-18).
Neurons in the PAG excite brainstem-activating systems (including serotonin and
noradrenaline neurons), which in turn project to the spinal cord, and inhibit neurons
in the spinal cord that form the ascending pain pathways.Activation in these inhibitory
circuits may explain in part why the sensation and perception of pain is lessened during
sleep. Stimulation of the PAG by implanted microelectrodes is one way of treating
pain that is resistant to all other therapies, including treatment with opioid drugs.
Many internal organs of the body, including the heart, the kidneys, and the blood
vessels, have pain receptors, but the ganglion neurons carrying information from these
receptors do not have their own pathway to the brain. Instead, these ganglion neurons
synapse with spinal-cord neurons that receive nocioceptive information from the
body’s surface. Consequently, the neurons in the spinal cord that relay pain and temperature
messages to the brain receive two sets of signals: one from the body’s surface
and the other from the internal organs.
These spinal-cord neurons cannot distinguish between the two sets of signals; nor
can we. As a result, pain in body organs is often felt as referred pain coming from the
surface of the body. For example, the pain in the heart associated with a heart attack
may be felt as pain in the left shoulder and upper arm (Figure 10-22). Pain in the
stomach is felt as pain in the midline of the trunk; pain in the kidneys is felt as pain in
the lower back. Pain in blood vessels in the head is felt as diffuse pain that we call a
headache (remember that the brain has no pain receptors).
The Vestibular System and Balance
The only localized part of the somatosensory system, the vestibular system, consists
of two organs, one located in each middle ear. As Figure 10-23A shows, each vestibular
organ is made up of two groups of receptors: the three semicircular canals and the
otolith organs, which consist of the utricle and the saccule. These vestibular receptors do
two jobs: (1) they tell us the position of the body in relation to gravity and (2) they signal
changes in the direction and the speed of movements of the head.
You can see in Figure 10-23A that the semicircular canals are oriented in three different
planes that correspond to the three dimensions in which we move. Each canal
furnishes information about movement in its particular plane. The semicircular canals
Periaqueductal gray matter (PAG).
Nuclei in the midbrain that surround the
cerebral aqueduct joining the third and
fourth ventricles; PAG neurons contain
circuits for species-typical behaviors (e.g.,
female sexual behavior) and play an
important role in the modulation of pain.
Referred pain. Pain felt on the surface
of the body that is actually due to pain in
one of the internal organs of the body.
Vestibular system. A set of receptors in
the middle ear that indicate position and
movement of the head
Area of
referred pain
Figure 10-22
Referred Pain During a heart attack,
pain from receptors in the heart is felt in
the left shoulder and upper arm.
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are filled with a fluid called endolymph. Immersed in the endolymph is a set of hair cells
very much like the hair cells described in Chapter 9 that mediate hearing.
When the head moves, the endolymph also moves, pushing against the hair cells
and bending the cilia at their tips. The force of the bending is converted into receptor
potentials in the hair cells and action potentials that are sent over vestibular nerve
axons to the brain. These axons are normally quite active: bending the hair cell cilia in
one direction increases neurotransmitter release, consequently increasing vestibular
nerve axon activity; bending them in the other direction decreases vestibular afferent
axon activity.
These responses are diagrammed in Figure 10-23B. Typically,when the head turns
in one direction, the message on the side of the body to which the turn is made is an
increase in neural firing. The message on the body’s opposite side is a decrease in
The utricle and saccule are located just beneath the semicircular canals. They also
contain hair cells, but these receptors are embedded in a gelatin-like substance that
contains small crystals of the salt calcium carbonate called otoconia.When you tilt your
head, the gelatin and otoconia press against the hair cells, bending them. The mechanical
action of the hair bending modulates the rate of action potentials in vestibular afferent
axons that convey messages about the position of the head in three-dimensional
The receptors in the vestibular system tell us about our location relative to gravity,
about acceleration and deceleration of our movements, and about changes in movement
direction. They also allow us to ignore the otherwise very destabilizing influence
that our movements might have on us. For example, when you are standing on a bus,
even slight movements of the vehicle could potentially throw you off balance, but they
do not. Similarly, when you make movements yourself, you easily avoid tipping over,
despite the constant shifting of your body weight. Your vestibular system enables you
to keep from tipping over.
378 ! CHAPTER 10
Nerve fibers exiting
a semicircular canal
Nerve impulses
Receptor potential Depolarization
Move right Move left
Increased impulse
Decreased impulse
Figure 10-23
The Vestibular System. (A) The
vestibular organs in each middle ear
consist of the three semicircular canals
and the otolith organs. Hair cells in
the vestibular system are sensitive to
movement of the head and to gravity.
(B) A vestibular neuron is normally active,
and its activity increases if the cilia of
its hair-cell receptors are bent in one
direction but decreases if the receptors
are bent in the opposite direction
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Here is an experiment that you can perform to illustrate the role of vestibular receptors
in helping you to compensate for your own movements. If you hold your hand
in front of you and shake it, your hand appears blurry. But, if you shake your head
instead of your hand, the hand remains in focus. Compensatory signals from your
vestibular system allow you to see the hand as stable even though you are moving
Not only do somatosensory neurons convey sensation to the brain but they also provide
our perceptions—of things that we describe as pleasant or unpleasant, of the
shape and texture of objects, of the effort required to complete tasks, and even of our
spatial world. These perceptual abilities are mediated
by the somatosensory cortex.
As illustrated in Figure 10-24, there are two
main somatosensory areas in the cortex. The primary
somatosensory cortex is the area that receives
projections from the thalamus. It consists
of Brodmann’s areas 3-1-2 (all shaded red in the
figure). The primary somatosensory cortex begins
the process of constructing perceptions from
somatosensory information. It mainly consists
of the postcentral gyrus just behind the central
fissure, which means that the primary somatosensory
cortex is adjacent to the primary motor
cortex. The secondary somatosensory cortex
(Brodmann’s areas 5 and 7, shaded orange and
yellow in the figure), located in the parietal lobe
just behind the primary somatosensory cortex,
continues the construction of perceptions.
The Somatosensory Homunculus
In his studies of human patients undergoing brain surgery,Wilder Penfield electrically
stimulated the somatosensory cortex and recorded the patients’ responses. Stimulation
at some sites elicited sensations in the foot,whereas stimulation of other sites produced
In Review .
Body senses contribute to the perception of hapsis (touch and pressure), proprioception
(location and movement), and nocioception (temperature and pain). Haptic–proprioceptive
information is carried by the dorsal spinothalamic tract; nocioceptive information is
carried by the ventral spinothalamic tract. The two systems interact in the spinal cord to
regulate the perception of pain by a pain gate. In the midbrain, the periaqueductal gray
matter effectively suppresses pain by activating neuromodulatory circuits that inhibit pain
pathways. The only localized somatosensory system, the vestibular system, helps us keep
our balance by signaling information about the head’s position and our movement through
Primary somatosensory
cortex receives sensory
information from the
Secondary somatosensory cortex
receives sensory information from
the primary somatosensory cortex.
Figure 10-24
Somatosensory Cortex Stimulation of
the primary somatosensory cortex in the
parietal lobe produces sensations that
are referred to appropriate body parts
by the motor cortex. Information from
the primary somatosensory cortex travels
to the secondary somatosensory cortex
for further perceptual analysis and
contribution to movement sequences
mediated in the frontal lobes.
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sensations in a hand, the trunk, or the face. By mapping these
responses, Penfield was able to construct a somatosensory
homunculus in the cortex, shown in Figure 10-25A.
Penfield’s work half a century ago demonstrates, for example,
that a dorsal-root ganglion neuron carrying finetouch
and pressure information from a finger through its
connections sends information to the finger region of the
somatosensory cortex. The sensory homunculus looks very
similar to the motor homunculus in that the areas of the
body most sensitive to sensory stimulation are accorded a
relatively larger cortical area.
Using smaller electrodes and more-precise recording
techniques in monkeys, John Kaas (1987) proposed that the
somatosensory cortex does not consist of a single homunculus
as proposed in Penfield’s original model. He stimulated
sensory receptors on the body and recorded the activity of
cells in the sensory cortex. He found that the somatosensory
cortex is actually composed of four representations of the
body. Each is associated with a certain class of sensory
The progression of these areas across the human cortex from front to
back is shown in Figure 10-25B. Area 3a cells are responsive to muscle receptors;
area 3b cells are responsive to slow-responding skin receptors. Area 1
cells are responsive to rapidly adapting skin receptors, and area 2 cells are responsive
to deep tissue pressure and joint receptors. In other studies, Hiroshi
Asanuma and his coworkers found still another sensory representation in the
motor cortex (area 4) in which cells respond to muscle and joint receptors
(Asanuma, 1989).
Research by Vernon Mountcastle (1978) showed that cells in the somatosensory
cortex are arranged in functional columns running from layer I
to layer VI, similar to columns found in the visual cortex. Every cell in a column
responds to a single class of receptors. Some columns of cells are activated
by rapidly adapting skin receptors, others by slowly adapting skin
receptors, still others by pressure receptors, and so forth. All neurons in a
column receive information from the same local area of skin. In this way,
neurons lying within a column seem to be an elementary functional unit of the
somatosensory cortex.
The construction of perceptions from sensations depends on a hierarchical organization
of the somatosensory cortex, with basic sensations being combined to form
more-complex perceptions. This combining of information takes place as areas 3a and
3b project onto area 1, which in turn projects onto area 2. For example, whereas a cell
in area 3a or 3b may respond to activity in only a certain area on a certain finger, cells
in area 1 may respond to similar information from a number of different fingers.
At the next level of synthesis, cells in area 2 may respond to stimulation in a number
of different locations on a number of different fingers, as well as to stimulation
from different kinds of receptors. Thus, area 2 contains multimodal neurons that are
responsive to movement force, orientation, and direction, all properties that we perceive
when we hold an object in our hands and manipulate it.
With each successive relay of information, both the size of the pertinent receptive
fields and the synthesis of somatosensory modalities increase. That the different kinds of
somatosensory information are both separated and combined in the cortex raises the
question of why both segregation and synthesis are needed. One reason that sensory in-
380 ! CHAPTER 10
Muscles Skin (slow) Skin (fast) Joints, pressure
Primary somatosensory
(A) Original model
(B) New model
In this model, the primary
somatosensory cortex is
organized as a single
homunculus with large areas
representing body parts that
are very sensitive to sensory
In this model, the primary
somatosensory cortex is
organized into four separate
homunculi consisting of areas
3a, 3b, 1, and 2. Information is
passed from other areas into
area 2, which is responsive to
combined somatosensory
Primary somatosensory
3a 3b 1
Figure 10-25
Two Models of Somatosensory
Cortex Organization (A) Penfield’s
single-homunculus model. (B) A fourhomunculus
model based on the
stimulation of sensory receptors on the
body surface and recording from the
somatosensory cortex.
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formation remains segregated at the level of the cortex could be that we often need to distinguish
between different kinds of sensory stimuli coming from different sources. For
example, we need to be able to tell the difference between tactile stimulation on the surface
of the skin, which is usually produced by some external agent, and stimulation coming
from muscles, tendons, and joints, which is likely produced by our own movements.
Yet, at the same time, we also often need to know about the combined sensory
properties of a stimulus. For instance, when we manipulate an object, it is useful to
“know”the object both in regard to its sensory properties, such as temperature and texture,
and in regard to the movements that we make as we handle it. For this reason, the
cortex provides for somatosensory synthesis, too. The tickle sensation seems rooted in
an “other versus us” somatosensory distinction, as described in “Tickling.”
Focus on New Research
Everyone knows the effects and consequences of tickling.
The perception of tickling is a curious mixture of pleasant
and unpleasant sensory stimulation. The tickle sensation is
experienced not only by humans but also by other primates,
cats, rats, and probably most mammals. Tickling is rewarding
in that people and animals will solicit tickles from others,
but it is also noxious because they will attempt to avoid
the stimulation when it becomes too intense.
It is well known, and even described in ancient historical
records, that a tickle stimulus is much more pronounced
when produced by another person than when produced by
ourselves. In other words, we find it hard, if not impossible, to
tickle ourselves as others can tickle us. What accounts for the
experience of a tickle and why can we not tickle ourselves?
Sara Blakemore and her colleagues (1998) attempted to
answer these questions by using a robot and brain-imaging
techniques. They designed the robot so that, when operated
by a human subject, it delivered one of two kinds of identical
tactile stimuli to the palm of the subject’s hand. In one
condition, the robot faithfully delivered the stimulus that the
subject commanded. In the other condition, the robot introduced
an unpredictable delay in the stimulus.
The faithfully delivered stimulation was not perceived
by the subject as tickles, but the unpredictable stimulus was.
Thus, it is not the stimulation itself but its unpredictability
that accounts in large part for the tickle perception.
Using the technique of functional magnetic resonance
brain imaging (fMRI, which measures blood flow and hence
brain activity), Blakemore and her colleagues found that the
predictable and unpredictable sensory stimulation had different
effects on the activity of a subject’s sensory cortex.
Even though the intensity of stimulation was the same in
both conditions, the sensory cortex was much less responsive
to the predictable than to the unpredictable stimulus. By
extension, the sensory cortex is relatively unresponsive when
we attempt to tickle ourselves in comparison with a tickle
delivered by someone else.
Why are we less responsive to self-stimulation? Brain
imaging of the cerebellum in the same two experimental
conditions shows that the anterior cerebellum is less
active during the predictable self-induced sensory stimulation
compared with the unpredictable stimulation. The researchers
propose, therefore, that, when we produce a
movement to tickle ourselves, the cortex sends out a command
to produce the movement and at the same time sends
a signal to the cerebellum instructing it to ignore the associated
sensory stimulation produced by the movement (see
Figure 10-15).
If the sensation produced by the movement is predictable,
feedback from the movement is muted by the cerebellum.
If the sensory stimulation is not predictable, the
cerebellum amplifies it. This brain circuitry, which is normally
used to correct errors in our own movements, may
thus underlie tickling. Perhaps the wriggly movements that
we make in response to tickles are attempts to make the stimuli
more predictable.
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382 ! CHAPTER 10
Effects of Damage to the Somatosensory Cortex
Damage to the primary somatosensory cortex impairs the ability to
make even simple sensory discriminations and movements.
Suzanne Corkin and her coworkers (1970) demonstrated this effect
by examining patients with cortical lesions that included most of
areas 3-1-2 in one hemisphere. The researchers mapped the sensory
cortices of these patients before they underwent elective surgery for
removal of a carefully defined piece of that cortex, including the
hand area. The patients’ sensory and motor skills in both hands were
tested on three different occasions: before the surgery, shortly after the surgery, and
almost a year afterward.
The tests included pressure sensitivity, two-point touch discrimination, position
sense (reporting the direction in which a finger was being moved), and haptic sense
(using touch to identify objects, such as a pencil, a penny, eyeglasses, and so forth). For
all the sensory abilities tested, the surgical lesions produced a severe and seemingly permanent
deficit in the contralateral hand. Sensory thresholds, proprioception, and hapsis
were all greatly impaired.
The results of other studies in both humans and animals have shown that damage
to the somatosensory cortex also impairs simple movements. For example, limb use in
reaching for an object is impaired, as is the ability to shape the hand to hold an object
(Leonard et al., 1991).Nevertheless, the somatosensory cortex is plastic, as is the motor
cortex. It can dramatically reorganize itself after deafferentation.
In 1991, Tim Pons and his coworkers reported a dramatic change in the somatosensory
maps of monkeys in which the ganglion cells for one arm had been deafferented
a number of years earlier. The researchers had wanted to develop an animal
model of damage to sensory nerves that could be a source of insight into human injuries,
but they were interrupted by a legal dispute with an animal advocacy group.
Years later, as the health of the animals declined, a court injunction allowed the mapping
experiment to be conducted.
Pons and his coworkers discovered that the area of the somatosensory cortex that
had formerly represented the arm no longer did so. Light touches on the lower face of
a monkey now activated cells in what had formerly been the cortical arm region. As illustrated
in Figure 10-26, the facial area in the cortex had expanded by as much as 10
to 14 mm, virtually doubling its original size by entering the arm area.
This massive change was completely unexpected. The stimulus–response patterns
associated with the new expanded facial area of the cortex appeared indistinguishable
from those associated with the original facial area. Furthermore, the trunk area, which
bounded the other side of the cortical arm area, did not expand into the vacated arm
What could account for this expansion of the face area into the arm area? One possibility
is that axons grew across the cortex from the face area into the arm area, but no
evidence supports this possibility. Another possibility is that the thalamic neurons representing
the facial area projected axon collaterals to the cortical neurons representing
the arm area. These collaterals might be preexisting or they might be new growths subsequent
to deafferentation.
There is evidence for preexisting collaterals that are not normally active, but these
collaterals would probably not be able to extend far enough to account for all of the
cortical reorganization. A third possibility is that,within the dorsal columns, facial-area
neurons projected collaterals to arm-area neurons. These neurons are close together,
and so the collaterals need travel only a millimeter or so.
Suzanne Corkin
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Whatever the mechanism, the very dramatic cortical reorganization observed in
this study eventually had far-reaching consequences for understanding other remarkable
phenomena, including phantom-limb sensations. We will return to this story in
Chapter 13, where we look at how the brain changes in response to experience.
The Somatosensory Cortex and
Complex Movement
This chapter began by describing the remarkable painting skills of Kamala the elephant.
Kamala first needs a plan—some idea of what she wants to paint. She must then
execute the movements required to apply paint to her canvas, and she must use somatosensory
information to confirm that she is producing the movements that she intends.
So to paint or to perform virtually any complex movement, the motor system
and the somatosensory system must work together. In this final section of the chapter,
we explore that interaction.
The secondary somatosensory cortex plays an important role in confirming which
movements have already taken place and in deciding which movements should follow.
Damage to the secondary somatosensory cortex does not disrupt the plans for making
movements, but it does disrupt how the movements are performed, leaving their execution
fragmented and confused. The inability to complete a plan of action accurately
In the control monkey, this area
of the somatosensory cortex
represents the arm and face.
This normal pattern
is illustrated by a
normal face.
In the deafferented monkey, the
area of the somatosensory cortex
that formerly represented the
arm has been taken over by
expansion of the face area.
This expansion is
illustrated by an
elongated face.
Figure 10-26
Somatosensory Plasticity Adapted
from “Massive Cortical Reorganization
after Sensory Deafferentation in Adult
Macaques,” by T. P. Pons, P. E. Garraghty,
A. K. Ommaya, J. H. Kaas, and M.
Mishkin, 1991, Science, 252, p. 1858.
CH10.qxd 1/6/05 3:21 PM Page 383

is called apraxia (from the Greek words for “no” and “action”). The following case
highlights the symptoms of apraxia:
A woman with a biparietal lesion [damage on both sides of the secondary somatosensory
cortex] had worked for years as a fish-filleter.With the development
of her symptoms, she began to experience difficulty in carrying on with
her job. She did not seem to know what to do with her knife. She would stick
the point in the head of a fish, start the first stroke, and then come to a stop.
In her own mind she knew how to fillet fish, but yet she could not execute the
maneuver. The foreman accused her of being drunk and sent her home for
mutilating fish.
The same patient also showed another unusual phenomenon that might
possibly be apraxic in nature. She could never finish an undertaking. She
would begin a job, drop it, start another, abandon that one, and within
a short while would have four or five uncompleted tasks on her hands.
This would cause her to do such inappropriate actions as putting the sugar
bowl in the refrigerator, and the coffeepot inside the oven. (Critchley, 1953,
pp. 158–159)
How does an intact secondary somatosensory cortex contribute to the organization
of movement? Recall from Chapter 8 that visual information influences
movement through the dorsal and ventral streams. The dorsal stream, working without
conscious awareness, provides vision for action, as when we use the visual form
of a cup to automatically shape a hand to grasp that cup. The ventral stream, in contrast,
works with conscious awareness and provides the vision needed to identify
As Figure 10-27 illustrates, the secondary somatosensory cortex participates in
both visual streams. The dorsal visual stream projects to the secondary somatosensory
cortex and then to the prefrontal cortex. In this way, visual information is integrated
with somatosensory information to produce movements that are appropriately shaped
and directed for their targets.
Much less is known about how the secondary somatosensory cortex
contributes to the ventral stream, but it is likely that somatosensory
information about the identity of objects and completed movements is
relayed by the ventral stream to the prefrontal cortex. The prefrontal
cortex can then select the appropriate actions that should follow from
those that are already complete. Consider the difference in the way we
would reach for an empty glass versus a glass filled to the brim with hot
Close interaction between the somatosensory system and the motor
system exists at all levels of the nervous system. It can be seen in the
spinal cord, where sensory information contributes to spinal reflexes. It
can also be seen in the brainstem, where various species-specific behaviors,
such as attack, withdrawal, and grooming, require both appropriate
patterns of movement and appropriate sensory information.
The close interrelation is found as well at the level of the neocortex,
where skilled movements elicited by the motor regions of the frontal
lobes require information about actions that have just taken place and about objects
that have been or could be manipulated. In short, an interaction between the
motor cortex, which decides what should be done, and the sensory cortex, which
knows what has been done, is central to how the brain produces movement in the
here and now.
384 ! CHAPTER 10
Information from the secondary
somatosensory cortex
contributes to the dorsal stream
by specifing the movement used
for grasping a target.
Information from the secondary
somatosensory cortex contributes to
the ventral stream by providing
information about object size and
Dorsal stream Visual
Ventral streamVentral stream
Figure 10-27
Visual Aid The secondary
somatosensory cortex contributes to
information flow in dorsal (how) and
ventral (what) visual streams
Apraxia. Inability to make voluntary
movements in the absence of paralysis or
other motor or sensory impairment,
especially an inability to make proper use
of an object
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How is the motor system organized? The organization of movement is hierarchical,
with almost the entire brain contributing to it in some way. The forebrain plans, organizes,
and initiates movements, whereas the brainstem coordinates regulatory functions,
such as eating and drinking, and controls neural mechanisms that maintain
posture and produce locomotion.Many reflexes are organized at the level of the spinal
cord and occur without any involvement of the brain.
How is the motor cortex organized? Maps produced by stimulating the motor cortex
show that it is organized topographically as a homunculus, with parts of the body capable
of fine movements associated with large regions of motor cortex. Two pathways
emerge from the motor cortex to the spinal cord. The lateral corticospinal tract consists
of axons from the digit, hand, and arm regions of the motor cortex. The tract
synapses with spinal interneurons and motor neurons located laterally in the spinal
cord, on the side of the cord opposite the side of the brain on which the corticospinal
tract started. The ventral corticospinal tract consists of axons from the trunk region of
the motor cortex. This tract synapses with interneurons and motor neurons located
medially in the spinal cord, on the same side of the cord as the side of the brain on
which the corticospinal tract started. Interneurons and motor neurons of the spinal
cord also are topographically organized, with more laterally located motor neurons
projecting to digit, hand, and arm muscles and more medially located motor neurons
projecting to trunk muscles.
How do motor-cortex neurons produce movement? Movements innate to a species are
organized as synergies, or movement patterns. Motor-cortex neurons initiate movement,
produce movement, control the force of movement, and indicate movement direction.
Different species of animals have topographic maps in which areas of the body
capable of the most-skilled movements have the largest motor-cortex representation.
Disuse of a limb, such as that which might follow motor-cortex injury, results in shrinkage
of that limb’s representation in the motor cortex. This shrinkage of motor-cortex
representation can be prevented, however, if the limb can be somehow forced into use.
How do the basal ganglia and the cerebellum contribute to controlling movement?
Damage to the basal ganglia or to the cerebellum results in abnormalities of movement.
This result tells us that both these brain structures somehow participate in movement
control. The results of experimental studies suggest that the basal ganglia regulate the
force of movements, whereas the cerebellum plays a role in movement timing and in
maintaining the accuracy of movements.
How is the somatosensory system organized? The somatosensory system is distributed
throughout the entire body and consists of more than 20 types of specialized receptors,
In Review\ .
The primary somatosensory cortex, which is arranged as a series of homunculi, provides
information to the secondary somatosensory cortex, which in turn contributes to the dorsal
(how) and ventral (what) visual streams. Damage to the secondary somatosensory cortex
produces apraxia, an inability to complete a series of movements. A person with this
condition has trouble knowing both what action has just been completed and what action
should follow in a movement sequence.
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each of which is sensitive to a particular form of mechanical energy. Each somatosensory
receptor projecting from skin,muscles, tendons, or joints is associated with a dorsal-
root ganglion neuron that carries the sensory information into the brain. Fibers
carrying proprioceptive (location and movement) information and haptic (touch and
pressure) information ascend the spinal cord as the dorsal spinothalamic tract. These
fibers synapse in the dorsal-column nuclei at the base of the brain, at which point axons
cross over to the other side of the brainstem to form the medial lemniscus, which ascends
to the ventrolateral thalamus. Most of the ventrolateral thalamus cells project
to the somatosensory cortex. Nocioceptive (pain and temperature) dorsal-root ganglion
neurons synapse on entering the spinal cord. Their relay neurons cross the spinal
cord to ascend to the thalamus as the ventral spinothalamic tract. Because there are two
somatosensory pathways that take somewhat different routes, unilateral spinal-cord
damage impairs proprioception and hapsis ipsilaterally below the site of injury and nocioception
contralaterally below the site.
How is somatosensory information represented in the neocortex? The somatosensory
system is represented topographically as a homunculus in the primary somatosensory
region of the parietal cortex (areas 3-1-2) such that the most sensitive parts of the body
are accorded the largest regions of neocortex. A number of homunculi represent different
sensory modalities, and these regions are hierarchically organized. If sensory input
from a part of the body is cut off from the cortex by damage to sensory fibers, adjacent
functional regions of the sensory cortex can expand into the now-unoccupied region.
How do the somatosensory system and the motor system interact? The somatosensory
system and the motor system are interrelated at all levels of the nervous system.
At the level of the spinal cord, sensory information contributes to motor reflexes; in
the brainstem, sensory information contributes to complex regulatory movements. At
the level of the neocortex, sensory information is used to record just-completed movements,
as well as to represent the sizes and shapes of objects. The somatosensory cortex
contributes to the dorsal visual stream to direct hand movements to targets. The
somatosensory cortex also contributes to the ventral visual stream to create representations
of external objects.
1. How are the somatosensory system and the motor system related?
2. Describe the pathways that convey somatosensory information to the brain.
apraxia, p. 384
autism, p. 349
cerebral palsy, p. 349
corticospinal tract, p. 355
deafferentation, p. 372
dissolution, p. 345
dorsal spinothalamic tract,
p. 373
glabrous skin, p. 369
hapsis, p. 370
homunculus, p. 354
hyperkinetic symptom,
p. 364
hypokinetic symptom,
p. 364
monosynaptic reflex, p. 375
motor sequence, p. 345
nocioception, p. 370
pain gate, p. 376
paraplegia, p. 350
periaqueductal gray matter
(PAG), p. 377
proprioception, p. 371
quadriplegia, p. 350
rapidly adapting receptor,
p. 371
referred pain, p. 377
scratch reflex, p. 351
slowly adapting receptor,
p. 371
synergy, p. 358
topographic organization,
p. 354
ventral spinothalamic tract,
p. 373
ventrolateral thalamus,
p. 373
vestibular system, p. 377
386 ! CHAPTER 10
neuroscience interact ive
Many resources are available for
expanding your learning on line:
Try some self-tests to reinforce your
mastery of the material. Look at some
of the updates on current research on
the brain. You’ll also be able to link to
other sites that will reinforce what
you’ve learned.
Go to this site to learn more about
current research on spinal-cord injury.
Learn more about Tourette’s syndrome,
an often misunderstood disorder, at the
home page of the Tourette’s Syndrome
On your CD-ROM, you’ll be able to
quiz yourself on your comprehension
of the chapter. The module on Control
of Movement offers interactive
illustrations to reinforce your
understanding of key concepts.
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3. Describe the pathways that convey motor instructions to the spinal cord.
4. What are the contributions of the cortex, the basal ganglia, and the cerebellum to
5. Describe two theories of how the human motor cortex moves a hand to a target
to grasp it.
6. Describe the changes that the somatosensory cortex and the motor cortex might
undergo in response to injury to the cortex or to a limb.
1. Why is the somatosensory system so much more intimately linked to movement
than the other sensory systems are?
2. Why might the dorsal and ventral streams be separate systems for controlling
hand movements?
Asanuma, H. (1989). The motor cortex. New York: Raven Press. An excellent summary of the
motor system by a scientist who made important advances in studying the role of the
motor cortex in behavior.
Cole, J. (1995). Pride and a daily marathon. London: MIT Press. At the age of 19, Ian
Waterman was struck down by a rare neurological condition that deprived him of joint
position and proprioception. This book tells the story of how he gradually adapted to
his strange condition by using vision and elaborate tricks to monitor his every
movement and regain his life.
Melzack, R. (1973). The puzzle of pain. New York: Basic Books. For ages, physicians and
scientists have attempted with little success to understand and control pain. Here, one
of the world’s leading researchers in the field of pain theory and treatment presents a
totally readable book to unravel the mystery of pain.
Sacks, O. (1974). Awakenings. New York: Vintage Books. This prize-winning book presents a
fascinating account of one of the mysteries of the motor system—how the great flu of
the 1920s produced the Parkinsonism that developed as the aftermath of the “sleeping
sickness.” This story presents wonderful insights into the function of the motor system.
Porter, R., & Lemon, R. (1993). Corticospinal function and voluntary movement. Oxford:
Clarendon Press. This book tells the story of the human brain’s great pathway, the
corticospinal tract.
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Focus on New Research: The Pain of Rejection
Identifying the Causes of Behavior
Behavior for Brain Maintenance
Drives and Behavior
Neural Circuits and Behavior
The Nature of Behavior: Why Cats Kill Birds
Biology, Evolution, and Environment
Evolutionary Influences on Behavior
The Chemical Senses
Environmental Influences on Behavior
Inferring Purpose in Behavior: To Know a Fly
Neuroanatomy of Motivated Behavior
Regulatory and Nonregulatory Behavior
The Hypothalamic Circuit’s Regulatory Function
The Limbic Circuit’s Organizing Function
The Frontal Lobes’ Executive Function
Focus on Disorders: Agenesis of the Frontal Lobe
Stimulating Emotion
The Amygdala and Emotional Behavior
The Prefrontal Cortex and Emotional Behavior
Emotional Disorders
Focus on Disorders: Anxiety Disorders
Control of Regulatory Behavior
Controlling Eating
Focus on Disorders: Weight-Loss Strategies
Controlling Drinking
Control of Nonregulatory Behavior
Effects of Sex Hormones on the Brain
Focus on Disorders: Androgen-Insensitivity Syndrome
and the Androgenital Syndrome
The Hypothalamus, the Amygdala, and Sexual
Sexual Orientation, Sexual Identity, and Brain
Cognitive Influences on Sexual Behavior
388 !
C H A P T E R 11
What Causes Emotional and
Motivated Behavior?
Left: Dr. Dennis Kunkel/Phototake. Middle: Photodisc. Right: Zephyr/Photo
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gions of the forebrain affected by physical pain are the anterior
cingulate cortex, which becomes more active when
physical pain is inflicted, and the orbital prefrontal cortex,
which becomes more active when physical distress is low.
The Eisenberger team found that emotional pain activates
the opposing reactions of these areas activate in exactly
the same way. Participants’ fMRI scans, recorded in
the accompanying images, reveal that the orbital cortex
may act to suppress the feelings of social distress, shown
here in the fMRI scan on the left, as well as the feelings of
physical distress, shown in the scan on the right.
These results suggest that the experience and regulation
of both physical and social pain have a common neuroanatomical
basis. Findings from this study are sources of
two insights about the range of emotional feelings, or affective
1. The same pattern of brain activation accompanies both
physical and emotional pain—in this case, “hurt feelings.”
Other investigators have shown parallel neural
correlates for a range of pleasant feelings, including the
craving for chocolate, winning the lottery, and sexual
2. Normalizing the activity of these brain regions likely
provides a basis for both physical and mental restorative
processes. Seeing the similarity in brain activation during
both social and physical pain helps us to understand
why social support can reduce physical pain, much as
it soothes emotional pain.
The Pain of Rejection
Focus on New Research
S orrow, grief, and heartbreak are words that we use
to describe a loss. Loss evokes painful feelings, as
does the pain inflicted by social exclusion. Exclusion leads
to “hurt” feelings. To discover whether painful or hurtful
feelings are manifested in the brain’s neural circuitry,
Naomi Eisenberger and colleagues (2003) performed an
Participants were scanned in an fMRI apparatus while
they played a virtual ball-tossing video game. Initially, the
subjects believed that they were merely observing the
game but, during the experimental phase, they became active
participants. Within a few throws, the other “players”
(actually computerized stooges) stopped throwing the ball
to the participants, leading them to feel excluded.
The question the researchers asked is whether this emotional
response activates the same neural systems that are
normally activated when people feel physical pain. Two rels
These fMRI scans showing activation in the orbial prefrontal
cortex are the result of averaging many individual images and
then using the subtraction process to produce a representative
image (see Figure 9-22).
Social pain Physical pain
Eisenberger, et al, Science, 302,
290–92, 2003.
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Knowing that the brain makes emotional experience real—more than mere
metaphors of “hurt” or “pain”—how do we incorporate our thoughts and
reasons for behaving as we do? Clearly, our subjective feelings and thoughts
influence our actions.The cognitive interpretation of subjective feelings are emotions—
anger, fear, sadness, jealousy, embarrassment, joy—but these feelings can operate outside
our immediate awareness as well.
This chapter begins by exploring the causes of behaviors in which human beings
and other animals engage. Sensory stimulation, neural circuits, and hormones are of
primary importance in explaining behavior.We focus both on emotions and on the underlying
reasons for motivation—behavior that seems purposeful and goal directed.
Like emotion, motivated behavior is both inferred and subjective and can occur without
awareness or intent.
Research on the neuroanatomy responsible for emotional and motivated behavior
focuses on a neural circuit formed by the hypothalamus, the limbic system, and the
frontal lobes. But behavior is influenced as much by the interaction of our social and
natural environments and by evolution as it is by biology. To explain all this interaction
in regard to how the brain controls behavior, we concentrate on the specific examples
of feeding and sexual activity. Our exploration leads finally to the topic of reward,
which plays another key role in explaining emotional and motivated behaviors.
We may think that the most obvious explanation for why we behave as we do is simply
that we want to. This explanation assumes that we act in a state of free will—that we always
have a choice. But the feeling of having free will is not a likely cause of behavior.
Consider Roger, a 25-year-old man whom we first met in the admissions ward of
a large mental hospital. Roger approached us and asked if we had any snacks.We had
chewing gum, which he accepted eagerly.We thought little about this encounter until
10 min later when we noticed Roger eating the flowers from the vase on a table.A nurse
took the flowers away but said little to Roger.
Later, as we wandered about the ward, we encountered a worker replacing linoleum
floor tiles. Roger was watching the worker and, as he did, he dipped his finger into the
pot of gluing compound and licked the glue from his finger, as if he were sampling
honey from a jar.When we asked Roger what he was doing, he said that he was really
hungry and that this stuff was not too bad. It reminded him of peanut butter.
One of us tasted the glue and concluded not only that it did not taste like peanut
butter but that it tasted awful. Roger was undeterred.We alerted a nurse, who quickly
removed him from the glue. Later, we saw him eating another flower bouquet.
Neurological testing revealed that a tumor had invaded Roger’s hypothalamus at
the base of his brain.He was indeed hungry all the time and could likely consume more
than 20,000 calories a day if allowed to do so.
Would you say that Roger had free will regarding his appetite and food preferences?
Probably not. Roger seemed compelled to eat whatever he could find, driven by
a ravenous hunger. In this case, the nervous system has produced behavior, not an act
of free will. If the nervous system can produce one such behavior, it can likely produce
many others.
Free will therefore does not adequately explain why we act as we do. If free will is
not a satisfactory explanation of behavior, what explanation is? One possibility is the
brain’s inherent need for stimulation.
This need was first demonstrated in the early 1950s by psychologists Donald
Hebb and Woodburn Heron (Hebb, 1955; Heron, 1957). They argued that people are
390 ! CHAPTER 11
Emotion. Cognitive interpretation of
subjective feelings.
Motivation. Behavior that seems
purposeful and goal directed.
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motivated to interact with the environment to maintain at least a minimum level of
brain stimulation, and they conducted a fascinating series of experiments that supports
this view.
Behavior for Brain Maintenance
Hebb and his coworkers studied the effects of sensory deprivation, depriving people
of nearly all sensory input. They wanted to see how well-fed, physically comfortable
college students who were paid handsomely for their time would react if they did nothing,
saw nothing, and heard or touched very little 24 hours a day. Figure 11-1 shows
the setting for this experiment.
Each man lay on a bed in a small sound-proofed room with his ears enveloped by
a hollowed-out pillow that muffled the monotonous hums of a nearby fan and air conditioner.
Cardboard tubes covered his hands and arms, cutting off his sense of touch,
and a translucent visor covered his eyes, blurring the visual world. The subjects were
given food on request and access to bathroom facilities. Otherwise, they were asked
simply to enjoy the peace and quiet. For doing so, they would receive $20 a day, which
was about four times what a student could earn even for a hard day’s labor half a century
Wouldn’t you think the subjects would be quite happy to contribute to scientific
knowledge in such a painless way? In fact, they were far from happy.Most subjects were
content for perhaps 4 to 8 hours, but then they became increasingly distressed. They
developed a need for stimulation of almost any kind. In one version of the experiment,
the subjects could listen, on request, to a talk for 6-year-old children on the dangers of
alcohol. Some of them requested to hear it 20 times a day. Few subjects lasted more
than 24 hours in these conditions.
The results of sensory deprivation studies are curious. After all, the subjects’ basic
needs were being met, except perhaps the need for sexual gratification. (But Hebb
assumed that, at the risk of insulting their virility, most of the young men in his study
were accustomed to stretches of at least 3 or 4 days without engaging in sexual activity.)
So what was the cause of the subjects’ distress? Why did they find sensory deprivation
so aversive? The answer, Hebb and his colleagues concluded, must be that the
brain has an inherent need for stimulation.
Psychologists Robert Butler and Harry Harlow (1954) came to a similar conclusion
through a series of experiments that they conducted at about the same time that
Hebb conducted his sensory-deprivation studies. Butler placed rhesus monkeys in a
EEG wires
Air conditioner
Sensory deprivation. Experimental
setup in which a subject is allowed
only restricted sensory input; subjects
generally have a low tolerance for
deprivation and may even display
Figure 11-1
Sensory Deprivation The subject lies
on a bed in an environmental cubicle
24 hours a day, with time out only for
meals and bathroom breaks. The room is
always dimly lit. A translucent plastic
visor restricts visual input; a U-shaped
pillow and the noise of a fan and air
conditioner limit the subject’s auditory
experience. In the experiment depicted
here, the subject is wired for EEG
recordings. The subject’s sense of touch
is restricted by cotton gloves and long
cardboard cuffs. Adapted from “The
Pathology of Boredom,” by W. Heron, 1957,
Scientific American, 197(4), p. 52.
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dimly lit room with a small door that could be opened to view
an adjoining room. As shown in Figure 11-2, the researchers
could vary the stimuli in the adjoining room so that the monkeys
could view different objects or animals each time they
opened the door.
Monkeys in these conditions spent a lot of time opening
the door and viewing whatever was on display, such as toy
trains in action. The monkeys were even willing to perform
various tasks just for an opportunity to look through the
door. The greater the amount of time during which they were
deprived of a chance to look, the more time that they spent
looking when finally given the opportunity.
These experiments, taken together with research on
sensory deprivation undertaken by Hebb and colleagues,
show that one reason that we engage in behavior is to stimulate
the brain. In the absence of stimulation, the brain will
seek it.
Drives and Behavior
Surely stimulating the brain is not the only reason for behavior. Consider the behavior
of a typical pet cat living in a house or apartment. It awakes in the morning, stretches,
wanders to its feeding place, and has a drink of water and some food. Then it sits and
cleans itself.Next, it wanders around and spots its favorite toy mouse, which it pounces
on and throws in the air. It may pounce and throw again and again for a number of
Eventually, seemingly bored with the toy, the cat wanders about looking for attention.
It sits on its owner’s lap, starts to purr, and falls asleep. Shortly thereafter, it gets
up and walks away, passes its food and mouse toy, and meows. It explores the apartment,
sniffing here and there, before napping in a sunbeam.On waking, the cat returns
to the food bowl, eats heartily, bats once at the toy in passing, and searches for its wool
ball, which it chases for a while. Later, it stares out the window and eventually settles
down for a long sleep.
This cat’s seemingly unremarkable actions provide three clues to the causes of
1. The cat’s response to a particular stimulus is not the same each time. Both the food
and the toy mouse elicit behavior on some occasions but not on others.
2. The strength of the cat’s behaviors varies. For instance, the mouse toy stimulates
vigorous behavior at one time and none at another.
3. The cat engages not only in behaviors that satisfy obvious biological needs (eating,
drinking, sleeping) but also in behaviors that are not so obviously necessary (playing,
affection seeking, exploring).
These same patterns of behavior are typical of dogs or even of people. People can
be amused by a puzzle or a book at one moment and completely bored by it the next.
They also respond to a certain object or situation vigorously on some occasions and
half-heartedly on others. And they engage in many behaviors that do not seem to have
any obvious function, such as tapping their toes to music.What generates all these different
392 ! CHAPTER 11
Figure 11-2
Brain Maintenance Monkeys quickly
learn to solve puzzles or perform other
tricks to gain access to a door that looks
out into an adjacent room. A toy train is
a strong visual incentive for the monkey
peeking through the door; a bowl of
fruit is less rewarding. Adapted from
“Persistence of Visual Exploration in Monkeys,”
by R. A. Butler and H. F. Harlow, 1954, Journal of
Comparative and Physiological Psychology, 47,
p. 260.
University of Wisconsin
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As psychologists and biologists began to ponder the causes of behavior in the
1930s, they concluded that some sort of internal energy must drive it. This internal energizing
factor had many names, including instincts and drives. (Actually, instincts and
drives are not identical concepts but, for our purposes, it does not matter.)
The concept of drives gave rise to what became known as drive theories of behavior.
Drive theorists assumed that, because animals perform many different behaviors,
they must have many different drives—a sexual drive, a curiosity drive, a hunger drive,
a thirst drive, and so on. According to drive theories, an animal engages in a particular
behavior because its drive for it is high, and it ceases engaging in that behavior because
its drive for it becomes low.Our cat, for example, played vigorously with the toy mouse
when its play drive was high and ceased playing when its play drive diminished to zero.
Notice how drive theory suggests that the brain is somehow storing energy for behavior.
That energy builds up until it reaches a level where it is released in action,
thereby becoming a cause of behavior. Ethologists (scientists who study animal behavior)
offer an interesting analogy to describe this process.
They compare behavior caused by drives to the flushing of a toilet.When the water
reservoir of a toilet is full, depressing the handle leads to a “whoosh” of water that, once
begun, cannot be stopped.When the reservoir is only partly full, depressing the handle
still produces a flush, but a less vigorous one. If the reservoir is empty, no amount
of handle pressing will cause the toilet to flush. Applying this analogy to our cat with
the toy mouse, the cat will play vigorously if the play reservoir is full, less vigorously if
it is partly full, and not at all if the reservoir is empty.
The “flush” model makes a couple assumptions about drive-induced behavior
(Figure 11-3). It assumes that such a behavior, once started, will continue until all the
energy in its reservoir is gone. Our cat keeps playing, although with decreasing vigor,
until all the energy held in reserve for play is depleted.
The flush model also assumes separate stores of energy for different behaviors. For
instance, cats have a drive to play, and they have a drive to kill. Engaging in one of these
behaviors does not reduce the energy stored for the other. That is presumably why a
cat may play with a mouse that it has caught for many minutes before finally killing it.
The cat will pounce and attack the mouse repeatedly until all its energy for play is used
up, and only then will it proceed to the next drive-induced behavior.
The flush model can be applied to many different kinds of actions and seems to
make some intuitive sense.We do seem to behave as if there were a store of energy for
various behaviors. For instance, males of most mammalian species typically have a refractory
period subsequent to sexual intercourse when they no longer have interest
in (or possibly energy for) sexual behavior. Later, the interest or energy returns. It is as
though a pent-up sexual urge, once satisfied, vanishes for a time, awaiting a new energy
Neural Circuits and Behavior
The problem with drive theories of behavior becomes clear when we try to relate drives
to brain activity. Researchers once assumed that physiologists would quickly discover
how the brain executes drives. Unfortunately, however, researchers were unable to establish
a link between drives and brain activity.
As they searched inside the brain for drives, they found instead that behavioral
change correlates with changes in hormones and cellular activity. For example, researchers
studying the sexual drive found that a man’s frequency of copulation is correlated
with his levels of male hormones, called androgens. Unusually high androgen
Action-specific energy, such
as a cat's desire to stalk and
attack prey, builds up in the
A sensory stimulus (in
this case, a rat) acts to
open the plunger and
release the attack
Drive. Hypothetical state of arousal that
motivates an organism to engage in a
particular behavior.
Androgen. Male hormone related to
level of sexual interest.
Figure 11-3
Flush Model of Motivation According
to drive theories, a reservoir of actionspecific
energy, once released, flows out
and produces behavior. Each type of
behavior is assumed to have its own
store of energy. The greater the energy
store, the longer the behavior persists.
Without an energy store, there is no
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levels are related to very high sexual interest, whereas abnormally low androgen levels
are linked to low sexual interest or perhaps no interest at all.
With knowledge of this correlation between sexual behavior and male hormones,
the concept of sexual drive no longer seemed needed. Rather than searching for a sexual
drive, researchers now sought to explain the action of androgens on neural circuits.
This physiological analysis provides more powerful explanations of behavior than
does simply invoking the concept of drives. It allows us to say exactly what particular
events in the brain can trigger a certain kind of behavior. For example, if an electrode
is used to stimulate the brain cells activated by androgens, sexual behavior can be induced.
In fact, such brain stimulation can produce amazing sexual activity in male rats,
sometimes allowing 50 ejaculations over a couple of hours. Clearly, the activity of neurons
is responsible for the behavior, not some hidden energy reservoir as drive theories
The idea of a neural basis for behavior has wide applications. For instance, we can
say that Roger had such a voracious and indiscriminate appetite either because his
brain circuits that initiated eating were excessively active or because his circuits that
terminated eating were inactive. Similarly, we can say that Hebb’s subjects were highly
upset by sensory deprivation because their neural circuits that responded to sensory
inputs were forced to be abnormally underactive. So the main reason why a particular
thought, feeling, or action occurs lies in what is going on in brain circuits.
The Nature of Behavior: Why Cats Kill Birds
Although neural circuits are somewhat plastic as they form during brain development,
they are not so easily changed later in life. It therefore follows that behaviors that are
caused by these neural circuits also are going to be hard to modify. The killing of prey
by cats is a good example.
One of the frustrating things about being a cat owner is that even well fed cats kill
birds—often lots of birds.Most people are not too bothered when their cats kill mice,
because they view mice as a nuisance. But birds are different. People enjoy watching
birds in their yards and gardens. Many cat owners wonder why their pets keep killing
To provide an answer, we can look to the activities of neural circuits. Cats must
have a brain circuit that controls prey killing. When this circuit is active, a cat makes
an appropriate kill. Viewed in an evolutionary context, it makes sense for cats to have
such a circuit because, in the days when cats were not owned by doting human beings,
they did not have food dishes that were regularly being filled.
Why does this prey-killing circuit become active when a cat does not need food?
One explanation is that, to secure survival, the activity of circuits such as the preykilling
circuit have become rewarding in some way—they make the cat “feel good.” As
a result, the cat is likely to engage in the pleasure-producing behavior often, which
helps to guarantee that it will usually not go hungry.
In the wild, after all, a cat that did not like killing would probably be a dead cat.
The idea of behaviors such as prey killing being rewarding was first proposed by Steve
Glickman and Bernard Schiff in the early 1960s. Because it is important to our understanding
of the causes of behavior, we will return to it at the end of this chapter when
we consider reward.
Killing behavior by cats is innate, not learned. It is triggered automatically in the
presence of the right stimulus. The innateness of killing in cats is demonstrated by a
motherless cat named Hunter that was found abandoned as a tiny kitten. Hunter was
bottle fed and raised without a mother cat to “teach” her to hunt.
394 ! CHAPTER 11
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She did not need an education in hunting. She got her name from her innate and
deadly skill at catching mice and other small prey. The prey-killing circuits in her brainstem
worked without training. They no doubt were influenced by practice, however,
because Hunter became more proficient at killing as she grew older. But the ultimate
underlying cause of the behavior is a neural circuit that, when activated, produces
stalking and killing responses.
Why does the sight of a bird or a mouse trigger stalking and killing in a cat? Why does
the female body stimulate sexual interest in men? We can address such questions by investigating
the evolutionary and environmental influences on brain-circuit activity
that contribute to behavior.
Evolutionary Influences on Behavior
The evolutionary explanation hinges on the concept of innate releasing mechanisms
(IRMs), activators for inborn, adaptive responses that aid in an animal’s survival. Innate
releasing mechanisms help an animal to successfully feed, reproduce, and escape
predators. The concept is best understood by analyzing its parts.
The term innate means that IRMs are present from birth rather than acquired
through experience. The term also implies that the mechanisms have proved adaptive
for the species and therefore have been maintained in the genome. The term releasing
means that IRMs act as triggers to set free behaviors for which there are internal
Let us return to our cat to illustrate. The brain of a cat must have a built-in mechanism
that triggers appropriate stalking and killing in response to stimuli such as a bird
or a mouse. Similarly, a cat must also have a built-in mechanism that triggers appropriate
mating behavior in the presence of a suitable cat of the opposite sex. Although
not all of a cat’s behaviors are due to IRMs, you can probably think of other innate releasing
mechanisms that cats possess, such as arching and hissing when encountering
a threat. For all these IRMs, the animal’s brain must have a set of norms against which
it can match stimuli so as to trigger an appropriate response.
The existence of such innate, internalized norms is suggested in the following experiment.
One of us (B. K.) and Arthur Nonneman allowed a litter of 6-week-old kittens
to play in a room and become familiar with it. After this adjustment period, we
introduced a two-dimensional image of an adult cat in a “Halloween posture,” as shown
in Figure 11-4.
In Review .
Free will is a not an adequate explanation of behavior, because the nervous system can
produce behaviors over which an organism has neither choice nor control. Researchers
have investigated causes of behavior, including the apparent need of the brain to maintain
at least a minimum level of stimulation, and the control exerted by the nervous system on
behavior. The older idea of internal, energizing drives that build up and are released in behavior
has given way to the more powerful explanation that behavior results from the hormone
actions and neural circuits inside the brain that control how we think, act, and feel.
Innate releasing mechanism (IRM).
Hypothetical mechanism that detects
specific sensory stimuli and directs an
organism to take a particular action.
Figure 11-4
Innate Releasing Mechanism in Cats
Displaying the “Halloween cat” (top)
stimulates cats to respond defensively,
with raised fur, arched backs, and bared
teeth. This behavior appears at about
6 weeks of age in kittens who have
never seen such a posture before.
The “Picasso” cat (bottom) evokes no
response at all.
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The kittens responded with raised fur, arched backs, and bared teeth, all
signs of being threatened by the image of the adult. Some even hissed at the
model. These kittens had no experience with any adult cat except their mother,
and there was no reason to believe that she had ever shown them this behavior.
Rather, some sort of template of this posture must be prewired in the kitten
brain.When the kittens saw the model that matched the preexisting template, a
threat response was automatically triggered. This innate triggering mechanism
is an IRM.
The IRM concept also applies to humans. In one study, Tiffany Field and
her colleagues (1982) had an adult display to young infants various exaggerated
facial expressions, such as happiness, sadness, and surprise. As Figure 11-5
shows, the babies responded with very much the same expressions as the adults
displayed. These newborns were too young to be imitating the adult faces intentionally.
Rather, their responses must have been due to an IRM.
The babies must have had an innate ability to match these facial expressions
to internal templates, which in turn triggered some prewired program to reproduce
the expressions in their own faces. Such ability would have adaptive value
if these facial expressions serve as important social signals for humans.
Evidence for a prewired motor program related to facial expressions also
comes from the study of congenitally blind children. These children spontaneously
produce the very same facial expressions that sighted people do, even
though they have never seen them in others.
Although IRMs such as those just described are prewired into the brain,
they can be modified by experience. For instance, our cat Hunter’s stalking skills
were not inherited fully developed at birth but rather matured functionally as
she grew older. The same is true of many human IRMs, such as those for responding
to sexually arousing stimuli.
Different cultures may emphasize different stimuli as arousing, and, even
within a single culture, there is variation in what different people find sexually
stimulating. Nonetheless, some human attributes are universally found to have
sexually arousing value. An example is the hip-to-waist ratio of human females
for most human males. This ratio is probably part of an IRM.
The IRM concept can be related to the Darwinian view of how the nervous
system evolves. According to this view, natural selection favors behaviors that prove
adaptive for an organism, and these behaviors are passed on to future generations. Because
behavior patterns are produced by the activity of neurons in the brain, the natural
selection of specific behaviors is really the selection of particular brain circuits.
Animals that survive long enough to reproduce and have healthy offspring are
more likely to pass on the genes for making their brain circuits than are animals with
traits that make them less likely to survive and successfully reproduce. Thus, cats with
brain circuits that made them adept at stalking prey or responding fiercely to threats
were more likely to survive and produce many offspring, passing on those adaptive
brain circuits and behaviors to their young. In this way, the behaviors became widespread
in the species over time.
Although the Darwinian view seems straightforward when considering how cats
evolved brain circuits for stalking prey or responding to threats, it is less so when applied
to many complex human behaviors. For instance, why have humans evolved the
behavior of killing other members of their species? At first glance, this behavior would
seem counterproductive to the survival of humans; so why has it endured?
A field of study called evolutionary psychology, which seeks to apply principles of
natural selection to understand the causes of human behavior, is a source of insight.
Consider how evolutionary psychologists account for homicide.When two men fight
396 ! CHAPTER 11
Figure 11-5
Innate Releasing Mechanism in
Humans Facial expressions made
by young infants in response to
expressions made by the experimenter.
From “Discrimination and Imitation of Facial
Expression by Neonates,” by T. M. Field, R.
Woodson, R. Greenberg, and D. Cohen, 1982,
Science, 218, p. 180.
Evolutionary psychology. Discipline
that seeks to apply principles of natural
selection to understand the causes of
human behavior.
Photographs courtesy of Dr. Tiffany M. Field
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a duel, one common-sense explanation might be that they are fighting over grievances.
But evolutionary psychologists would look at a duel differently, asking why a behavior
pattern that risks people’s lives is sustained in a population. Their answer is that fights
are about social status.
Evolutionary psychologists assume that any behavior, including dueling, exists because
the neural circuits producing it have been favored through natural selection. In
this case, men who fought and won duels passed on their genes to future generations,
whereas those who lost duels did not. Through time, therefore, the traits associated
with successful dueling—strength, aggression, agility—became more prevalent among
humans, and so, too, did dueling itself.
Martin Daly and Margot Wilson (1988) extended this type of analysis to further
account for homicide. In their view, homicide may endure in our society despite its severe
punishment because it is related to behaviors that were adaptive in the human
past. Suppose, for example, that natural selection favored sexually jealous males who
effectively intimidated their rivals and bullied their mates so as to guarantee their own
paternity of any offspring produced by their mates.As a result,male jealousy would become
a prevalent motive for interpersonal violence, including homicide.
Note that, in this view, homicide itself does not help a man produce more children.
But men who are apt to commit homicides are more likely to engage in other behaviors
(bullying and intimidation) that improve their social status and therefore their reproductive
fitness. Homicide therefore is related to adaptive traits that have been
selected through millennia.
The evolutionary psychology view is introduced here not to account for all human
behavior and perhaps not even to account for homicide; rather, it demonstrates
that evolutionary theory can generate hypotheses about how natural selection might
have shaped the brain and behavior. In this way, evolutionary psychology can sometimes
provide an additional and intriguing perspective on the neurological bases of
The Chemical Senses
Just as chemical reactions play a central role in nervous system activity, chemical signals
(chemosignals) play a central role in the motivated and emotional behavior of
mammals. Mammals identify group members by odor, mark their territories with
urine and other odorants, identify favorite and forbidden foods by taste, and form associations
between odors, tastes, and emotional events.We thus consider the chemical
senses here in the context of emotional and motivated behavior.
Odor is the most puzzling of the sensory systems. We can discriminate thousands of
odors, yet we have great difficulty finding words to describe what we smell.We may like
or dislike smells or compare one smell to another, but we lack a vocabulary for our olfactory
Wine experts rely on olfaction to tell them about wines, but they must learn to use
smell to do so. There are courses for training people in wine sniffing, courses that are
typically one full day a week for a year, and most people who take such courses still have
great difficulty in passing the final test. The degree of difficulty contrasts with that of vision
and audition, which are designed to analyze specific qualities of the sensory input
(such as pitch in audition or color in vision). In contrast, olfaction seem to be designed
to determine whether information is familiar—for example, is a food or a friend—or to
identify a signal such as a receptive mate.
Visit the Web site at www.worth to
learn more about evolutionary
CH11.qxd 2/3/05 4:19 PM Page 397

Receptors for Smell The identification of chemosignals
is conceptually similar to the identification of
other sensory stimuli (light, sound, touch) except that,
instead of converting physical energy such as light or
sound waves into receptor potentials, scent interacts
with chemical receptors. This constant chemical interaction
appears to be tough on the receptors and so, in
contrast with the receptors for light, sound, and touch,
chemical receptors are constantly being replaced. The
life of an olfactory receptor is about 60 days.
The receptor surface for olfaction is the olfactory
epithelium, which lies in the nasal cavity, as illustrated
in Figure 11-6. The epithelium is composed of receptor
cells and support cells. Each receptor cell sends a
process, which ends in 10 to 20 cilia, into a mucous
layer known as the olfactory mucosa. Chemicals in the
air that we breathe dissolve in the mucosa to interact with the cilia. If the receptors are
affected by an olfactory chemosignal, metabotropic activation of a specific G protein
leads to an opening of sodium channels and a change in membrane potential (see
Chapter 5).
The receptor surface of the epithelium varies widely across species. In humans, the
area is estimated to range from 2 to 4 cm2; in dogs, the area is about 18 cm2; and, in
cats, it is about 21 cm2. No wonder our sensitivity to odors is less acute than that of
dogs and cats: they have 10 times as much receptor area as humans have. Roughly analogous
to the tuning characteristics of cells in the auditory system, olfactory receptor
neurons in vertebrates do not respond to specific odors but rather to a range of odors.
How does a limited number of receptor types allow us to smell many different
odors? The simplest explanation is that any given odorant stimulates a unique pattern
of receptors, and the summed activity, or pattern of activity, produces our perception
of a particular odor. Analogously, the visual system enables us to identify many different
colors with only three receptor types in the retina: the summed activity of the three
cones leads to our rich color life.
A fundamental difference, however, is that there are far more receptors in the olfactory
system than in the visual system. Richard Axel and Linda Buck won the Nobel
Prize in medicine in 2004 for their discovery that a novel gene family (about 350 genes
in humans) encodes a very large and diverse set of olfactory receptors. The combination
of these receptors allows us to discriminate about 10,000 different smells.
Olfactory Pathways Olfactory receptor cells project to the olfactory bulb, ending in
ball-like tufts of dendrites called glomeruli (see Figure 11-6). There they form synapses
with the dendrites of mitral cells. The mitral cells send their axons from the olfactory
bulb to a broad range of forebrain areas summarized in Figure 11-7. Although many
of the olfactory targets, such as the amygdala and pyriform cortex, have no connection
through the thalamus, as do other sensory systems, a thalamic connection (to the dorsomedial
nucleus) does project to the orbitofrontal cortex. As we shall see, the orbitofrontal
cortex plays a central role in a variety of emotional and social behaviors as
well as in eating.
Accessory Olfactory System A unique class of odorants are pheromones, biochemicals
released by one animal that act as chemosignals and can affect the physiology or
behavior of another animal. For example, Karen Stern and Martha McClintock (1998)
398 ! CHAPTER 11
To pyriform cortex
bulb Mitral cells
Cilia Support
Olfactory mucosa cells
Figure 11-6
Olfactory Epithelium
Olfactory bulb
To amygdala
To thalamus and
orbitofrontal cortex
To hypothalamus
Pyriform and
entorhinal cortex
Figure 11-7
Olfactory Pathways
CH11.qxd 2/3/05 4:19 PM Page 398

found that, when women reside together they begin to cycle together, a phenomenon
referred to as the Whitten effect. Furthermore, the researchers found that the synchronization
of menstrual cycles is conveyed by odors.
Pheromones appear to be able to affect more than sex-related behavior. A human
chemosignal, androstadienone, has been shown to alter glucose utilization in the neocortex—
that is, how the brain uses energy (Jacob et al., 2001). Thus, a chemosignal
appears to affect cortical processes even though the signal was not actually detected
consciously. The puzzle is why we would evolve such a mechanism and how it might
actually affect cerebral functioning.
Pheromones are unique odors because they are detected by a special olfactory receptor
system known as the vomeronasal organ, which is made up of a small group of
sensory receptors that are connected by a duct to the nasal passage. The receptor cells
in the vomeronasal organ send their axons to the accessory olfactory bulb, which lies
adjacent to the main olfactory bulb. The vomeronasal organ connects primarily with
the amygdala and hypothalamus by which it likely plays a role in reproductive and social
The vomeronasal organ probably does not participate in general olfactory behavior
but rather in the analysis of pheromones such as those in urine. You may have seen
bulls or cats engage in a behavior known as flehmen, which is illustrated in Figure11-8.
When exposed to novel cat or human urine, these animals raise their upper lip to close
off the nasal passages and suck air into the mouth. The air flows through the duct on
the roof of the mouth en route to the vomeronasal organ.
Curiously, cats respond to novel cat or human urine but do not respond to dog,
rodent, or monkey urine or feces (Kolb & Nonneman, 1975). Damage to the orbitofrontal
cortex eliminates the behavior, suggesting that the orbitofrontal cortex
plays a key role in analyzing the pheromones in urine.
Research reveals significant differences in taste preferences both between and within
species. Humans and rats like sucrose and saccharin solutions, but dogs reject saccharin,
and cats are indifferent to both, inasmuch as they do not detect sweetness at all.
The failure of cats to taste sweetness may not be surprising; they are pure carnivores,
and nothing that they normally eat is sweet.
Similarly, within the human species, clear differences in taste thresholds and preferences
are obvious.An example is the preference for or dislike of bitter tastes—the flavor
of brussels sprouts, for instance. People tend either to love them or hate them.
Linda Bartoshuk (2000) showed absolute differences among adults: some perceive certain
tastes as very bitter, whereas others are indifferent to them. Presumably, the latter
group is more tolerant of brussels sprouts.
There are also differences in taste thresholds as we age. Children are much more
responsive to tastes than adults and are often intolerant of spicy foods, because they
Figure 11-8
Response to Pheromones (Left) A
cat sniffs a urine-soaked cotton ball,
(middle) raises its upper lip to close off
the nasal passages, and (right) follows
with the full gape response characteristic
of flehmen, a behavior mediated by the
accessory olfactory system. Photographs
courtesy Arthur Nonneman and Bryan Kolb.
Pheromone. Odorant biochemical
released by one animal that acts as a
chemosignal and can affect the
physiology or behavior of another animal.
CH11.qxd 2/3/05 4:19 PM Page 399

have more taste receptors than adults have. By age 20, humans have lost
at least an estimated 50 percent of their taste receptors. No wonder children
and adults have different food preferences.
Receptors for Taste Taste receptors are found within taste buds located
in several distinct subpopulations: on the tongue, under the tongue, on
the soft palate on the roof of the mouth, on the sides of the mouth, and
at the back of the mouth on the nasopharnyx. Each of the five different
taste-receptor types responds to a different chemical component of food.
The four most familiar are sweet, sour, salty, and bitter. The fifth type,
sometimes called the umami receptor, is specially sensitive to glutamate and perhaps
to protein (see Chapter 5).
Taste receptors are grouped into taste buds, each containing several receptor types,
as illustrated in Figure 11-9. Gustatory stimuli interact with the receptor tips, the microvilli,
to open ion channels, leading to changes in membrane potential. The base of
the taste bud is contacted by the branches of afferent nerves that come from cranial
nerves 7 (facial nerve), 9 (glossopharyngeal nerve), or 10 (vagus). You can review these
cranial nerves in Figure 2-26.
Gustatory Pathways Cranial nerves 7, 9, and 10 form the main gustatory nerve,
the solitary tract. On entering the brainstem, the tract divides in two as illustrated in
Figure 11-10. One route travels through the posterior medulla to the ventroposterior
medial nucleus of the thalamus, which in turn sends out two pathways, one to the primary
somatosensory cortex and the other to a region just rostral to the secondary somatosensory
cortex in the gustatory cortex of the insula.
The gustatory region is dedicated to taste, whereas the primary somatosensory region
is also responsive to tactile information and is probably responsible for localizing
tastes on the tongue. The gustatory cortex sends a projection to the orbital cortex in a
region near the input of the olfactory cortex. The mixture of olfactory and gustatory
input in the orbital cortex likely gives rise to our perception of flavor.
The second pathway from the gustatory nerve projects through the pons to the hypothalamus
and amygdala. Researchers hypothesize that this input plays some role in
feeding behavior.
Environmental Influences on Behavior
Many psychologists have emphasized learning as a cause of behavior.
No one would question that we modify our behavior as we learn, but
B. F. Skinner went much farther.He believed that behaviors are selected
by environmental factors.
His argument is simple. Certain events function as rewards, or
reinforcers, and,when a reinforcing event follows a particular response,
similar responses are more likely to occur again. Skinner argued that reinforcement
can be manipulated to encourage the display of complex
forms of behavior.
The power of experience to shape behavior by pairing stimuli and rewards is typified
by one of Skinner’s experiments. A pigeon is placed in a box that has a small disc
on one wall (the stimulus). If the pigeon pecks at the disc (the response), a food tray
opens and the pigeon can feed (the reinforcement or reward). A pigeon quickly learns
the association between the stimulus and the response, especially if the disc has a small
400 ! CHAPTER 11
Reinforcer. In operant conditioning, any
event that strengthens the behavior that it
Tongue Taste pore
Processes of cranial
nerves 7, 9, 10
Figure 11-9
Anatomy of a Taste Bud Adapted from
Smith and Shepherd, 2003, p. 720.
nucleus of
cortex (insula)
Cranial nerves
7, 9, 10
Nucleus of
solitary tract
Figure 11-10
Gustatory Pathways
B. F. Skinner

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kesehatan biology dan Meditasi

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