Carlson 11e Ch08 W

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for
Physiology of Behavior 11th Edition
by
Neil R. Carlson
Prepared by Grant McLaren, Edinboro University of Pennsylvania

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Control of Movement
Chapter 8
2 COPYRIGHT © ALLYN & BACON 2012
Skeletal Muscle
Skeletal Muscle
• one of the striated muscles attached to bones
• Skeletal muscles are the ones that move us (our skeletons) around and thus are
responsible for our actions.
• Most of them are attached to bones at each end and move the bones when they
contract. (Exceptions include eye muscles and some abdominal muscles, which are
attached to bone at one end only.)
• Muscles are fastened to bones via tendons, strong bands of connective tissue.

Skeletal Muscle
Skeletal Muscle
• Several different classes of movement can be accomplished by the skeletal muscles, but I will
refer principally to two of them: flexion and extension.
• Contraction of a flexor muscle produces flexion, the drawing in of a limb.
• Extension, which is the opposite movement, is produced by contraction of extensor muscles.

These are the so-called antigravity muscles—the ones we use to stand up.
• Muscles contract; limbs flex.

Skeletal Muscle
Skeletal Muscle
• Flexion
• a movement of a limb that tends to bend its joints; the opposite of extension
• Extension
• a movement of a limb that tends to straighten its joints; the opposite of flexion

Skeletal Muscle
Anatomy
• The detailed structure of a skeletal muscle is shown in Figure 8.1.
• The extrafusal muscle fibers are served by axons of the alpha motor neurons. Contraction of
these fibers provides the muscle’s motive force.
• The intrafusal muscle fibers are specialized sensory organs that are served by two axons,
one sensory and one motor.
• These organs are also called muscle spindles because of their shape.

Skeletal Muscle
Anatomy
• Extrafusal Muscle Fiber

• one of the muscle fibers responsible for the force exerted by contraction of a skeletal
muscle
• Alpha Motor Neuron

• A neuron whose axon forms synapses with extrafusal muscle fibers of a skeletal muscle:
activation contracts the muscle fibers.

Skeletal Muscle
Anatomy
• Intrafusal Muscle Fiber

• a muscle fiber that functions as a stretch receptor; arranged parallel to the extrafusal
muscle fibers, thus detecting changes in muscle length

Figure 8.1, page 257

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Skeletal Muscle
Anatomy
• The central region (capsule) of the intrafusal muscle fiber contains sensory endings that are
sensitive to stretch applied to the muscle fiber.
• Actually, there are two types of intrafusal muscle fibers, but for simplicity’s sake, only one
kind is shown here.
• The efferent axon of the gamma motor neuron causes the intrafusal muscle fiber to contract;
however, this contraction contributes an insubstantial amount of force.
• Gamma Motor Neuron

• a neuron whose axons form synapses with intrafusal muscle fibers

Skeletal Muscle
Anatomy
• In muscles that move the fingers or eyes, the ratio can be less than one to ten; in muscles
that move the leg, it can be one to several hundred.
• An alpha motor neuron, its axon, and associated extrafusal muscle fibers constitute a motor
unit.
• A single muscle fiber consists of a bundle of myofibrils, each of which consists of overlapping
strands of actin and myosin.

Skeletal Muscle
Anatomy
• Motor Unit
• a motor neuron and its associated muscle fibers
• Myofibril
• an element of muscle fibers that consists of overlapping strands of actin and myosin;
responsible for muscular contractions

Skeletal Muscle
The Physical Basis of Muscular Contraction
• The synapse between the terminal button of an efferent neuron and the membrane of a
muscle fiber is called a neuromuscular junction.
• The terminal buttons of the neurons synapse on motor endplates, located in grooves along
the surface of the muscle fibers.

Skeletal Muscle
• When an axon fires, acetylcholine is liberated by the terminal buttons and produces a
depolarization of the postsynaptic membrane—an endplate potential.
• The endplate potential is much larger than an excitatory postsynaptic potential in synapses
between neurons; an endplate potential always causes the muscle fiber to fire, propagating
the potential along its length.
• This action potential induces a contraction, or twitch, of the muscle fiber.

Skeletal Muscle
• Neuromuscular Junction
• the synapse between the terminal buttons of an axon and a muscle fiber
• Motor Endplate
• the postsynaptic membrane of a neuromuscular junction
• Endplate Potential
• the postsynaptic potential that occurs in the motor endplate in response to release of
acetylcholine by the terminal button

Skeletal Muscle
• The depolarization of a muscle fiber opens the gates of voltage-dependent calcium channels,
permitting calcium ions to enter the cytoplasm.
• This event triggers the contraction.
• Calcium acts as a cofactor that permits the myofibrils to extract energy from the ATP that is
present in the cytoplasm.

Skeletal Muscle
• The myosin cross bridges alternately attach to the actin strands, bend in one direction,
detach themselves, bend back, reattach to the actin at a point farther down the strand, and so
on.
• Thus, the cross bridges “row” along the actin filaments.
• Figure 8.2 illustrates this rowing sequence and shows how this sequence results in
shortening the muscle fiber. (See Figure 8.2.)

Figure8.2, page 259

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Skeletal Muscle
• Figure 8.3 shows how the physical effects of a series of action potentials can overlap,
causing a sustained contraction by the muscle fiber.
• A single motor unit in a leg muscle of a cat can raise a 100-gram weight, which attests to the
remarkable strength of the contractile mechanism. (See Figure 8.3.)


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Skeletal Muscle
Sensory Feedback from Muscles
• As we saw, the intrafusal muscle fibers contain sensory endings that are sensitive to stretch.
• The intrafusal muscle fibers are arranged in parallel with the extrafusal muscle fibers.
• Therefore, they are stretched when the muscle lengthens and are relaxed when it shortens.
Thus, even though these afferent neurons are stretch receptors, they serve as muscle length
detectors.

Skeletal Muscle
• This distinction is important. Stretch receptors are also located within the tendons, in the
Golgi tendon organ.
• Golgi Tendon Organ

• the receptor organ at the junction of the tendon and muscle that is sensitive to stretch

Skeletal Muscle
• Figure 8.4 shows the response of afferent axons of the muscle spindles and Golgi tendon
organ to various types of movements.
• Figure 8.4(a) shows the effects of passive lengthening of muscles, the kind of movement that
would be seen if your forearm, held in a completely relaxed fashion, were slowly lowered by
someone who was supporting it.
• The rate of firing of one type of muscle spindle afferent neuron (MS1) increases, while the
activity of the afferent of the Golgi tendon organ remains unchanged. (See Figure 8.4a.)

Skeletal Muscle
• Figure 8.4(b) shows the results when the arm is dropped quickly; note that this time the
second type of muscle spindle afferent neuron (MS2) fires a rapid burst of impulses.
• This fiber, then, signals rapid changes in muscle length. (See Figure 8.4b.)
• Figure 8.4(c) shows what would happen if a weight were suddenly dropped into your hand
while your forearm was held parallel to the ground.

Figure 8.4a, page 260

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Figure 8.4b, page 260

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Figure 8.4c, page 260

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Skeletal Muscle
Section Summary
• Our bodies possess skeletal muscle, smooth muscle, and cardiac muscle.
• Skeletal muscles contain extrafusal muscle fibers, which provide the force of contraction.
• The alpha motor neurons form synapses with the extrafusal muscle fibers and control their
contraction.

Skeletal Muscle
Section Summary
• The force of muscular contraction is provided by long protein molecules called actin and
myosin, arranged in overlapping parallel arrays.
• When an action potential—initiated by the synapse at the motor endplate—causes calcium

ions to enter the muscle fiber, the myofibrils extract energy from ATP and cause a twitch of
the muscle fiber, producing a ratchetlike “rowing” movement of the myosin cross bridges.

Reflexive Control of Movement
• Although behaviors are controlled by the brain, the spinal cord possesses a certain degree of
autonomy.
• Particular kinds of somatosensory stimuli can elicit rapid responses through neural
connections located within the spinal cord.
• These reflexes constitute the simplest level of motor integration.

The Monosynaptic Stretch Reflex
• Figure 8.5 shows the effects of placing a weight in a person’s hand.
• This time I have included a piece of the spinal cord, with its roots, to show the neural circuit
that composes the monosynaptic stretch reflex.
• First, follow the circuit: Starting at the muscle spindle, afferent impulses are conducted to
terminal buttons in the gray matter of the spinal cord.

• These terminal buttons synapse on an alpha motor neuron that innervates the extrafusal
muscle fibers of the same muscle.
• Only one synapse is encountered along the route from receptor to effector—hence the term
monosynaptic. (See Figure 8.5a.)
• Monosynaptic Stretch Reflex

• a reflex in which a muscle contracts in response to its being quickly stretched; involves a
sensory neuron and a motor neuron, with one synapse between them

Figure 8.5a, page 262

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• Now consider a useful function this reflex performs.
• If the weight the person is holding is increased, the forearm begins to move downward.
• This movement lengthens the muscle and increases the firing rate of the muscle spindle
afferent neurons, whose terminal buttons then stimulate the alpha motor neurons, increasing
their rate of firing.
• Consequently, the strength of the muscular contraction increases, and the arm pulls the
weight up. (See Figure 8.5b.)


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• To stand, we must keep our center of gravity above our feet, or we will fall.
• As we stand, we tend to oscillate forward and back and from side to side.
• Our vestibular sacs and our visual system play important roles in the maintenance of posture.

• However, these systems are aided by the activity of the monosynaptic stretch reflex.
• For example, consider what happens when a person begins to lean forward.
• The large calf muscle (gastrocnemius) is stretched, and this stretching elicits compensatory
muscular contraction that pushes the toes downward, thus restoring upright posture. (See
Figure 8.6.)


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The Gamma Motor System
• We have already seen that the afferent axons of the muscle spindle help to maintain limb
position even when the load carried by the limb is altered.
• Efferent control of the muscle spindles permits these muscle length detectors to assist in
changes in limb position as well.
• Consider a single muscle spindle. When its efferent axon is completely silent, the spindle is
completely relaxed and extended.

• As the firing rate of the efferent axon increases, the spindle gets shorter and shorter.
• If, simultaneously, the rest of the entire muscle also gets shorter, there will be no stretch on
the central region that contains the sensory endings, and the afferent axon will not respond.
• However, if the muscle spindle contracts faster than does the muscle as a whole, there will
be a considerable amount of afferent activity.

• If there is little resistance, both the extrafusal and intrafusal muscle fibers will contract at
approximately the same rate, and little activity will be seen from the afferent axons of the
muscle spindle.
• However, if the limb meets with resistance, the intrafusal muscle fibers will shorten more than
the extrafusal muscle fibers, and hence sensory axons will begin to fire and cause the
monosynaptic stretch reflex to strengthen the contraction.
• Thus, the brain makes use of the gamma motor system in moving the limbs.
• By establishing a rate of firing in the gamma motor system, the brain controls the length of
the muscle spindles and, indirectly, the length of the entire muscle.

Polysynaptic Reflexes
• The monosynaptic stretch reflex is the only spinal reflex we know of that involves only one
synapse.
• All others are polysynaptic.
• Examples include relatively simple ones, such as limb withdrawal in response to noxious
stimulation, and relatively complex ones, such as the ejaculation of semen.
• Spinal reflexes do not exist in isolation; they are normally controlled by the brain.

• There are two populations of afferent axons from the Golgi tendon organ, with different
sensitivities to stretch.
• The more sensitive afferent axons tell the brain how hard the muscle is pulling. The less
sensitive ones have an additional function.
• Their terminal buttons synapse on spinal cord interneurons—neurons that reside entirely
within the gray matter of the spinal cord and serve to interconnect other spinal neurons.

• These interneurons synapse on the alpha motor neurons serving the same muscle.
• The terminal buttons liberate glycine and hence produce inhibitory postsynaptic potentials on
the motor neurons. (See Figure 8.7.)
• The function of this reflex pathway is to decrease the strength of muscular contraction when
there is danger of damage to the tendons or bones to which the muscles are attached.


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• The discovery of the inhibitory Golgi tendon organ reflex provided the first real evidence of
neural inhibition, long before the synaptic mechanisms were understood.
• A decerebrate cat, whose brain stem has been cut through, exhibits a phenomenon known as
decerebrate rigidity.
• The animal’s back is arched, and its legs are extended stiffly from its body.
• This rigidity results from excitation originating in the caudal reticular formation, a region of the
brain stem, which greatly facilitates all stretch reflexes, especially of extensor muscles, by
increasing the activity of the gamma motor system.

• Rostral to the brain stem transection is an inhibitory region of the reticular formation that
normally counterbalances the excitatory one.
• The transection removes the inhibitory influence, leaving only the excitatory one. If you
attempt to flex the outstretched leg of a decerebrate cat, you will meet with increasing
resistance, which will suddenly melt away, allowing the limb to flex
• It almost feels as though you were closing the blade of a pocketknife—hence the term clasp-
knife reflex.
• The sudden release is, of course, mediated by activation of the Golgi tendon organ reflex.

• Decerebrate
• describes an animal whose brain stem has been transected
• Decerebrate Rigidity
• simultaneous contraction of agonistic and antagonistic muscles; caused by
decerebration or damage to the reticular formation
• Clasp-Knife Reflex
• A reflex that occurs when force is applied to flex or extend the limb of an animal showing
decerebrate rigidity: resistance is replaced by sudden relaxation.

Section Summary
• Reflexes are simple circuits of sensory neurons, interneurons (usually), and efferent neurons
that control simple responses to particular stimuli.
• In the monosynaptic stretch reflex, the terminal buttons of axons that receive sensory
information from the intrafusal muscle fibers synapse with alpha motor neurons that innervate
the same muscle.

Section Summary
• Thus, a sudden lengthening of the muscle causes the muscle to contract.
• By setting the length of the intrafusal muscle fibers, and hence their sensitivity to increases in
muscle length, the motor system of the brain can control limb position.
• Changes in a weight being held that cause the limb to move will be quickly compensated for
by means of the monosynaptic stretch reflex.

Control of Movement by the Brain
• Movements can be initiated by several means.
• For example, rapid stretch of a muscle triggers the monosynaptic stretch reflex, a stumble
triggers righting reflexes, and the rapid approach of an object toward the face causes a startle
response, a complex reflex consisting of movements of several muscle groups.
• Other stimuli initiate sequences of movements that we have previously learned.
• For example, the presence of food causes eating, and the sight of a loved one evokes a hug
and a kiss.
• Because there is no single cause of behavior, we cannot find a single starting point in our
search for the neural mechanisms that control movement.

• The brain and spinal cord include several different motor systems, each of which can
simultaneously control particular kinds of movements.
• Walking, postural adjustments, talking, movement of the arms, and movements of the fingers
all involve different specialized motor systems.

Organization of the Motor Cortex
• The primary motor cortex lies on the precentral gyrus, just rostral to the central sulcus.
• Stimulation studies (including those in awake humans) have shown that the activation of
neurons located in particular parts of the primary motor cortex causes movements of
particular parts of the body.
• Somatotopic Organization
• a topographically organized mapping of parts of the body that are represented in a
particular region of the brain

• In other words, the primary motor cortex shows somatotopic organization (from soma, “body,”
and topos, “place”).
• Figure 8.8 shows a motor homunculus based on the observations of Penfield and
Rasmussen (1950).
• Note that a disproportionate amount of cortical area is devoted to movements of the fingers
and the muscles used for speech. (See Figure 8.8.)


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• Figure 8.9 shows the results of a combined fMRI and DTI study by Wahl et al. (2007), which
shows an image of regions of the primary motor cortex and the axons of the corpus callosum
that unite regions of the left and right primary motor cortex.
• The cortical regions that control movements in the lips, hand, and foot are shown in light red,
light green, and light yellow, respectively.
• The axons of the corpus callosum that unite these regions are shown in darker versions of
the same colors. (See Figure 8.9.)


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• It is important to recognize that the primary motor cortex is organized in terms of particular
movements of particular parts of the body.
• Each movement may be accomplished by the contraction of several muscles.
• This fact means that complex neural circuitry is located between individual neurons in the
primary motor cortex and the motor neurons in the spinal cord that cause motor units to
contract.

• For example, stimulation of one region caused the hand to close and then approach the
mouth—and the mouth then to open.
• Stimulation of another region caused the face to squint, the head to turn quickly to one side,
and the arms to fling up, as if to protect the face from something that was going to hit it.
• Stimulation of different zones of the motor cortex caused different categories of actions. The
map of these categories was consistent from animal to animal. (See Figure 8.10.)


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• The principal cortical input to the primary motor cortex is the frontal association cortex,
located rostral to it.
• Two regions immediately adjacent to the primary motor cortex—the supplementary motor
area and the premotor cortex—are especially important in the control of movement.
• Both regions receive sensory information from the parietal and temporal lobes, and both send
efferent axons to the primary motor cortex.

• The supplementary motor area (SMA) is located on the medial surface of the brain, just
rostral to the primary motor cortex.
• The premotor cortex is located primarily on the lateral surface, also just rostral to the primary
motor cortex. The roles that these regions play in the control of movement is discussed later
in this chapter. (Refer to Figure 8.8.)

• Supplementary Motor Area (SMA)

• a region of motor association cortex of the dorsal and dorsomedial frontal lobe; rostral to
the primary motor cortex
• Premotor Cortex
• a region of motor association cortex of the lateral frontal lobe; rostral to the primary
motor cortex

Cortical Control of Movement: The Descending Pathways
• Neurons in the primary motor cortex control movements by two groups of descending tracts,
the lateral group and the ventromedial group, named for their locations in the white matter of
the spinal cord.
• The lateral group consists of the corticospinal tract, the corticobulbar tract, and the
rubrospinal tract.

• Lateral Group
• the corticospinal tract, the corticobulbar tract, and the rubrospinal tract
• Ventromedial Group
• the vestibulospinal tract, the tectospinal tract, the reticulospinal tract, and the ventral
corticospinal tract

• This system is primarily involved in control of independent limb movements, particularly

movements of the hands and fingers.
• Independent limb movements mean that the right and left limbs make different movements or
one limb moves while the other remains still.
• These movements contrast with coordinated limb movements, such as those involved in
locomotion.

• The ventromedial group consists of the vestibulospinal tract, the tectospinal tract, the
reticulospinal tract, and the ventral corticospinal tract.
• These tracts control more automatic movements: gross movements of the muscles of the
trunk and coordinated trunk and limb movements involved in posture and locomotion.

• The corticospinal tract consists of axons of cortical neurons that terminate in the gray matter
of the spinal cord.
• The largest concentration of cell bodies responsible for these axons is located in the primary
motor cortex, but neurons in the parietal and temporal lobes also send axons through the
corticospinal pathway.

• The axons leave the cortex and travel through subcortical white matter to the ventral
midbrain, where they enter the cerebral peduncles.
• They leave the peduncles in the medulla and form the pyramidal tracts, so called because of
their shape.
• At the level of the caudal medulla, most of the fibers decussate (cross over) and descend
through the contralateral spinal cord, forming the lateral corticospinal tract.

• The rest of the fibers descend through the ipsilateral spinal cord, forming the ventral
corticospinal tract.
• Because of its location and function, the ventral corticospinal tract is actually part of the
ventromedial group. (See the light and dark blue lines in Figure 8.11.)

• Corticospinal Tract
• the system of axons that originates in the motor cortex and terminates in the ventral gray
matter of the spinal cord
• Pyramidal Tract
• the portion of the corticospinal tract on the ventral border of the medulla

• Lateral Corticospinal Tract

• the system of axons that originates in the motor cortex and terminates in the
contralateral ventral gray matter of the spinal cord; controls movements of the distal
limbs
• Ventral Corticospinal Tract

• the system of axons that originates in the motor cortex and terminates in the ipsilateral
ventral gray matter of the spinal cord; controls movements of the upper legs and trunk

• The rest of the fibers descend through the ipsilateral spinal cord, forming the ventral
corticospinal tract.
• Because of its location and function, the ventral corticospinal tract is actually part of the
ventromedial group. (See the light and dark blue lines in Figure 8.11.)


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• Most of the axons in the lateral corticospinal tract originate in the regions of the primary motor
cortex and supplementary motor area that control the distal parts of the limbs: the arms,
hands, and fingers and the lower legs, feet, and toes.
• They form synapses, directly or via interneurons, with motor neurons in the gray matter of the
spinal cord—in the lateral part of the ventral horn.
• These motor neurons control muscles of the distal limbs, including those that move the arms,
hands, and fingers. (See the light blue lines in Figure 8.11.)

• The axons in the ventral corticospinal tract originate in the upper leg and trunk regions of the
primary motor cortex.
• They descend to the appropriate region of the spinal cord and divide, sending terminal
buttons into both sides of the gray matter.
• They control motor neurons that move the muscles of the upper legs and trunk. (See the dark
blue lines in Figure 8.11.)

• The second of the lateral group of descending pathways, the corticobulbar tract, projects to
the medulla (sometimes called the bulb).
• This pathway is similar to the corticospinal pathway, except that it terminates in the motor
nuclei of the fifth, seventh, ninth, tenth, eleventh, and twelfth cranial nerves (the trigeminal,
facial, glossopharyngeal, vagus, spinal accessory, and hypoglossal nerves).
• These nerves control movements of the face, neck, and tongue and parts of the extraocular
eye muscles. (See the green lines in Figure 8.11.)

• Corticobulbar Tract
• a bundle of axons from the motor cortex to the fifth, seventh, ninth, tenth, eleventh, and
twelfth cranial nerves; controls movements of the face, neck, tongue, and parts of the
extraocular eye muscles

• The third member of the lateral group is the rubrospinal tract. This tract originates in the red
nucleus (nucleus ruber) of the midbrain.
• The red nucleus receives its most important inputs from the motor cortex via the corticorubral
tract and (as we shall see later) from the cerebellum.
• Rubrospinal Tract
• the system of axons that travels from the red nucleus to the spinal cord; controls
independent limb movements

• Axons of the rubrospinal tracts terminate on motor neurons in the spinal cord that control
independent movements of the forearms and hands—that is, movements that are
independent of trunk movements. (They do not control the muscles that move the fingers.)
(See the red lines in Figure 8.11.)
• Corticorubral Tract
• the system of axons that travels from the motor cortex to the red nucleus

• The second set of pathways originating in the brain stem is the ventromedial group.
• This group includes the vestibulospinal tracts, the tectospinal tracts, and the reticulospinal
tracts, as well as the ventral corticospinal tract (already described).
• Vestibulospinal Tract
• a bundle of axons that travels from the vestibular nuclei to the gray matter of the spinal
cord; controls postural movements in response to information from the vestibular system
• Tectospinal Tract
• a bundle of axons that travels from the tectum to the spinal cord; coordinates head and
trunk movements with eye movements

• These tracts control motor neurons in the ventromedial part of the spinal cord gray matter.
• Neurons of all these tracts receive input from the portions of the primary motor cortex that
control movements of the trunk and proximal muscles (that is, the muscles located on the
parts of the limbs close to the body).

• In addition, the reticular formation receives a considerable amount of input from the premotor
cortex and from several subcortical regions, including the amygdala, hypothalamus, and
basal ganglia.
• The cell bodies of neurons of the vestibulospinal tracts are located in the vestibular nuclei.

• These neurons control several automatic functions, such as muscle tonus, respiration,
coughing, and sneezing; they are also involved in behaviors that are under direct neocortical
control, such as walking. (See Figure 8.12.)
• Table 8.1 summarizes the names of these pathways, their locations, and the muscle groups
they control. (See Table 8.1.)


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Table 8.1, page 270

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Planning and Initiating Movement: Role of the Motor Association Cortex
• The supplementary motor area and the premotor cortex are involved in the planning of
movements, and they execute these plans through their connections with the primary motor
cortex.
• Functional-imaging studies show that when people execute sequences of movements—or

even imagine them—these regions become activated (Roth et al., 1996)
• More recent evidence indicates that the motor association cortex is also involved in imitating
the actions of other people (an ability that makes it possible to learn new behaviors from
them) and even in understanding the functions of other people’s behavior.

• Besides receiving information about space from the visual system, the parietal lobe receives
information about spatial location from the somatosensory, vestibular, and auditory systems
and integrates this information with visual information.
• Thus, the regions of the frontal cortex that are involved in planning movements receive the
information they need about what is happening and where it is happening from the temporal
and parietal lobes.

• Because the parietal lobes contain spatial information, the pathway from them to the frontal
lobes is especially important in controlling both locomotion and arm and hand movements.
• After all, meaningful locomotion requires us to know where we are, and meaningful
movements of our arms and hands require us to know where objects are located in space.
(See Figure 8.13.)


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The Supplemental Motor Area
• The supplementary motor area plays a critical role in behavioral sequences.
• Damage to this region disrupts the ability to execute well-learned sequences of responses in
which the performance of one response serves as the signal that the next response must be
made.
• Chen et al. (1995) found that lesions of the supplementary motor area severely impaired
monkeys’ ability to perform a simple sequence of two responses: pushing a lever in and then
turning it to the left, receiving a peanut after each response. (See Figure 8.14.)


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• Shima and Tanji (2000) taught monkeys six sequences of three motor responses. For
example, one of the sequences was push, then pull, then turn.
• They recorded from neurons in the supplementary motor area and found neurons whose
activity appeared to encode elements of these sequences.

• For example, some neurons responded just before a particular sequence of three movements
occurred; some neurons responded between two particular responses; and some neurons
responded as the monkey was preparing the make the last response of the sequence.
• Presumably, these neurons were members of circuits that encoded the information necessary
to perform the six sequences.
• Figure 8.15 shows the response of a neuron that responded during a pulling movement, but
only if it was to be followed by a pushing movement. (See Figure 8.15.)


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• A region just anterior to the supplementary motor area, the pre-SMA, appears to be involved
in control of spontaneous movements—or at least in the perception of control.
• It has long been known that although electrical stimulation of the motor cortex causes
movements, it does not produce the desire to move.
• The movement is perceived as automatic and involuntary.
• In contrast, electrical stimulation of the medial surface of the frontal lobes (including the SMA
and pre-SMA) often provokes the urge to make a movement or at least the anticipation that a
movement is about to occur (Fried et al., 1991).

• Evidence suggests that the decision to move is not made by neurons in the SMA.
• Sirigu et al. (2004) used a task similar to the one in the study by Lau et al. to investigate
decision making in people with lesions of the posterior parietal cortex.
• They found that people with these lesions could accurately report when they started the
movement, but they were not aware of an intention to move prior to making the movement.
• The investigators suggest that neural activity in the posterior parietal cortex “generates a
predictive internal model of the upcoming movement.”

• What neural circuits are actually responsible for making a decision to move?
• Sirigu and her colleagues (2004) note that lesions of the prefrontal cortex (even more anterior
than the pre-SMA) disrupt people’s plans for voluntary action.
• People with prefrontal lesions will react to events but show deficits in initiating behavior, so
perhaps the prefrontal cortex is an important source of these decisions.
• The posterior parietal cortex may be involved in monitoring one’s own plans and intentions
rather than directly forming these intentions.

The Premotor Cortex
• The premotor cortex is involved in learning and executing complex movements that are
guided by sensory information.
• The results of several studies suggest that the premotor cortex is involved in using arbitrary
stimuli to indicate what movement should be made.
• For example, reaching for an object that we see in a particular location involves nonarbitrary
spatial information; that is, the visual information provided by the location of the object
specifies just where we should target our reaching movement.

The Premotor Cortex
• Kurata and Hoffman (1994) trained monkeys to move their hand toward the right or left in
response to either a spatial or a nonspatial signal.
• The spatial signal required the animals to move in the direction indicated by signal lights
located to the right and left of its hand. The nonspatial signal consisted of a pair of lights, one
red and one green, located in the middle of the display.

The Premotor Cortex
• The red light signaled a movement to the left, and the green light signaled a movement to the
right. The investigators temporarily inactivated the premotor cortex with injections of
muscimol.
• When this region was inactivated, the monkeys could still move their hand toward a signal
light located to the left or right (a nonarbitrary signal), but they could no longer make the
appropriate movements when the red or green signal lights were illuminated.

The Premotor Cortex
• Similar results are seen in people with damage to the premotor cortex.
• Halsband and Freund (1990) found that patients with these lesions could learn to make six
different movements in response to spatial cues—but not in response to arbitrary visual cues.
• That is, they could learn to point to one of six locations in which they had just seen a visual
stimulus, but they could not learn to use a set of visual, auditory, and tactile cues to make
particular movements.

Imitating and Comprehending Movements: Role of the Mirror Neuron System
• Investigators found that neurons in an area of the rostral part of the ventral premotor cortex in
the monkey brain (area F5) became active when monkeys saw people or other monkeys
perform various grasping, holding, or manipulating movements with objects or when they
performed these movements themselves.
• Thus, the neurons responded to either the sight or the execution of particular movements.
• The investigators named these cells mirror neurons.
• Mirror Neurons
• neurons located in the ventral premotor cortex and inferior parietal lobule that respond
when the individual makes a particular movement or sees another individual making that
movement

• Figure 8.16 shows the anatomy of the major regions of the parietal lobe of the human brain
that I will discuss in the next several subsections of this chapter. (See Figure 8.16.)
• Several functional-imaging studies have shown that the human brain also contains a circuit of
mirror neurons in the rostral part of the inferior parietal lobule (a region of the posterior
parietal cortex) and the ventral premotor area.
• For example, in a functional imaging study, Buccino et al. (2004) had nonmusicians watch
and then imitate video clips of an expert guitarist placing his fingers on the neck of a guitar to
play a chord.
• Both watching and imitating the guitarist’s movements activated the mirror neuron circuit.


105
• These neurons, located in the ventral premotor cortex, are reciprocally connected with
neurons in the posterior parietal cortex, and further investigation found that this region also
contains mirror neurons.
• Given the characteristics of mirror neurons, we might expect that they play a role in a monke
y’s ability to imitate the movements of other monkeys—and Rizzolatti and his colleagues
found that this inference was correct.

• Mirror neurons are activated not only by the performance of an action or the sight of someone
else performing that action, but also by sounds that indicate the occurrence of a familiar
action.
• Haslinger et al. (2005) found that the interaction between audition and vision worked in the
other direction as well.
• The investigators showed professional pianists silent videos of a hand playing the piano or
making meaningless finger movements above a piano keyboard. (See Figure 8.17.)


108
• A functional-imaging study by Iacoboni et al. (2005) suggests that the mirror neuron system
helps us to understand other people’s intentions.
• The researchers showed subjects video clips of an arm and hand reaching for and grasping a
drinking mug.
• The actions were shown in isolation or in the context of objects set out for a snack (mug,
teapot, milk pitcher, sugar bowl, sealed jam jar, plate of cookies, etc.) or the same objects
after the snack had been eaten (mug, milk pitcher overturned, cookies missing from the plate,
open jam jar, etc.).

• The first context suggests that the intent of the action is that of drinking, and the second
suggests that the intent is that of cleaning up.
• The investigators found that watching the reaching action activated the mirror neuron system
of the ventral premotor cortex, but there were differences in the activation when the action
occurred in the two different contexts.
• (There were no differences in the activation caused by simply looking at the contexts.) The
authors concluded that the mirror neuron system encodes not only an action but the intent of
that action. (See Figure 8.18.)


111
Control of Reaching and Grasping
• Connolly, Andersen, and Goodale (2003) found that when people were about to make a
pointing or reaching movement to a particular location, this region became active.
• Presumably, the parietal cortex determines the location of the target and supplies information
about this location to motor mechanisms in the frontal cortex. (See Figure 8.19 and refer to
Figure 8.16.)


113

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Control of Reaching and Grasping
• As we saw in Chapter 6, several regions of the visual association cortex are named for
particular types of objects that we perceive, for example, fusiform face area, extrastriate body
area, and parahippocampal place area.
• One region of the medial posterior parietal cortex has been named the parietal reach region.
• Parietal Reach Region

• region in the medial posterior parietal cortex that plays a critical role in control of
pointing or reaching with the hands

Deficits of Skilled Movements: The Apraxias
• Damage to the frontal or parietal cortex on the left side of the brain can produce a category of
deficits called apraxia.
• Literally, the term means “without action,” but apraxia differs from paralysis or weakness that
occurs when motor structures such as the precentral gyrus, basal ganglia, brain stem, or
spinal cord are damaged.

• Apraxia refers to the inability to imitate movements or produce them in response to verbal
instructions or inability to demonstrate the movements that would be made in using a familiar
tool or utensil (Leiguarda and Marsden, 2000).
• Apraxia
• difficulty in carrying out purposeful movements, in the absence of paralysis or muscular
weakness

• There are four major types of apraxia, two of which I will discuss in this chapter.
• Limb apraxia refers to problems with movements of the arms, hands, and fingers.
• Oral apraxia refers to problems with movements of the muscles used in speech.
• Apraxic agraphia refers to a particular type of writing deficit.
• Constructional apraxia refers to difficulty in drawing or constructing objects.

Limb Apraxia
• Limb apraxia is characterized by movement of the wrong part of the limb, incorrect movement
of the correct part, or correct movements but in the incorrect sequence.
• It is assessed by asking patients to perform movements—for example, imitating hand

gestures made by the examiner.
• The most difficult movements involve pantomiming particular acts without the presence of the
objects that are normally acted upon.

Limb Apraxia
• To perform behaviors on verbal command without having a real object to manipulate, a

person must comprehend the command and be able to imagine the missing article as well as
to make the proper movements; therefore, these requests are the most difficult to carry out.
• Somewhat easier are tasks that involve imitating behaviors performed by the experimenter.

Limb Apraxia
• Although the frontal and parietal lobes are both involved in imitating hand gestures made by
other people, the frontal cortex appears to play a more important role in recognizing the
meaning of these gestures.
• Pazzaglia et al. (2008) tested patients with limb apraxia caused by damage to the left frontal
or parietal lobes.

Limb Apraxia
• They tested the patients’ recognition of hand gestures by having them watch video clips in
which a person performed the gestures correctly or incorrectly.
• For example, incorrect gestures included playing a broom as if it were a guitar or pretending
to hitchhike by extending the little finger instead of the thumb.
• Apraxic patients with damage to the inferior frontal gyrus, but not to the parietal cortex,
showed deficits in comprehension of the gestures. (See Figure 8.21.)


123
Constructional Apraxia
• Constructional apraxia is caused by lesions of the right hemisphere, particularly the right
parietal lobe.
• People with this disorder do not have difficulty making most types of skilled movements with
their arms and hands.
• Constructional Apraxia
• difficulty in drawing pictures or diagrams or in making geometrical constructions of
elements such as building blocks or sticks; caused by damage to the right parietal lobe

• They have no trouble using objects properly, imitating their use, or pretending to use them.
• However, they have trouble drawing pictures or assembling objects from elements such as
toy building blocks.

• The primary deficit in constructional apraxia appears to involve the ability to perceive and
imagine geometrical relations.
• Because of this deficit, a person cannot draw a picture, say, of a cube, because he or she
cannot imagine what the lines and angles of a cube look like—not because of difficulty
controlling the movements of his or her arm and hand. (See Figure 8.22.)
• Besides being unable to draw accurately, a person with constructional apraxia invariably has
trouble with other tasks involving spatial perception, such as following a map.


127
The Basal Ganglia
• The basal ganglia constitute an important component of the motor system.
• We know that they are important because their destruction by disease or injury causes
severe motor deficits.
• The motor nuclei of the basal ganglia include the caudate nucleus, putamen, and globus
pallidus.

The Basal Ganglia
• The basal ganglia constitute an important component of the motor system. We know that they
are important because their destruction by disease or injury causes severe motor deficits.
• The motor nuclei of the basal ganglia include the caudate nucleus, putamen, and globus
pallidus.
• The basal ganglia receive most of their input from all regions of the cerebral cortex (but
especially the primary motor cortex and primary somatosensory cortex) and the substantia
nigra.

The Basal Ganglia
• They have two primary outputs: the primary motor cortex, supplementary motor area, and
premotor cortex (via the thalamus); and motor nuclei of the brain stem that contribute to the
ventromedial pathways.
• Through these connections, the basal ganglia influence movements under the control of the
primary motor cortex and exert some direct control over the ventromedial system.

The Basal Ganglia
• Figure 8.23(a) illustrates the components of the basal ganglia: the caudate nucleus, the
putamen, and the globus pallidus.
• It also shows some nuclei associated with the basal ganglia: the ventral anterior nucleus and
ventrolateral nucleus of the thalamus, the subthalamic nucleus, and the substantia nigra of
the ventral midbrain. (See Figure 8.23a.)

The Basal Ganglia
• Caudate Nucleus
• a telencephalic nucleus; one of the input nuclei of basal ganglia; involved with control of
voluntary movement
• Putamen
• a telencephalic nucleus; one of the input nuclei of the basal ganglia; involved with
control of voluntary movement
• Globus Pallidus
• a telencephalic nucleus; the primary output nucleus of the basal ganglia; involved with
control of voluntary movement

The Basal Ganglia
• Ventral Anterior Nucleus (of Thalamus)

• a thalamic nucleus that receives projections from the basal ganglia and sends
projections to the motor cortex
• Ventrolateral Nucleus (of Thalamus)

• a thalamic nucleus that receives projections from the basal ganglia and sends
projections to the motor cortex
• Subthalamic Nucleus
• a nucleus located ventral to the thalamus; an important part of the subcortical motor
system that includes the basal ganglia; a target of deep-brain stimulation for treatment of
Parkinson’s disease

Figure8.23a, page 279

134
The Basal Ganglia
• Figure 8.23(b) shows some of the more important connections of the basal ganglia and helps
to explain the role these structures play in the control of movement.
• For the sake of clarity, this figure leaves out many connections, including inputs to the
substantia nigra from the basal ganglia and other structures.


136
The Basal Ganglia
• The frontal, parietal, and temporal cortex send axons to the caudate nucleus and the
putamen, which then connect with the globus pallidus.
• The globus pallidus sends information back to the motor cortex via the ventral anterior and
ventrolateral nuclei of the thalamus, completing the loop.

The Basal Ganglia
• Thus, the basal ganglia can monitor somatosensory information and are informed of
movements being planned and executed by the motor cortex.
• Using this information (and other information they receive from other parts of the brain), they
can then influence the movements controlled by the motor cortex.

The Basal Ganglia
• Throughout this circuit, information is represented somatotopically.
• That is, projections from neurons in the motor cortex that cause movements in particular
parts of the body project to particular parts of the putamen, and this segregation is
maintained all the way back to the motor cortex. (See Figure 8.23b.)


140
The Basal Ganglia
• The caudate nucleus and putamen receive excitatory input from the cerebral cortex.
• They send inhibitory axons to the external and internal divisions of the globus pallidus (the
GPi and the GPe, respectively).
• The subthalamic nucleus also receives excitatory input from the cerebral cortex, and it sends
excitatory input to the GPi.

The Basal Ganglia
• The subthalamic nucleus also receives excitatory input from the cerebral cortex, and it sends
excitatory input to the GPi.
• Direct Pathway (in Basal Ganglia)

• the pathway that includes the caudate nucleus and putamen, the internal division of the
globus pallidus, and the ventral anterior/ventrolateral thalamic nuclei; has an excitatory
effect on movement

The Basal Ganglia
• The pathway shown in solid lines that includes the GPi is known as the direct pathway.
• Neurons in GPi sends inhibitory axons to the ventral anterior and ventrolateral thalamus
(VA/VL thalamus), which send excitatory projections to the motor cortex.
• The net effect of the loop is excitatory because it contains two inhibitory links. Each inhibitory
link (red arrow) reverses the sign of the input to that link.

The Basal Ganglia
• Thus, excitatory input to the caudate nucleus and putamen causes the these structures to
inhibit neurons in the Gpi.
• This inhibition removes the inhibitory effect of the connections between the GPi on the VA/VL
thalamus; in other words, neurons in the VA/VL thalamus become more excited.
• This excitation is passed on to the motor cortex, where it facilitates movements. (See Figure
8.23b.)

The Basal Ganglia
• The pathway shown in broken lines, which includes the GPe, is known as the indirect
pathway.
• Neurons in GPe send inhibitory input to the subthalamic nucleus, which sends excitatory input
to the GPi. From there on, the circuit is identical to the one we just examined—except that the
ultimate effect of this loop on the thalamus and frontal cortex is inhibitory.

The Basal Ganglia
• The globus pallidus also sends axons to various motor nuclei in the brain stem that contribute
to the ventromedial system. The effect of this pathway is to inhibit the motor cortex. (See
Figure 8.23b.)
• Indirect Pathway (in Basal Ganglia)

• the pathway that includes the caudate nucleus and putamen, the external division of the
globus pallidus, the subthalamic nucleus, the internal division of the globus pallidus, and
the ventral anterior/ventrolateral thalamic nuclei; has an inhibitory effect on movement

The Basal Ganglia
• A third pathway is known as the hyperdirect pathway (arrows with dotted lines).
• Neurons in the cerebral cortex send excitatory input to the subthalamic nucleus, which sends
excitatory input to the Gpi.
• As we just saw, the GPi has an inhibitory effect on the motor cortex, so the hyperdirect
pathway inhibits movements.

Parkinson’s Disease
• Now that you understand the roles played by the three cortical–basal ganglia loops, you can
understand the symptoms and treatment of two important neurological disorders: Parkinson’s
disease and Huntington’s disease.
• The primary symptoms of Parkinson’s disease are muscular rigidity, slowness of movement,
a resting tremor, and postural instability.

• Thus, a person with Parkinson’s disease cannot easily pace back and forth across a room.
• Reaching for an object can be accurate, but the movement usually begins only after a
considerable delay, and the individual components of the movement (a series of trunk, arm,
hand, and finger movements) are poorly coordinated (Poizner et al., 2000).

• Disruption of the normal functions of the basal ganglia means that people with Parkinson’s
disease have difficulty performing tasks automatically.
• As the disease progresses, they must “think through” actions that were previously automatic,
which means that the actions become slower and demand more brain resources for their
accomplishment.

• Parkinson’s disease also produces a resting tremor—vibratory movements of the arms and
hands that diminish somewhat when the individual makes purposeful movements. The tremor
is accompanied by rigidity; the joints appear stiff.
• However, the tremor and rigidity are not the cause of the slow movements. In fact, some
patients with Parkinson’s disease show extreme slowness of movements but little or no
tremor.

• Normal movements require an appropriate balance between the direct (excitatory) and
indirect (inhibitory) pathways.
• The caudate nucleus and putamen consist of two different zones, both of which receive input
from dopaminergic neurons of the substantia nigra.
• One of these zones contains D1 dopamine receptors, which produce excitatory effects.
Neurons in this zone send their axons to the GPi.

• Neurons in the other zone contain D2 receptors, which produce inhibitory effects. These
neurons send their axons to the GPe. (See Figure 8.23b.)
• The first of these circuits, beginning with the black arrow from the substantia nigra, goes
through two inhibitory synapses (red arrows) before it reaches the VA/VL thalamus; thus, this
circuit has an excitatory effect on behavior.

• The second of these circuits begins with an inhibitory input to the caudate nucleus and
putamen, but it goes through four inhibitory synapses in the following pathway: substantia
nigra  caudate/putamen  GPe  subthalamic nucleus  GPi  VA/VL thalamus.
• Thus, the effect of this pathway, too, is excitatory; thus, dopaminergic input to the caudate
nucleus and putamen facilitate movements.
• Note that the GPi also sends axons to the ventromedial system.
• A decrease in this inhibitory output is probably responsible for the muscular rigidity and poor
control of posture seen in Parkinson’s disease. (See Figure 8.23b.)

• As we saw in Chapter 4, the standard treatment for Parkinson’s disease is L-DOPA, the
precursor of dopamine.
• When an increased amount of L-DOPA is present, the remaining nigrostriatal dopaminergic

neurons in a patient with Parkinson’s disease will produce and release more dopamine.

• But this compensation often produces dyskinesias and dystonias—involuntary movements

and postures that are presumably caused by too much stimulation of dopamine receptors in
the basal ganglia.
• In addition, L-DOPA does not work indefinitely; eventually, the number of nigrostriatal
dopaminergic neurons declines to such a low level that the symptoms become worse.
• Some patients—especially those whose symptoms began when they were relatively young—
eventually become bedridden, scarcely able to move.

• In recent years, clinicians have worked on developing new ways to treat Parkinson’s disease,
including stereotaxic surgery and implantation of stimulating electrodes in various regions of
the basal ganglia.
• In addition, much research has been done on discovering the causes of the disease.

Huntington’s Disease
• Another basal ganglia disease, Huntington’s disease, is caused by degeneration of the

caudate nucleus and putamen, especially of GABAergic and acetylcholinergic neurons. (See
Figure 8.24.)
• Whereas Parkinson’s disease causes a poverty of movements, Huntington’s disease,

formerly called Huntington’s chorea, causes uncontrollable ones, especially jerky limb
movements.

• (The term chorea derives from the Greek khoros, meaning “dance.”)
• The movements of Huntington’s disease look like fragments of purposeful movements, but
occur involuntarily. This disease is progressive and eventually causes death.
• Huntington’s Disease
• a fatal inherited disorder that causes degeneration of the caudate nucleus and putamen;
characterized by uncontrollable jerking movements, writhing movements, and dementia


160
• The symptoms of Huntington’s disease usually begin in the patient’s thirties or forties, but can
sometimes begin in the early twenties.
• The first signs of neural degeneration occur in the caudate nucleus and the putamen—
specifically, in the medium-sized spiny inhibitory neurons whose axons travel to the external
division of the globus pallidus.

• The loss of inhibition provided by these GABA-secreting neurons increases the activity of the
GPe, which then inhibits the subthalamic nucleus.
• As a consequence, the activity level of the GPi decreases, and excessive movements occur.
(Refer to Figure 8.23b.) As the disease progresses, the caudate nucleus and putamen
degenerate until almost all of their neurons disappear.
• The patient dies from complications of immobility. Unfortunately, there is at present no

effective treatment for this disorder.

• Huntington’s disease is a hereditary disorder, caused by a dominant gene on chromosome 4.
• In fact, the gene has been located, and its defect has been identified as a repeated
sequence of bases that code for the amino acid glutamine (Collaborative Research Group,
1993).

The Cerebellum
• The cerebellum is an important part of the motor system. It contains about 50 billion neurons,
compared to the approximately 22 billion neurons in the cerebral cortex (Robinson, 1995).
• Its outputs project to every major motor structure of the brain.
• When it is damaged, people’s movements become jerky, erratic, and uncoordinated.

The Cerebellum
• The cerebellum consists of two hemispheres that contain several deep nuclei situated
beneath the wrinkled and folded cerebellar cortex.
• Thus, the cerebellum resembles the cerebrum in miniature.

The Cerebellum
• The medial part of the cerebellum is phylogenetically older than the lateral part, and it
participates in control of the ventromedial system.
• The flocculonodular lobe, located at the caudal end of the cerebellum, receives input from the
vestibular system and projects axons to the vestibular nucleus.
• Flocculonodular Lobe
• a region of the cerebellum; involved in control of postural reflexes

The Cerebellum
• You will not be surprised to learn that this system is involved in postural reflexes. (See the
green lines in Figure 8.25.)
• The vermis (“worm”), located on the midline, receives auditory and visual information from the
tectum and cutaneous and kinesthetic information from the spinal cord.
• Vermis
• the portion of the cerebellum located at the midline; receives somatosensory information
and helps to control the vestibulospinal and reticulospinal tracts through its connections
with the fastigial nucleus

The Cerebellum
• Neurons in the fastigial nucleus send axons to the vestibular nucleus and to motor nuclei in
the reticular formation.
• Thus, these neurons influence behavior through the vestibulospinal and reticulospinal tracts,
two of the three ventromedial pathways. (See the blue lines in Figure 8.25.)
• Fastigial Nucleus
• a deep cerebellar nucleus; involved in the control of movement by the reticulospinal and
vestibulospinal tracts

The Cerebellum
• The rest of the cerebellar cortex receives most of its input from the cerebral cortex, including
the primary motor cortex and association cortex.
• This input is relayed to the cerebellar cortex through the pontine tegmental reticular nucleus.

The Cerebellum
• The intermediate zone of the cerebellar cortex projects to the interposed nuclei, which in turn
project to the red nucleus.
• Thus, the intermediate zone influences the control of the rubrospinal system over movements
of the arms and legs.
• The interposed nuclei also send outputs to the ventrolateral thalamic nucleus, which projects
to the motor cortex. (See the red lines in Figure 8.25.)
• Interposed Nuclei
• a set of deep cerebellar nuclei; involved in the control of the rubrospinal system


171
The Cerebellum
• Both the frontal association cortex and the primary motor cortex send information about
intended movements to the lateral zone of the cerebellum via the pontine nucleus.
• The lateral zone also receives information from the somatosensory system, which informs it
about the current position and rate of movement of the limbs—information that is necessary
for computing the details of a movement.
• Pontine Nucleus
• a large nucleus in the pons that serves as an important source of input to the cerebellum

The Cerebellum
• When the cerebellum receives information that the motor cortex has begun to initiate a
movement, it computes the contribution that various muscles will have to make to perform
that movement.
• The results of this computation are sent to the dentate nucleus, another of the deep
cerebellar nuclei. Neurons in the dentate nucleus pass the information on to the ventrolateral
thalamus, which projects to the primary motor cortex.
• Dentate Nucleus
• a deep cerebellar nucleus; involved in the control of rapid, skilled movements by the
corticospinal and rubrospinal systems

The Cerebellum
• The projection from the ventrolateral thalamus to the primary motor cortex enables the
cerebellum to modify the ongoing movement that was initiated by the frontal cortex.
• The lateral zone of the cerebellum also sends efferents to the red nucleus (again, via the
dentate nucleus); thus, it helps to control independent limb movements through this system
as well. (See Figure 8.26.)


175
The Reticular Formation
• The reticular formation consists of a large number of nuclei located in the core of the medulla,
pons, and midbrain.
• The reticular formation controls the activity of the gamma motor system and hence regulates
muscle tonus. In addition, the pons and medulla contain several nuclei with specific motor
functions.

The Reticular Formation
• The reticular formation also plays a role in locomotion.
• Stimulation of the mesencephalic locomotor region, located ventral to the inferior colliculus,
causes a cat to make pacing movements (Shik and Orlovsky, 1976).
• The mesencephalic locomotor region does not send fibers directly to the spinal cord, but
apparently controls the activity of reticulospinal tract neurons.
• Mesencephalic Locomotor Region

• a region of the reticular formation of the midbrain whose stimulation causes alternating
movements of the limbs normally seen during locomotion

Section Summary
• The motor systems of the brain are complex.
• The rapid movement of your head and eyes is controlled by mechanisms that involve the
superior colliculi and nearby nuclei.
• The head movement and corresponding movement of the trunk are mediated by the
tectospinal tract.

Section Summary
• Even before your hand moves, the ventral corticospinal tract and the ventromedial pathways
(vestibulospinal and reticulospinal system, largely under the influence of the basal ganglia)
begin adjusting your posture so that you will not fall forward when you suddenly reach in front
of you.
• The corticobulbar pathway, under the control of speech mechanisms in the left hemisphere,
causes the muscles of your vocal apparatus to speak.

Section Summary
• The supplementary motor area (SMA) and the premotor cortex receive information from the
parietal lobe and help to initiate movements through their connections with the primary motor
cortex.
• The SMA is involved in well-learned behavioral sequences.
• Neurons there fire at particular points in behavioral sequences, and disruption or damage
impairs the ability to perform these sequences.
• The pre-SMA is involved in awareness of our decisions to make spontaneous movements.

Section Summary
• The dorsal stream of your visual association cortex also contributes spatial information to the
parietal reaching region in your left hemisphere, which calculates the reaching movement you
must make and transmits this information to the motor association cortex in your left frontal
lobe.
• The muscles of your arm and hand are controlled through a cooperation between the
corticospinal, rubrospinal, and ventromedial pathways.
• Even before your hand moves, the ventral corticospinal tract and the ventromedial pathways
(vestibulospinal and reticulospinal system, largely under the influence of the basal ganglia)
begin adjusting your posture so that you will not fall forward when you suddenly reach in front
of you.

Section Summary
• The premotor cortex is involved in learning and executing complex movements that are
guided by arbitrary sensory information, such as verbal instructions.
• This region and the inferior parietal lobule constitute a mirror neuron system that plays an
important role in imitation and understanding the actions and intentions of others.

Section Summary
• A person with apraxia will have difficulty making controlled movements of the limb in
response to a verbal request or an attempt to imitate another person’s action.
• Most cases of apraxia are produced by lesions of the left frontal or parietal cortex.
• The left parietal cortex directly controls movement of the right limb by activating neurons in
the left primary motor cortex and indirectly controls movement of the left limb by sending
information to the right frontal association cortex.

Section Summary
• The basal ganglia are part of a circuit that includes the cerebral cortex, the subthalamic
nucleus, thalamic motor nuclei, and the substantia nigra.
• The direct pathway is involved in excitation of cortical mechanisms of motor control, and the
indirect and hyperdirect pathways are involved in the inhibition of these mechanisms.
• Parkinson’s disease is caused by degeneration of dopamine-secreting neurons of the

substantia nigra that send axons to the basal ganglia.
• An important symptom of this disorder is disruption of automatic behaviors.

Section Summary
• Huntington’s disease—a fatal disease caused by a mutation that causes production of

abnormal huntingtin protein—causes degeneration of the caudate nucleus and putamen.
• Although identification of the faulty protein provides hope for understanding the causes of the
neural degeneration, there is still no treatment for this disorder.

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• one of the striated muscles attached to bones

3 COPYRIGHT © ALLYN & BACON 2012

• Contraction of a flexor muscle produces flexion, the drawing in of a limb.

• Extension, which is the opposite movement, is produced by contraction of extensor muscles.

• Muscles contract; limbs flex.

4 COPYRIGHT © ALLYN & BACON 2012

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• The detailed structure of a skeletal muscle is shown in Figure 8.1.

6 COPYRIGHT © ALLYN & BACON 2012

• Extrafusal Muscle Fiber

• Alpha Motor Neuron

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• Intrafusal Muscle Fiber

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• Gamma Motor Neuron

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• This action potential induces a contraction, or twitch, of the muscle fiber.

14 COPYRIGHT © ALLYN & BACON 2012

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• This event triggers the contraction.

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• Thus, the cross bridges “row” along the actin filaments.

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• Golgi Tendon Organ

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• When an action potential—initiated by the synapse at the motor endplate—causes calcium

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• These reflexes constitute the simplest level of motor integration.

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• Figure 8.5 shows the effects of placing a weight in a person’s hand.

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• Monosynaptic Stretch Reflex

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• Now consider a useful function this reflex performs.

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• All others are polysynaptic.

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