Human Physiology, 14th edition (2016)

216 Chapter 8

be discussed shortly) send GABA-releasing inhibitory axons to

the thalamus. The thalamus, in turn, sends excitatory axons

to the motor areas of the cerebral cortex, thereby completing

a motor circuit ( fig.  8.12 ). The motor circuit allows intended

movements to occur while inhibiting unintended movements.

The subthalamic nucleus of the diencephalon and the sub-

stantia nigra of the midbrain are often included among the

basal nuclei. The substantia nigra is particularly noteworthy

because degeneration of dopaminergic (dopamine-releasing)

neurons that project from the substantia nigra to the corpus

striatum—the nigrostriatal tract —causes Parkinson’s disease.

Cerebral Lateralization

By way of motor fibers originating in the precentral gyrus,

each cerebral cortex controls movements of the contralateral

(opposite) side of the body. At the same time, somatesthetic

sensation from each side of the body projects to the contralat-

eral postcentral gyrus as a result of decussation (crossing over)

of fibers. In a similar manner, images falling in the left half of

each retina project to the right occipital lobe, and images in the

right half of each retina project to the left occipital lobe. Each

cerebral hemisphere, however, receives information from both

sides of the body because the two hemispheres communicate

with each other via the corpus callosum, a large tract com-

posed of about 200 million fibers.

The corpus callosum has been surgically cut in some people

with severe epilepsy as a way of alleviating their symptoms. These

split-brain procedures isolate each hemisphere from the other,

but, surprisingly, to a casual observer split-brain patients do not

show evidence of disability as a result of the surgery. However,

in specially designed experiments in which each hemisphere is

CLINICAL APPLICATION

Dyskinesia refers to involuntary movements, which can occur

as a side effect of certain drugs or as a symptom of some

neurodegenerative diseases. For example, chorea —rapid

involuntary movements of the limbs or writhing movements—

is characteristic of Huntington’s disease. As described

in chapter 3, Huntington’s disease is caused by a mutation

involving extensive CAG repeats that is inherited as an auto-

somal dominant trait. In addition to chorea, Huntington’s

disease is accompanied by a decline in mental function and

progressively serious psychiatric conditions. There is degen-

eration of the caudate nucleus, and evidence suggests a lack

of new neurons in the striatum that are derived from neural

stem cells near the lateral ventricles.

In addition to dyskinesia, Parkinson’s disease symptoms

include muscle tremor, slow movements, speech impairments,

and muscle rigidity. These symptoms are produced by the

degeneration of dopaminergic neurons that extend to the cau-

date nucleus from the substantia nigra, a small nucleus in the

midbrain. The causes of Parkinson’s disease are poorly under-

stood; however, scientists have discovered that affected neu-

rons produce proteins called a -synuclein, which stick together

to form tiny fibrils of Lewy bodies that appear to promote

neurodegeneration. As discussed in chapter 7, Parkinson’s

disease is treated with L-dopa (also called Levodopa ), which

can enter the brain and be converted into the neurotransmitter

dopamine, as well as with other drugs that act as dopamine

agonists and MAO inhibitors (chapter 7, section 7.5). Some

Parkinson’s disease patients benefit from deep brain stimu-

lation, where an electrode is implanted into the subthalamic

nucleus or globus pallidus.

Caudate

Putamen

Globus pallidus

Thalamus

Glutamate neurotransmitter

(excitatory)

Dopamine neurotransmitter

(excitatory)

GABA neurotransmitter

(inhibitory)

Subthalamic

nucleus

Substantia nigra

Figure 8.12 The motor
circuit. The motor circuit is formed by
interconnections between motor areas of
the cerebral cortex, the basal nuclei (basal
ganglia), and other brain regions. Note the
extensive inhibitory, GABA-ergic effects
(shown in red) made by the globus pallidus
on other structures of this circuit. The
excitatory neurotransmitters of this circuit
are glutamate (green) and dopamine (blue).