BASIC BASAL GANGLIA CIRCUITRY AND NEUROTRANSMITTERS

Radiographic anatomy
The basal ganglia (caudate nucleus, putamen, and globus pallidus) form characteristic
anatomical relationships with the internal capsule. The head and body of the caudate
nucleus are found medial to the anterior limb; the thalamus is found medial to the
posterior limb; and the globus pallidus and putamen are found lateral to the anterior and
posterior limbs.

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Clinical Anatomy
Basal ganglia disorders are characterized by movement disorders, although emotional
and cognitive symptoms also are seen. Some movement disorders involve actual
degeneration of basal ganglia and related structures; these disorders include
Huntingtons chorea and degeneration of the head of the caudate nucleus as well as
Parkinsons disease and degeneration of the dopaminergic pars compacta of the
substantia nigra.

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CLINICAL POINT
The basal ganglia assist the cerebral cortex in planning and generating desired
programs of activity and suppressing undesired programs of activity. The most
conspicuous arena in which these functions are observed is motor activity. Basal
ganglia disorders produce movement problems that are often involuntary in nature and
are commonly accompanied by cognitive and affective symptoms (e.g., Huntingtons
disease). The principal route of information flow from the basal ganglia is from the
thalamus and cerebral cortex to the striatum (caudate nucleus and putamen), then to
the globus pallidus, then back to the thalamus and cortex, completing the loop.
Disruption of this loop can produce excessive movements (e.g., choreiform and athetoid
movements, tremor) or diminished movements (bradykinesia).
DOPAMINERGIC PATHWAYS
DA neurons are found in the midbrain and hypothalamus. In the midbrain, neurons in
the substantia nigra pars compacta (A9) project axons (along the nigrostriatal pathway)
mainly to the striatum (caudate nucleus and putamen) and to the globus pallidus and
subthalamus. This nigrostriatal projection is involved in basal ganglia circuitry that aids
in the planning and execution of cortical activities, the most conspicuous of which
involve the motor system. Damage to the nigrostriatal system results in Parkinsons
disease, a disease characterized by resting tremor, muscular rigidity, bradykinesia
(difficulty initiating movements or stopping them once they are initiated), and postural
deficits. The antiparkinsonian drugs such as levodopa target this system and its
receptors.

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BASIC BASAL GANGLIA CIRCUITRY AND NEUROTRANSMITTERS

Inputs from the cerebral cortex and thalamus to the striatum are excitatory (glutamate).
The striatopallidal connection is inhibitory (GABA), and the pallidothalamic connection is
inhibitory (GABA) too, resulting in a net drive over the thalamocortical (and resultant
corticospinal) output. However, extensive inhibitory and excitatory circuitry also exists
through the internal segment of the globus pallidus, the substantia nigra, and the
subthalamic nucleus, producing complex modulation of basal ganglia output. The
dopaminergic nigrostriatal connections can exert both inhibitory and excitatory effects
on the striatum. Thus, with loss of nigrostriatal dopamine axons in Parkinsons disease,
both negative symptoms (bradykinesia) and positive symptoms (resting tremor,
muscular rigidity, and postural instability) exist side by side. Additional interneurons are
found in some basal ganglia structures such as the excitatory cholinergic
interneurons in the striatum.

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END
-----------------------------------------------Source: Extracts modified from: Felten, D L. Netter's Atlas of Neuroscience, Second Ed.
Sanders, 2010
Companion Cases: Parkinsonism, Parkinsons disease, and Huntington's disease.
Inside Brown TA, Shah SJ.Neurology. Case 17-2 and Case 17-3. Pgs. 528-34. USMLE
Step 1 Secrets, 3rd ed. Sanders 2013

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