basal ganglia

The basal ganglia (or basal nuclei) comprise multiple subcortical nuclei, of varied origin, in the brains of vertebrates, which are situated at the base of the forebrain. Basal ganglia nuclei are strongly interconnected with the cerebral cortex, thalamus, andbrainstem, as well as several other brain areas. The basal ganglia are associated with a variety of functions including: control of voluntary motor movements, procedural learning, routine behaviors or “habits” such as bruxism, eye movements, cognition[1] and emotion.[2]

The main components of the basal ganglia – as defined functionally – are the dorsal striatum (caudate nucleus and putamen),ventral striatum (nucleus accumbens and olfactory tubercle), globus pallidus, ventral pallidum, substantia nigra, and subthalamic nucleus.[3] It is important to note, however, that the dorsal striatum and globus pallidus may be considered anatomically distinct from the substantia nigra, nucleus accumbens, and subthalamic nucleus. Each of these components has a complex internal anatomical and neurochemical organization. The largest component, the striatum (dorsal and ventral), receives input from many brain areas beyond the basal ganglia, but only sends output to other components of the basal ganglia. The pallidum receives input from the striatum, and sends inhibitory output to a number of motor-related areas. The substantia nigra is the source of the striatal input of the neurotransmitter dopamine, which plays an important role in basal ganglia function. The subthalamic nucleus receives input mainly from the striatum and cerebral cortex, and projects to the globus pallidus.

Currently, popular theories implicate the basal ganglia primarily in action selection; that is, it helps determine the decision of which of several possible behaviors to execute at any given time. In more specific terms, the basal ganglia’s primary function is likely to control and regulate activities of the motor and premotor cortical areas so that voluntary movements can be performed smoothly.[1][4]Experimental studies show that the basal ganglia exert an inhibitory influence on a number of motor systems, and that a release of this inhibition permits a motor system to become active. The “behavior switching” that takes place within the basal ganglia is influenced by signals from many parts of the brain, including the prefrontal cortex, which plays a key role in executive functions.[2][5]

The importance of these subcortical nuclei for normal brain function and behavior is emphasized by the numerous and diverse neurological conditions associated with basal ganglia dysfunction, which include: disorders of behavior control such as Tourette syndrome, hemiballismus, and obsessive–compulsive disorder; dystonia; addiction; and movement disorders, the most notable of which are Parkinson’s disease, which involves degeneration of the dopamine-producing cells in the substantia nigra pars compacta, and Huntington’s disease, which primarily involves damage to the striatum.[1][3] The basal ganglia have a limbic sector whose components are assigned distinct names: the nucleus accumbens, ventral pallidum, and ventral tegmental area (VTA). There is considerable evidence that this limbic part plays a central role in reward learning, particularly a pathway from the VTA to the nucleus accumbens that uses the neurotransmitter dopamine. A number of highly addictive drugs, including cocaine, amphetamine, andnicotine, are thought to work by increasing the efficacy of this dopamine signal. There is also evidence implicating overactivity of the VTA dopaminergic projection in schizophrenia.[6]

Although the role of the basal ganglia in motor control is clear, there are also many indications that it is involved in the control of behavior in a more fundamental way, at the level of motivation. In Parkinson’s disease, the ability to execute the components of movement is not greatly affected, but motivational factors such as hunger fail to cause movements to be initiated or switched at the proper times. The immobility of Parkinsonian patients has sometimes been described as a “paralysis of the will”.[11] These patients have occasionally been observed to show a phenomenon called kinesia paradoxica, in which a person who is otherwise immobile responds to an emergency in a coordinated and energetic way, then lapses back into immobility once the emergency has passed.

The role in motivation of the “limbic” part of the basal ganglia—the nucleus accumbens (NA), ventral pallidum, and ventral tegmental area (VTA)—is particularly well established. Thousands of experimental studies combine to demonstrate that the dopaminergic projection from the VTA to the NA plays a central role in the brain’s reward system. Animals with stimulating electrodes implanted along this pathway will bar-press very energetically if each press is followed by a brief pulse of electric current. Numerous things that people find rewarding, including addictive drugs, good-tasting food, and sex, have been shown to elicit activation of the VTA dopamine system. Damage to the NA or VTA can produce a state of profound torpor.

Although it is not universally accepted, some theorists have proposed a distinction between “appetitive” behaviors, which are initiated by the basal ganglia, and “consummatory” behaviors, which are not. For example, an animal with severe basal ganglia damage will not move toward food even if it is placed a few inches away, but, if the food is placed directly in the mouth, the animal will chew it and swallow it.


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