Abstract

The basal ganglia are nodal points in corticobasal ganglia circuits that have been implicated in a range of cognitive and motor disorders (1–4). In normal individuals, the basal ganglia may be essential to the development of the kinds of automatic or semiautomatic behaviors that underlie habits in everyday life (5–9). There is no definitive link yet between normal habits and the symptomatology present in the particular clinical disorders attributable to basal ganglia dysfunction. But there is great interest in the possibility that the neural mechanisms that make the habit learning possible are malfunctional in basal ganglia disorders. At the heart of this view is the idea that in order to form a habit, it may be necessary to “chunk” together movements, complex acts or sequences, or cognitive acts by means of developing novel neural firing patterns that represent the entire action sequences or that, at minimum, release the action sequences when triggered by an external or internal stimulus (10). Current electrophysiological evidence suggests that much of the temporal and spatial organization of behavioral sequences is built up in the neocortex, especially in the regions of the frontal and prefrontal cortex, including the supplementary motor areas (11,12). Yet, there is strong experimental evidence that neurons in the basal ganglia also become active preferentially in relation to sequences of movements (13–18). There are massive inputs to the basal ganglia from the frontal cortex, so that much of the neuronal activity in the basal ganglia may depend on the neocortex for its patterning. However, because corticobasal ganglia circuits lead from large parts of the cerebral cortex through basal ganglia nuclei to the frontal cortex, the basal ganglia may actually be important for the development of sequence representation in the frontal cortex.

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