Topical Review: Basal Ganglia: Functional Anatomy and Physiology. Part 1

Abstract

Advances in knowledge about basal ganglia structure and connectivity from 1925 to date are reviewed. Current concepts about neuronal populations, transmitters, and input and output of each of the basal ganglia nuclei are presented. The portrayal by Wilson, in 1925, of the striatum as a simple homogeneous structure has been replaced by the recognition, based on staining characteristics, connectivity, and function, that the neostriatum is compartmentalized into striosomes, matrisomes, and matrix compartments. Electrophysiologic studies have further shown the existence, in the neostriatum, of neuronal clusters that represent basic functional units much like the functional columns described much earlier for the cerebral cortex. Whereas the neostriatum is considered the major receiving area of the basal ganglia, the globus pallidus and substantia nigra pars reticulata constitute the major output nuclei. Combined neuroanatomic and neurophysiologic studies have revealed precise somatotopic organization throughout the basal ganglia system such that the leg, arm, and face areas of the cerebral cortex related to respective topographic areas within the striatum, pallidum, substantia nigra, and subthalamus. The previous concept of an inhibitory role for dopamine on striatal neurons has been modified. It is now acknowledged that dopamine exerts an inhibitory effect on striatal neurons that project to the external pallidum and a facilitatory effect on striatal neurons that project to the internal pallidum and substantia nigra pars reticulata. The previous concept of serial connectivity of the neostriatum (funnel concept) has been replaced by the concept of parallel connectivity. Within the internal connectivity of the basal ganglia, there is a fast system in which the neurotransmitter is γ aminobutyric acid (GABA) and a slow system modulated by neuropeptides. The slow system is believed to give identity to an otherwise homogenous GABAergic system. (J Child Neurol 1994;9:249-260).