Abstract
The striatum is composed principally of GABAergic, medium spiny striatal projection neurons (MSNs) that can be categorized based on their gene expression, electrophysiological profiles, and input–output circuits. Major subdivisions of MSN populations include (1) those in ventromedial and dorsolateral striatal regions, (2) those giving rise to the direct and indirect pathways, and (3) those that lie in the striosome and matrix compartments. The first two classificatory schemes have enabled advances in understanding of how basal ganglia circuits contribute to disease. However, despite the large number of molecules that are differentially expressed in the striosomes or the extra-striosomal matrix, and the evidence that these compartments have different input–output connections, our understanding of how this compartmentalization contributes to striatal function is still not clear. A broad view is that the matrix contains the direct and indirect pathway MSNs that form parts of sensorimotor and associative circuits, whereas striosomes contain MSNs that receive input from parts of limbic cortex and project directly or indirectly to the dopamine-containing neurons of the substantia nigra, pars compacta. Striosomes are widely distributed within the striatum and are thought to exert global, as well as local, influences on striatal processing by exchanging information with the surrounding matrix, including through interneurons that send processes into both compartments. It has been suggested that striosomes exert and maintain limbic control over behaviors driven by surrounding sensorimotor and associative parts of the striatal matrix. Consistent with this possibility, imbalances between striosome and matrix functions have been reported in relation to neurological disorders, including Huntington’s disease, L-DOPA-induced dyskinesias, dystonia, and drug addiction. Here, we consider how signaling imbalances between the striosomes and matrix might relate to symptomatology in these disorders.
Highlights
The striatum is the primary input side of the basal ganglia, a set of subcortical brain regions that are important for the control of voluntary movement and our ability to learn patterns of behavior that maximize reward
Striosomes are heavily innervated by limbic cortices, which may be related to the preferential degeneration of striosomes and cingulate cortex in individuals with mood disorders associated with Huntington’s disease (HD)
Evidence for imbalance between striosome and matrix functions in Parkinson’s disease (PD) is primarily associated with l-DOPA treatment that can produce dyskinesias
Summary
The striatum is the primary input side of the basal ganglia, a set of subcortical brain regions that are important for the control of voluntary movement and our ability to learn patterns of behavior that maximize reward. Considering its key function in reward-based learning, it is no surprise that the striatum is implicated in a wide variety of behaviors This breadth of function is strikingly exhibited in the range of clinical disorders for which abnormal functioning of the striatum has been found, including classical motor disorders: Parkinson’s disease (PD), Huntington’s disease (HD), and dystonia, and habit formation and drug addiction, impulsivity and attention-deficit hyperactivity disorder (ADHD), compulsivity and obsessive compulsive disorder, emotional control, and depression (for review, see Graybiel and Mink, 2009). Medium spiny striatal projection neurons (MSNs) that are part of a circuit that promotes movement express the Drd (D1) dopamine receptor, which boosts MSN cell excitability. MSNs that are part of a circuit that suppresses movement express the Drd (D2) dopamine receptor, which diminishes excitability of this MSN
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