Abstract
The striatum receives inputs from all areas of the cerebral cortex and also from the intralaminar nucleus of the thalamus. These inputs are considered to be excitatory, probably utilising glutamate as the neurotransmitter (Fonnum et al., 1981; McGeer et al., 1977). Indeed, stimulation of the corticostriatal pathway evokes fast excitatory postsy-naptic potentials (EPSPs) in the striatal output neurones (medium spiny neurones, MSNs) which are inhibited by antagonists of ionotropic glutamate receptors (iGluRs; Cherubini et al., 1988). The regulation of MSN activity is crucial to the functioning of the basal ganglia, indeed, overactivity MSNs may contribute to dysfunctioning of the output regions of the basal ganglia seen in Parkinson’s disease (Albin, 1991; Mitchell et al., 1989). Overactivity of glutamatergic inputs may also play a role in the pathophysiology of Huntington’s disease where there is degeneration of striatal neurones (Vonsattel et al., 1985). This idea is based partly on the fact that the pathology of Huntington’s disease can be closely mimicked in rats by intrastriatal injections of the iGluR agonist quinolinate (Beal et al., 1991).
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East, S.J., Brotchie, J.M. (1996). Modulation of Glutamatergic Transmission in the Striatum by Metabotropic Glutamate Receptors. In: Ohye, C., Kimura, M., McKenzie, J.S. (eds) The Basal Ganglia V. Advances in Behavioral Biology, vol 47. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0194-1_20
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