Abstract
Output from the basal ganglia reaches the cerebral cortex via the thalamus. In the primate, GABAergic axons from the internal pallidal segment (GPi) and the substantia nigra, pars reticulata (SNr) provide an inhibitory input to the ventral anterior (VA), oral, and some of the caudal portions of the ventrolateral (VLo and VLc), the ventromedial (VM), and to some extent, the dorsomedial (MD) thalamic nuclei (Sakai et al., 1996; Kultas-Ilinsky et al., 1997; Ilinsky et al., 1993; DeVito and Anderson, 1982). Changes in this inhibition are presumed to be major contributors to the symptoms of Parkinson’s disease (Hutchison et al., 1994; Wichmann et al., 1999), and several therapeutic interventions, such as pallidotomy or deep brain stimulation, are directly targeted at modification of pallidal output.
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Anderson, M.E., Ruffo, M., Buford, J.A., Inase, M. (2001). Pallidal and Cortical Determinants of Thalamic Activity. In: Kultas-Ilinsky, K., Ilinsky, I.A. (eds) Basal Ganglia and Thalamus in Health and Movement Disorders. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1235-6_8
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DOI: https://doi.org/10.1007/978-1-4615-1235-6_8
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