Abstract
Current models of basal ganglia dysfunction in Parkinson’s disease (PD) attribute the motor disturbances largely to hyperactivity of the internal segment of the globus pallidus (GPi) (Delong, 1990; Alexander and Crutcher, 1991). Since the GPi neurons are inhibitory, their hyperactivity is believed to produce excessive inhibition of the GPi target neurons in the motor thalamus. This in turn reduces the activity of the cortical targets of these neurons, thereby depressing motor performance and giving rise to akinesia and bradykinesia, and possibly to tremor. When thalamic neurons are hyperpolarized, as occurs during sleep, their firing pattern is dramatically altered into a bursting pattern, consisting of bursts with a very characteristic intraburst firing pattern caused by a low threshold calcium spike (Steriade et al., 1997). It is possible that in PD the increased inhibition in thalamus resulting from the GABAergic inputs from GPi could lead to such bursting, and it has been proposed that such activity may lead to the generation of tremor (Pare et al., 1990).
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Dostrovsky, J.O., Molnar, G.F., Pilliar, A., Hutchison, W.D., Davis, K.D., Lozano, A.M. (2001). Neuronal Activity in Motor Thalamus of Parkinson’s Disease Patients. 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_23
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DOI: https://doi.org/10.1007/978-1-4615-1235-6_23
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