Abstract

Pharmacological manipulations of brain dopamine (DA) systems modify motor behavior. Current models of basal ganglia function predict that dopamine agonist-induced motor activation, such as rotation or stereotypic behavior, is mediated by decreases in activity in the output nuclei of the basal ganglia, the substantia nigra pars reticulata (SNPR) and entopeduncular nucleus (EPN), brought about by activation of striatal DA receptors. These decreases in activity are thought to lead to disinhibition in motor thalamocortical and tectofugal circuits. Electrophysiology has provided some support for these models: in animals with nigrostriatal lesions, the D1/D2 agonist apomorphine or high doses of the partial D1 agonist SKF 38393 cause decreases in firing rate in most neurons of the SNPR19,20 or the primate homolog of the EPN.3 KeywordsFiring RateRotational BehaviorAverage Firing RateOutput NucleusEntopeduncular NucleusThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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