Abstract
Lesion of the nigrostriatal dopaminergic pathway in the rat by 6-hydroxydopamine enhances the ability of pergolide to increase striatal acetylcholine levels and prevents the haloperidol-induced decrease in acetylcholine concentrations. This supersensitive response of striatal cholinergic cells is already maximal 6 days after lesion but tends to decrease thereafter. As the time course of the development of the supersensitivity of cholinergic cells differs from that of increased dopamine binding site density, the two are probably not causally related, the former reflecting rather a change occurring beyond the dopamine recognition site.
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