Abstract
The effect of dopamine on the K +-depolarized overflow of 3H-acetylcholine from rat striatal slices was investigated to determine whether drug-induced changes in neuronal sensitivity to dopamine might be manifested in changes in striatal cholinergic activity. Dopamine was found to produce a dose-dependent inhibition of the K +-evoked release of 3H-Ach. This inhibition could be blocked by prior exposure of the slices to haloperidol, a dopamine receptor blocker. Dopamine receptors localized on striatal cholinergic axon terminals and possibly postsynaptic dopamine receptors on cholinergic perikarya and dendrites may mediate the DA inhibition of 3H-Ach release induced by high K +. Chronic pretreatment with haloperidol followed by alpha-methyl-p-tyrosine resulted in a significant shift to the left in the dose-dependent inhibition of K +-stimulated overflow of 3H-Ach by dopamine. This shift to the left in the dose-response curve may be the result of an increase in the number of striatal dopamine receptors produced by chronic dopamine receptor blockade and inhibition of dopamine synthesis.
Published Version
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