Inhibitory effect of dopamine on acetylcholine release from caudate nucleus.
It has been shown that dopamine inhibits the release of acetylcholine (ACh) from nerve terminals of caudate cholinergic interneurons, and the imbalance between dopaminergic and cholinergic system by 6-hydroxydopamine pretreatment leads to an increased ACh release. The Parkinson-syndrome induced by drugs which depress dopaminergic function either by reducing the output of dopamine, such as reserpine, or by antagonizing its action on DA receptors, as for instance haloperidol or chlorpromazine, can be attributed to the augmented release of ACh from caudate cholinergic nerve terminals and a consequent increase of cholinergic outflow from caudate nucleus. However, athetoid and choreiform hyperkinesis in patients and hypermotility in animals might result from increased dopaminergic outflow of nigro-striatal pathway and a consequent reduction in cholinergic neurosecretion of caudate nucleus.
D000109:Acetylcholine / Q000037:antagonists & inhibitors*; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001479:Basal Ganglia / Q000187:drug effects; D002415:Cats; D002421:Caudate Nucleus / Q000187:drug effects*; D004298:Dopamine / Q000494:pharmacology*; D005246:Feedback; D005260:Female; D006168:Guinea Pigs; D006220:Haloperidol / Q000494:pharmacology; D008297:Male; D008954:Models, Biological; D009489:Neurosecretion / Q000187:drug effects; D051381:Rats; D011954:Receptors, Dopamine / Q000187:drug effects
D011954:Receptors, Dopamine; D006220:Haloperidol; D001058:Apomorphine; D000109:Acetylcholine; D004298:Dopamine