Cholinergic-dopaminergic interactions in experimental catalepsy.
The 'pinch-induced' model of catalepsy in the mouse was disrupted by atropine sulfate (4 mg/kg IP), confirming an earlier finding, and also by the antinicotinic mecamylamine (4 mg/kg). Either anticholinergic, when given concurrently with haloperidol (5 mg/kg), interfered with the typical haloperidol-induced enhancement of catalepsy. In mice pretreated with a peripheral cholinergic blocker, the cholinomimetic pilocarpine (10 mg/kg) enhanced catalepsy. The dopamine (DA) agonist apomorphine (5 mg/kg) reversed the enhancement that was normally caused by pilocarpine. Apomorphine did not stimulate open field locomotion in mice that were pretreated with pilocarpine. This lack of correlation between catalepsy and open field activity indicates that catalepsy in a unique state that involves more than mere absence of movement. The DA mechanisms, thus, appear to be specifically antagonistic to catalepsy or, conversely, cholinergic mediation of catalepsy involves reduced influence of DA systems.
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D002375:Catalepsy / Q000139:chemically induced / Q000503:physiopathology*; D004298:Dopamine / Q000502:physiology*; D004347:Drug Interactions; D006220:Haloperidol / Q000494:pharmacology; D006801:Humans; D008297:Male; D051379:Mice; D010275:Parasympathetic Nervous System / Q000503:physiopathology*; D010276:Parasympatholytics / Q000494:pharmacology; D010862:Pilocarpine / Q000494:pharmacology
D010276:Parasympatholytics; D010862:Pilocarpine; D006220:Haloperidol; D001058:Apomorphine; D004298:Dopamine