Evidence for a cholinergic role in haloperidol-induced catalepsy.
Experiments in mice tested previous evidence that activation of cholinergic systems promotes catalepsy and that cholinergic mechanisms need to be intact for full expression of neuroleptic-induced catalepsy. Large doses of the cholinomimetic, pilocarpine, could induce catalepsy when peripheral cholinergic receptors were blocked. Low doses of pilocarpine caused a pronounced enhancement of the catalepsy that was induced by the dopaminergic blocker, haloperidol. A muscarinic receptor blocker, atropine, disrupted haloperidol-induced catalepsy. Intracranial injection of an acetylcholine-synthesis inhibitor, hemicholinium, prevented the catalepsy that is usually induced by haloperidol. These findings suggest the hypothesis that the catalepsy that is produced by neuroleptics such as haloperidol is actually mediated by intrinsic central cholinergic systems. Alternatively, activation of central cholinergic systems could promote catalepsy by suppression of dopaminergic systems.
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001921:Brain / Q000187:drug effects*; D002375:Catalepsy / Q000139:chemically induced*; D002799:Cholinergic Fibers / Q000187:drug effects; D004357:Drug Synergism; D006220:Haloperidol / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D006426:Hemicholinium 3 / Q000494:pharmacology; D006801:Humans; D008297:Male; D008464:Mecamylamine / Q000494:pharmacology; D051379:Mice; D010862:Pilocarpine / Q000494:pharmacology
D010862:Pilocarpine; D006426:Hemicholinium 3; D008464:Mecamylamine; D001285:Atropine; D006220:Haloperidol