Inhibition of apomorphine-induced hypermotility in rats by chlorpromazine, perphenazine, thioridazine and melperone.
Hypermotility in rats produced by various subcutaneous doses of apomorphine (ap) was studied. The neuroleptics chlorpromazine, perphenazine, thioridazine and melperone were administered subcutaneously 30 minutes before ap. The four neuroleptics were found to inhibit ap-induced hypermotility. When the dose of ap was increased, higher doses of the neuroleptics were required to inhibit the hypermotility. By varying the dose of chlorpromazine, thioridazine and melperone partial ap-antagonism was found, but increase of the perphenazine-dose resulted in complete ap-inhibition. Hypermotility produced by ap is presumably dependent on direct stimulation of dopamine (DA)-receptors. Neuroleptics blocking some, but not all, DA-receptors may cause no, or weak parkinsonian side effects.
D000818:Animals; D001058:Apomorphine / Q000008:administration & dosage / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D002090:Butyrophenones / Q000008:administration & dosage / Q000494:pharmacology*; D002746:Chlorpromazine / Q000008:administration & dosage / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D007279:Injections, Subcutaneous; D009043:Motor Activity / Q000187:drug effects*; D010546:Perphenazine / Q000008:administration & dosage / Q000494:pharmacology*; D051381:Rats; D013881:Thioridazine / Q000008:administration & dosage / Q000494:pharmacology*; D013997:Time Factors
D002090:Butyrophenones; D010546:Perphenazine; D001058:Apomorphine; D013881:Thioridazine; D002746:Chlorpromazine