Possible involvement of prostaglandins in cataleptic behavior in rats.
Involvement of prostaglandin (PG) in cataleptic behavior was investigated by a high bar test method in rats. PG F2 alpha (F2a) and E2 administered intracerebroventricularly (ICV) elicited cataleptic behavior in a dose-dependent manner. The cataleptic behaviors produced by PGs were markedly inhibited by ICV pretreatment with propranolol. The cataleptic behaviors induced by haloperidol were also inhibited by propranolol. The PG F2a- and haloperidol-induced cataleptic behaviors were almost abolished by the thermal coagulation of bilateral striatum where the dopaminergic and cholinergic link is found. The pilocarpine-induced cataleptic behavior was potentiated by ICV treatment with PG F2a. On the other hand, the cataleptic behavior elicited by haloperidol was reduced after oral treatment with aspirin, a PG synthesis inhibitor. These results suggest that PGs seem to be participated in incidence of cataleptic behavior, which might involve alteration of brain beta-adrenoceptor activity.
D000818:Animals; D001921:Brain / Q000187:drug effects*; D002375:Catalepsy / Q000139:chemically induced*; D015237:Dinoprost; D015232:Dinoprostone; D007276:Injections, Intraventricular; D008297:Male; D011433:Propranolol / Q000494:pharmacology; D011458:Prostaglandins E / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D011460:Prostaglandins F / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D011943:Receptors, Adrenergic, beta / Q000187:drug effects*
D011458:Prostaglandins E; D011460:Prostaglandins F; D011943:Receptors, Adrenergic, beta; D011433:Propranolol; D015237:Dinoprost; D015232:Dinoprostone