Endogenous opioids mediate ECS-induced catalepsy at supraspinal levels.
Several lines of evidence point to the involvement of endogenous opioids in the mediation of electroconvulsive shock (ECS)-induced catalepsy. Although the site of action of these agents has not yet been determined, the spinal cord has been a likely candidate. Using intrathecal and systemic administrations of morphine and naltrexone, the present experiments were designed to test this possibility directly. The data obtained were consistent with the involvement of endogenous opioids in mediating ECS-induced catalepsy, but it was clearly evident that the site of action of these agents was at supraspinal, not spinal levels.
D000818:Animals; D001921:Brain / Q000503:physiopathology*; D002375:Catalepsy / Q000209:etiology / Q000503:physiopathology*; D004597:Electroshock; D004723:Endorphins / Q000502:physiology*; D006801:Humans; D008297:Male; D009020:Morphine; D009271:Naltrexone; D051381:Rats; D011919:Rats, Inbred Strains; D011957:Receptors, Opioid / Q000502:physiology; D012640:Seizures / Q000503:physiopathology; D013116:Spinal Cord / Q000503:physiopathology*
D004723:Endorphins; D011957:Receptors, Opioid; D009271:Naltrexone; D009020:Morphine