Dopaminergic mediation of beta-endorphin-induced catalepsy.
Acute intracisternal administration of human beta-endorphin produced catalepsy and increased striatal concentrations of 3,4-dihydroxyphenylacetic acid (DOPA) and homovanillic acid (HVA). All of these effects were blocked by naloxone. Apomorphine, a dopamine receptor antagonist, also prevented beta-endorphin-induced catalepsy and the increase in striatal DOPAC and HVA. The combination of subcataleptic doses of haloperidol and beta-endorphin produced catalepsy and large increases in striatal DOPAC and HVA. These data provide evidence for a role for nigrostriatal dopamine neurons in beta-endorphin-induced catalepsy. The apparent increase in striatal dopamine turnover following beta-endorphin administration may be compensatory.
D015102:3,4-Dihydroxyphenylacetic Acid / Q000032:analysis; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001923:Brain Chemistry / Q000187:drug effects; D002375:Catalepsy / Q000139:chemically induced*; D003342:Corpus Striatum / Q000187:drug effects* / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism*; D004357:Drug Synergism; D004723:Endorphins / Q000037:antagonists & inhibitors*; D006220:Haloperidol / Q000494:pharmacology*; D006801:Humans; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D051381:Rats
D004723:Endorphins; D015102:3,4-Dihydroxyphenylacetic Acid; D009270:Naloxone; D006220:Haloperidol; D001058:Apomorphine; D004298:Dopamine