Dopaminergic mediation of beta-endorphin-induced prolactin secretion.
Intracisternal administration of synthetic human beta-endorphin increases plasma praolactin concentration, and this effect is blocked by naloxone. Drugs which stimulate dopamine receptors (apomorphine or bromocriptine) or increase availability of dopamine (pargyline) inhibited the effect of beta-endorphin on plasma prolactin. Drugs which antagonize dopamine receptors (haloperidol) or decrease availability of dopamine (alpha-methyltyrosine) potentiated the effect of beta-endorphin on plasma prolactin. Some of these drugs act only in neurons and not in anterior pituitary, supporting a brain site of action for these drug interactions with beta-endorphin which altered prolactin secretion. These pharmacological studies provide support for a concept of dopaminergic mediation of beta-endorphin-induced prolactin secretion.
D000818:Animals; D004298:Dopamine / Q000502:physiology*; D004347:Drug Interactions; D004723:Endorphins / Q000494:pharmacology*; D007031:Hypothalamus / Q000378:metabolism; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D011388:Prolactin / Q000097:blood*; D051381:Rats; D011954:Receptors, Dopamine / Q000187:drug effects; D001615:beta-Endorphin
D004723:Endorphins; D011954:Receptors, Dopamine; D009270:Naloxone; D001615:beta-Endorphin; D011388:Prolactin; D004298:Dopamine