Stress-induced release of prolactin: blockade by dexamethasone and naloxone may indicate beta-endorphin mediation.
Basal levels of immunoreactive (ir) beta-endorphin, corticotropin (ACTH), and prolactin (PRL) in plasma of male rats decrease after dexamethasone pretreatment (400 microgram/kg at 24 hr and 200 microgram/kg at 2 hr before). Inescapable electric footshocks increase ir-beta-endorphin, ACTH, and PRL plasma levels and this effect is blocked by dexamethasone pretreatment. Morphine (20 mg/kg) also increases ir-beta-endorphin, ACTH, and PRL levels. Dexamethasone pretreatment blocks the morphine-induced release of ir-beta-endorphin but does not prevent the morphine-induced release of PRL. Naloxone, the opiate antagonist, decreases basal plasma levels of PRL and partially blocks the stress-induced increase of PRL, but it has no effect on the basal or stress-induced release of ir-beta-endorphin. These results are consistent with the proposal that beta-endorphin may interact with an opiate receptor involved in the regulation of PRL secretion.
D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000818:Animals; D003907:Dexamethasone / Q000494:pharmacology*; D004723:Endorphins / Q000378:metabolism*; D009020:Morphine / Q000494:pharmacology; D009270:Naloxone / Q000494:pharmacology*; D010902:Pituitary Gland / Q000378:metabolism; D011388:Prolactin / Q000378:metabolism*; D051381:Rats; D012636:Secretory Rate / Q000187:drug effects; D013312:Stress, Physiological / Q000503:physiopathology*
D004723:Endorphins; D009270:Naloxone; D009020:Morphine; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D011388:Prolactin