Arcuate Nucleus and Preoptic Area Involvement in Beta‐Endorphin‐lnduced Release of Prolactin in Conscious Ovariectomized Rats†

Abstract

Abstract The ability of ss-endorphin (ss-END) to release prolactin and the ability of naloxone to block prolactin's release when delivered to specific hypothalamic areas via push-pull perfusion was studied in unrestrained, conscious, Ovariectomized rats. Perfusion of either the arcuate nucleus or the preoptic area with ss-END for 15 to 30 min caused a large, brief increase in plasma prolactin levels. Perfusion for a longer time period (120 min) resulted in peak prolactin levels at 60 min, with a return to baseline by 120 min, suggesting that ss-END primarily acts to induce a sequence of events that culminates in prolactin release, but other factors are needed to maintain this release over long periods of time. Perfusion of the arcuate nucleus for two 15-min periods 90 min apart resulted in two surges of prolactin. When naloxone, the opiate receptor antagonist, was added to the perfusate, ss-END was not capable of stimulating prolactin release. These results provide a model to answer whether endogenous ss-END has a role in the neuroendocrine regulation of prolactin surges and what the location is of the opiate neurons involved in this neuronal pathway.