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Arcuate Nucleus and Preoptic Area Involvement in Beta‐Endorphin‐lnduced Release of Prolactin in Conscious Ovariectomized Rats †
Author(s) -
Voogt James L.,
Reseh Garth,
Turkington Susan
Publication year - 1989
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.1989.tb00146.x
Subject(s) - prolactin , medicine , endocrinology , ovariectomized rat , arcuate nucleus , (+) naloxone , preoptic area , opiate , chemistry , hypothalamus , perfusion , antagonist , receptor , hormone
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.