BETA-ENDORPHIN REGULATION OF LUTEINIZING-HORMONE-RELEASING HORMONE-RELEASE AT THE MEDIAN-EMINENCE IN EWES - IMMUNOCYTOCHEMICAL AND PHYSIOLOGICAL EVIDENCE

Beta-endorphin (beta-END) is an inhibitory factor in the neuroendocrin e control of luteinizing hormone (LH) release and thus, presumably als o of hypophysiotropic luteinizing hormone-releasing hormone (LHRH) rel ease. In order to address if the median eminence (ME) is a site of bet a-END action, we studied its functional role in ewes by assessing: (a) the hypothalamic distribution of beta-END using immunolabeling and by comparing this distribution with our data on the localization of LHRH ; (b) the ME in vivo release of LHRH and beta-END during the luteal (d ay 12) and the follicular (day 15) phases of the estrous cycle, (c) th e in vivo release of LHRH from the posterior-lateral ME, as assessed b y push-pull cannula (PPC) sampling, before, during, and after infusion of increasing doses of beta-END or naloxone through the PPC, during t he follicular phase; and (d) the in vivo release of ME-LHRH and serum LH, before, during, and after infusion of beta-END or naloxone in lute al and follicular ewes. In the ewe, beta-END-containing perikarya are located in and around the arcuate nucleus. Their processes are also pr esent in the diagonal band, medial septal nucleus, and medial and late ral hypothalamic areas, including the preoptic region and posterior ME . Perikarya containing LHRH are located in the preoptic area and proje ct also to the ME, providing opportunities for synaptic interactions b etween beta-END and LHRH-containing perikarya and processes at these l evels. ME in vivo release of LHRH and beta-END increase from the lutea l (low LH/high progesterone, P4) to the follicular phase (high LH/low P4). In follicular ewes, in vivo LHRH and LH release is decreased, in a dose-dependent manner, by beta-END infused through the PPC probe int o the posterior-lateral ME. In contrast, infusion of naloxone under si milar conditions increases LHRH and LH release, also in a dose-depende nt fashion. The inhibitory effect of beta-END on LHRH and LH, well as the stimulatory effect of naloxone on LHRH and LH, were only marginall y apparent in luteal ewes. These results suggest that the ME is a majo r control site where beta-END exerts its influence on hypophysiotropic LHRH release. The strength of this inhibitory effect apparently incre ases throughout the follicular phase, and might prevent the premature onset of the preovulatory surge of LHRH and LH.