ADRENERGIC MEDIATION OF THE NALOXONE-INDUCED GNRH RELEASE FROM HYPOTHALAMI OF OVARIECTOMIZED, STEROID-TREATED IMMATURE RATS

The present study examines the effect of naloxone on GnRH release in v itro under different steroid milieus. Naloxone (6.1-mu-mol/kg) adminis tered 30 min before decapitation was highly effective in evoking GnRH release from superfused hypothalamic tissues derived from ovariectomiz ed, estradiol- and progesterone-treated immature rats, while ineffecti ve in altering GnRH release from intact, ovariectomized and vehicle- o r estradiol-treated rats. To further explore the possible involvement of catecholamines in the naloxone-stimulated GnRH release, diethyldith iocarbamic acid (2.9 mmol/kg), an inhibitor of noradrenalin synthesis, was administered ip 30 min before naloxone injection into ovariectomi zed, estradiol- and progesterone-treated rats. Diethyldithiocarbamic a cid markedly reduced the naloxone-evoked GnRH release, although it was ineffective in modifying the spontaneous release of GnRH. A blockade of alpha-adrenergic receptor with phenoxybenzamine significantly suppr essed the naloxone-stimulated GnRH release, whereas treatment with pro pranolol, a beta-adrenergic receptor blocker, failed to alter GnRH rel ease. The present data suggest that the endogenous opioid peptide may participate in the regulation of GnRH release under a particular stero id milieu, and the inhibitory action of endogenous opioid peptide seem s to require the mediation of adrenergic neurotransmission, presumably through alpha-adrenergic receptor.