The purpose of the present study was to investigate the effect of time of beta-endorphin (beta-EP) administration on lordosis in ovariectomized female rats injected subcutaneously (sc) with estradiol benzoate (EB) and progesterone (Prog). Intracerebroventricular (icv) injections of beta-EP and naloxone (NLX), an opioid receptor antagonist, were administered at the various stages of sc steroid hormone priming. Facilitation of lordosis induced by 10 microg beta-EP was observed exclusively within the initial 6 h of estrogen action, after which inhibition of lordosis occurred. At 12 h after EB priming, at the time of sc Prog treatment (or 43 h after EB priming), icv injection of 10 microg beta-EP significantly inhibited lordosis. Lordosis was significantly facilitated by icv injections of 1 and 10 microg beta-EP at the time of sc EB priming, but not by 0.1 microg beta-EP. A dose-response relationship was identified for lordosis in experimental animals receiving icv injection of beta-EP. Lordosis was inhibited by icv injections of 1 and 10 microg beta-EP at 1 h before the test (or 47 h after EB priming). Lordosis was significantly inhibited by icv injection of NLX at all stages. From the present results, it seems that two different mechanisms are involved in endorphinergic modulation of rats' sexual receptivity: (a) the endorphinergic system at the initial stages of estrogen action facilitates the estrogen activation of lordosis; (b) the endorphinergic system at the final stages of steroid action inhibits lordosis. Moreover, there exists a critical time between 6 and 12 h after estrogen priming for endorphinergic mediation to modulate estrogen action.
Copyright 1999 Academic Press.