Abstract

The action of two antagonist analogs and an antibody to luteinizing hormone-releasing hormone (LHRH) on sexual receptivity was studied in avariectomized, estrogen-progesterone primed female rats. Small amounts of each LHRH substance or saline was infused through a cannula positioned in either the third ventricle or arcuate-ventromedial (ARC-VMH) area of the hypothalamus. Infusions were carried out at the time of progesterone priming, which was 42 hrs post-estrogen treatment, and sexual receptivity, as denoted by the lordosis-to-mount ratio, was measured six hrs later. One antagonist analog, [D-pGlu1, D-Phe2, D-Trp3,6]-LHRH[1], had little or no effect on sexual receptivity when tested in either site. Similarly, an antibody to LHRH, tested only in the ARC-VMH, had no observable effect on lordotic behavior. However, the second and the most potent antagonist analog, [Ac-dehydro-Pro1, pCl-D-Phe2, D-Trp3,6]-LHRH[2], produced a marked and significant decrement in lordotic behavior when infused into either the third ventricle or ARC-VMH. These results suggest that this potent and long-acting, competitive antagonist analog of LHRH prevented endogenous LHRH from exerting its normal role in the induction of sexual receptivity and provide evidence to support the contention that the role of LHRH in mediating receptivity in the female rat is physiologically relevant.

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