The present study was designed to assess the participation of
gonadotropin-releasing hormone (
GnRH) in the display of estrous behavior induced by application of vaginal-cervical stimulation (VCS) and by the intracerebroventricular (icv) administration of
progesterone and its ring A-reduced metabolites to ovariectomized (ovx),
estradiol benzoate (E2B) primed rats. Icv injection of
Antide, a GnRH-1 receptor antagonist, significantly depressed
lordosis behavior in ovx, E2B-primed rats treated with icv
GnRH. Application of VCS to ovx, E2B-primed rats facilitated both
lordosis and proceptivity. These behavioral responses were significantly depressed by the icv administration of
Antide. Similarly, icv
Antide blocked the stimulatory effect on both
lordosis and proceptive behaviors elicited by
progesterone and its ring A-reduced metabolites: 5alpha-pregnandione (5alpha-DHP), 5alpha-pregnan-3alpha-ol-20-one (5alpha,3alpha-Pgl) and 5beta-pregnan-3beta-hydroxy-20-one (5beta,3beta-Pgl) in ovx, E2B-primed rats. By contrast, icv injection of
Antide failed to interfere with the facilitatory effect of the
synthetic progestin megestrol acetate on
lordosis and proceptive behaviors. This
progestin is not reduced in ring A. The results suggest that
GnRH release is an important process in the chain of events leading to the display of estrous behavior in response to
progesterone, its ring A-reduced metabolites, and VCS in female rats.