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Prostaglandin E, (PGE,) is involved in the luteinizing hormone-releasing hormone-stimulated luteinizing hormone surge in female rats and may act via specific membrane receptors. The following studies were performed to determine whether there were any changes in the hypothalamic PGE, binding and/or PGE, content which were specific to proestrus and not to the rest of the estrous cycle. Groups of female Wistar rats were sacrificed at 3-h intervals throughout the estrous cycle to determine both the circadian and circaestral changes in the hypothalamic PGE, content and [3H]PGE, binding. The hypothalamic PGE, content was maximal at 1700 h on each of the 4 consecutive days of the estrous cycle but was independent of the stage of the cycle.[3H]PGE, binding also displayed a circadian rhythm; the lowest binding occurred near the circadian peak of PGE,, suggesting that the PGE, binding sites were occupied by endogenous PGE,. Since such circadian rhythms were not observed in the hypothalamus of male rats, they may be under the control of ovarian steroids. Also, since PGE, binding and the PGE, content both exhibit a diurnal pattern independent of the day of the cycle, there may be changes in the PGE, receptor-mediated process coupled to an adenylyl cyclase which could explain the luteinizing hormone surge in proestrus.Prostaglandin E, (PGE,) induces the release of Iuteinizing hormone (LH) by stimulating luteinizing hormonc-rclcasing hormone (LHRH) release (1-5). There are also sevcral indications that PGs are involved in the modulation of LHRH release by steroids. The cyclo-oxygenase inhibitor, indomcthacin, prevents the steroidinduced release of gonadotrophin and lowcrs the elevated LH level of castrated animals (6). The preovulatory increase in PGE, synthesis, which precedes the LH surge, indicates that PGE, affects LH release in female rats (7,8), and a peak of PGE, release into the cerebrospinal fluid precedes the LH surge by 20 to 40 min (9). PGE, may act on LHRH release via specific membrane receptors (lo), since specific binding of [3H]PGE, to hypothalamic membranes is correlated with LHRH rclcase in vitro (1 1 ) .The preovulatory LH surge which occurs during proestrus in rats also requires a neural LHRH surge. This, in turn, depends upon adequate circulating titres of ovarian steroids (12). The effect of such a neurogenic stimulus was reported to be dependent on the time of day (1 3). In vitro PGE,-stimulated LHRH release from the median eminence (ME) also depcnds upon the stages of both the estrous and 24-h cycles (14). Such a change in M E sensitivity to PGE, could reflect a modification o f its PGE, binding capacity. However, LHRH release may be differently affected by PGE, and steroids, depending on the area of the hypothalamus: the comparative effect of norepinephrine (N E) on PGE, or LHRH release by the ME alone or hy the ME linkcd to the mediobasal hypothalamus (MBH/ME complex) suggests a regulation of the PGE,-stimulated LHRH release by neurons with cell body located in the MBH (15, 16). Moreover, thc...