Alterations in the Responsiveness of Median Eminence Luteinizing Hormone-Releasing Hormone Nerve Terminals to Norepinephrine and Prostaglandin E2in Vitro during the Rat Estrous Cycle*

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Abstract
The present study was conducted to determine if the response of median eminence (ME) nerve terminals to norepinephrine (NE) and prostaglandin E2 (PGE2) varies during the 4-day estrous cycle and if so, whether these changes could play a role in neural mechanisms regulating cyclic gonadotropin release. Groups of adult female rats were decapitated at either 1300 or 1600 h on each day of the cycle, blood was collected, and ME fragments (two MEs per flask) were incubated in an in vitro system. After a 15-min preincubation period, basal LHRH and PGE2 release was measured by RIA during a 30-min incubation period, and ME responses to either PGE2 (0.28 /IM) or NE (60 /AM) were tested during a second 30-min incubation period. The basal release of PGE2 and LHRH did not differ significantly among days of the cycle at any time examined. The release of LHRH in response to PGE2 markedly declined between 1300 h on diestrus day 2 (diestrus-2) and 1300 h on proestrus. Coincident with the preovulatory LH surge, the LHRH response to PGE2 increased during the afternoon of proestrus, remained elevated at 1300 h on estrus, and was again low by 1600 h on estrus. The PGE2 response to NE was high at 1300 h and low at 1600 h on diestrus-2, proestrus, and estrus. Likewise, the release of LHRH in response to NE on diestrus-2 and estrus was high at 1300 h and low at 1600 h. In contrast, increments in NE-induced LHRH release on proestrus paralleled the LHRH response to PGE2 on proestrus; that is, the release of LHRH was low at 1300 h and high at 1600 h. In additional experiments, treatment of proestrous rats with pentobarbital to block spontaneous gonadotropin surges completely suppressed ME responsiveness to both NE and PGE2 at 1600 h. Furthermore, the injection of progesterone at 1000 h on proestrus advanced both the onset of the LH/FSH surge and the increased in vitro LHRH response to PGE2 compared with oil-treated controls. Collectively, the results indicate that the preovulatory release of LHRH from ME terminals on proestrus may be due initially to an increased release of PGE2 by NE. Further LHRH release on proestrus may occur as a result of an increased response of these terminals to PGE2. Moreover, this sequence of events can be blocked by in vitro barbiturate treatment, thus providing evidence for a site (ME) as well as a possible mechanism of action of pentobarbital in suppressing the preovulatory discharge of gonadotropins.

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