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Alterations in the Responsiveness of Median Eminence Luteinizing Hormone-Releasing Hormone Nerve Terminals to Norepinephrine and Prostaglandin E₂ in Vitro during the Rat Estrous Cycle^*

LOUIS V. DEPAOLO, SÉRGIO R. OJEDA, ANDRES NEGRO-VILAR and AMUEL M. McCANN

Department of Physiology, University of Texas Health Science Center at Dallas, Dallas, Texas 75235

Address all correspondence to: Dr. S. M. McCann, Department of Physiology, University of Texas Health Science Center at Dallas, 5323 Harry Hines Boulevard, Dallas, Texas 75235.

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.

Footnotes

^* This work was supported by NIH Grant HD-09988 and the Ford Foundation.

Supported by NIH Postdoctoral Fellowship 1-F32-HD-05776. Present address: Department of Physiology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78284.

Received August 19, 1981.