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Endocrinology, doi:10.1210/endo-105-4-875
Endocrinology Vol. 105, No. 4 875-878
Copyright © 1979 by the Endocrine Society.
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Circulating Luteinizing Hormone and Prolactin Concentrations in Intact or Castrated Male Rats Treated with 5-Hydroxytryptamine*

NANCY S. PILOTTE and JOHN C. PORTER

Cecil H. and Ida Green Center for Reproductive Biology Sciences, the Departments of Obstetrics and Gynecology and Physiology, The University of Texas Health Science Center at Dallas, Southwestern Medical School Dallas, Texas 75235

Address all correspondence and requests for reprints to: Dr. Nancy S. Pilotte, Department of Obstetrics and Gynecology, The University of Texas Health Science Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235.

Abstract

The effects of sc administered 5-hydroxytryptamine (serotonin) on LH and PRL release, as reflected by circulating concentrations of these hormones, were investigated in intact and castrated male rats. In the initial experiment, the animals were given serotonin or its solvent vehicle and were decapitated 30 min later. In all serotonin-treated animals (intact or castrated 2 or 30 days before use), the serum PRL concentration was increased markedly (at least 5 times) over that of the vehicle-treated animals, but the serum LH concentration was affected significantly only in rats that had been castrated for 2 days. In these animals, the serum LH concentration was 230 ± 21 ng/ml (mean ± SE) compared to 395 ± 39 ng/ml in thecontrols. However, in intact male rats or male rats that had been castrated for 30 days, the serum LH concentration was not significantly depressed in serotonin-treated animals. In subsequent experiments, an indwelling cannula was inserted into the right atrium by way of the right jugular vein at the time of castration, and the animals were used 2 days later. Blood was withdrawn through the cannula before and after serotonin or the solvent vehicle was administered sc to these rats. Within 30 min after the injection of serotonin, the serum concentration of PRL was significantly increased and that of LH was significantly (P < 0.01) decreased relative to the preinjection levels. When bromocriptine was given to these acutely castrated rats 3 h before the administration of serotonin, PRL release was completely inhibited; however, LH release was still reduced significantly (P < 0.01) relative to the controls. These findings are in accord with the hypothesis that treatment with serotonin can lead to an increase in PRL release and, conversely, to an inhibition of LH release in acutely castrated male rats. Moreover, the effect of serotonin on LH release is not dependent on PRL release.

Footnotes

* This work was supported by Research Grants AM-01237, AG-00306, and HD-11149 from the NIH, Bethesda, MD.

Received March 9, 1979.




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