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      Somatostatin Messenger RNA in Hypothalamic Neurons Is Increased by Testosterone through Activation of Androgen Receptors and Not by Aromatization to Estradiol

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          Abstract

          Growth hormone (GH) secretory patterns are influenced by sex steroids, at least in part, through modulation of the secretion of hypothalamic somatostatin (SS) and GH-releasing hormone. Neurons in the periventricular nucleus (PeN) expressing the messenger RNA (mRNA) for SS are modulated by physiological levels of testosterone. However, it is uncertain whether testosterone’s action is mediated directly by androgen receptor activation or indirectly through aromatization to estradiol and subsequent binding to the estrogen receptor. We examined this question by evaluating the effectiveness of 17β-estradiol and the nonaromatizable androgen, dihydrotestosterone (DHT), to mimic the effects of testosterone. Adult male rats were castrated and implanted subcutaneously with a Silastic capsule that contained either testosterone, 17β-estradiol or DHT, or a sham capsule. Intact animals were sham-operated. We used in situ hybridization to assess the effect of these treatments on SS mRNA signal levels in individual neurons of the hypothalamus. Following castration, SS mRNA content was reduced in cells of the PeN (intact, 195 ± 12 grains/cell, vs. castrated, 139 ± 4 grains/cell). Replacement with physiological levels of testosterone prevented the decline in SS mRNA signal levels (castrated testosterone-replaced, 214 ± 15 grains/cell) as did replacement with the nonaromatizable androgen DHT (castrated DHT-replaced, 213 ± 16 grains/cell). Treatment with 17β-estradiol failed to prevent the postcastration decline in SS mRNA content (castrated estrogen-replaced, 145 ± 4 grains/cell). Castrated 17β-estradiol-treated animals were not significantly different from the castrated sham-treated animals (castrated, 139 ± 4 grains/cell, vs. castrated estrogen-replaced, 145 ± 4 grains/cell). These results show that, whereas testosterone and DHT prevented the postcastration decline in SS mRNA signal levels, 17β-estradiol had no such effect. Based on these observations, we conclude that the ability of testosterone to stimulate SS gene expression in neurons of the PeN is likely to be mediated through activation of androgen receptors and not through aromatization to estradiol.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1990
          1990
          03 April 2008
          : 52
          : 4
          : 342-349
          Affiliations
          Departments of aObstetrics and Gynecology, bPhysiology and Biophysics and cZoology, and dPopulation Center for Research in Reproduction, University of Washington, Seattle, Wash., USA
          Article
          125618 Neuroendocrinology 1990;52:342–349
          10.1159/000125618
          1979839
          © 1990 S. Karger AG, Basel

          Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

          Page count
          Pages: 8
          Categories
          Original Paper

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