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      Effect of Estrogen on Hypothalamic Transforming Growth Factor Alpha and Gonadotropin-Releasing Hormone Gene Expression in the Female Rhesus Monkey

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          Abstract

          In order to study whether hypothalamic transforming growth factor alpha (TGFα) gene expression in the monkey is estrogen-sensitive, long-term ovariectomized rhesus macaques were implanted subcutaneously with either estradiol-containing (n = 3) or blank (n = 3) Silastic capsules. Blood samples were collected every other day while the animals were lightly sedated with ketamine hydrochloride to monitor circulating LH and estradiol concentrations. Animals were killed with a lethal dose of pentobarbital sodium after a marked suppression of LH secretion was confirmed (81 days of estradiol treatment); the preoptic area (POA), mediobasal hypothalamus (MBH) and samples of cerebral cortex were dissected out, snap-frozen in liquid nitrogen and processed for the determination of TGFα messenger RNA (mRNA) by ribonuclease protection assay using a cRNA probe. The opportunity was also taken to study the action of estrogen on hypothalamic GnRH mRNA levels. Although circulating estradiol concentrations of 50–150 pg/ml achieved in the steroid-treated group produced a decrease in hypothalamic GnRH mRNA levels, which was significant in the MBH, TGFα mRNA levels in this hypothalamic region and in the POA were not influenced by estrogen treatment. These findings indicate that TGFα is probably not involved in mediating the inhibitory action of estradiol on GnRH neurons. Additionally, the relevance of our results to the understanding of the neurobiological mechanisms underlying the initiation of puberty in primates is discussed.

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          Targeting transforming growth factor alpha expression to discrete loci of the neuroendocrine brain induces female sexual precocity.

          Precocious puberty of cerebral origin is a poorly understood disorder of human sexual development, brought about by the premature activation of those neurons that produce luteinizing hormone-releasing hormone (LHRH), the neuropeptide controlling sexual maturation. An increased production of transforming growth factor alpha (TGF alpha) in the hypothalamus has been implicated in the mechanism underlying both normal and precocious puberty. We have now used two gene delivery systems to target TGF alpha overexpression near LHRH neurons in immature female rats. Fibroblasts infected with a retroviral construct in which expression of the human TGF alpha gene is constitutively driven by the phosphoglycerate kinase promoter, or transfected with a plasmid in which TGF alpha expression is controlled by an inducible metallothionein promoter, were transplanted into several regions of the hypothalamus. When the cells were in contact with LHRH nerve terminals or in the vicinity of LHRH perikarya, sexual maturation was accelerated. These results suggest that precocious puberty of cerebral origin may result from a focal disorder of TGF alpha production within the confines of the LHRH neuron microenvironment.
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            Estradiol stimulates preoptic area-anterior hypothalamic proGnRH-GAP gene expression in ovariectomized rats

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              Author and article information

              Journal
              NEN
              Neuroendocrinology
              10.1159/issn.0028-3835
              Neuroendocrinology
              S. Karger AG
              0028-3835
              1423-0194
              1998
              March 1998
              11 April 1998
              : 67
              : 3
              : 228-235
              Affiliations
              Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine, Pittsburgh, Pa., USA
              Article
              54318 Neuroendocrinology 1998;67:228–235
              10.1159/000054318
              9588692
              © 1998 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
              Figures: 4, Tables: 1, References: 27, Pages: 8
              Categories
              Gonadotropins and Gonadal Steroids

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