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      Trophic Effects of Estradiol on Fetal Rat Hypothalamic Neurons

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          Abstract

          Sex steroids play an important role in the development and functioning of the central nervous system (CNS); however, the mechanisms by which such hormones exert these effects are not well understood. We addressed the question as to whether sex steroids affect the development of the hypothalamus, at least in part, by acting as a trophic factor to modulate the number of neurons in the hypothalamus. To this end, primary hypothalamic cultures were prepared from the brains of embryonic (day 15) fetuses. Cultures received either 17β-es-tradiol (10<sup>–12</sup> M) or vehicle 6 h after seeding and everyday throughout the study. As early as 24 h later, cultures receiving 17β-estradiol had significantly more neurons (44%, p < 0.001) than the control cultures. This effect not only continued throughout the duration of the study, but the difference between the two groups increased so that after 5 days, 17β-estradiol-treated cultures had 209% more neurons than control cultures (p < 0.001). Thus, addition of 17β-estradiol to fetal hypothalamic cultures produced a significant increase in the number of neurons surviving in vitro. The presence of glia was not required for this phenomenon, since the number of neurons surviving in glial-free cultures was also significantly increased by the addition of 17β-estradiol. The neuron survival promoting effect of 17β-estradiol was saturable and could be blocked by the estrogen antagonist tamoxifen (10<sup>-7</sup> M). Testosterone (10<sup>–10</sup> M), but not the nonaromatizable androgen dihydrotestosterone (10<sup>–10</sup> M), could mimic the neuron survival-promoting effects of estradiol. Furthermore, estradiol had no significant effect on the in vitro survival of cerebral cortical neurons. These results suggest that one mechanism by which sex steroids may affect the development of the hypothalamus is through the modulation of the number of neurons that survive and that this effect is most likely mediated, at least in part, through the estrogen receptor.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1992
          1992
          07 April 2008
          : 56
          : 6
          : 895-901
          Affiliations
          Cajal Institute, CSIC, Madrid, Spain
          Article
          126321 Neuroendocrinology 1992;56:895–901
          10.1159/000126321
          1369599
          © 1992 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: 7
          Categories
          Original Paper

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