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      Changes in the Hypothalamic Interaction between Norepinephrine and Prostaglandin E 2 during Sexual Maturation in Female Rats

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          Abstract

          The present experiments describe the study of the metabolism of <sup>14</sup>C-arachidonic acid and the effect of exogenous norepinephrine (NE) on prostanoid production in the anterior preop-tic area and medial basal hypothalamus (APOA-MBH) of prepubertal (16 days of age) and peripubertal female rats (30 days old). Four prostanoids were produced from <sup>14</sup>C-arachidonic acid (6-keto-prostaglandin(PG)F<sub>1α</sub>, PGF2<sub>α</sub>, PGE<sub>2</sub> and thromboxane (TX)B<sub>2)</sub> and were released to the incubating medium. The basal percent of conversion was not significantly different between them. In prepubertal rats the addition of NE (10<sup>–5</sup> M) to the medium did not modify on the synthesis of these eicosanoids. In peripubertal rats there are no significant differences in the basal production of 6-keto-PGF<sub>1α</sub>, PGF2<sub>α</sub>, PGE<sub>2</sub> and TXB<sub>2</sub> as compared to prepubertal rats. Moreover, the percentage of conversion of arachidonic acid into the different prostanoids was similar in prepubertal and peripubertal hypothalamus. Nevertheless, when NE (10<sup>–5</sup> M) was added to the incubation medium of peripubertal hypothalamus, a significant increase in the synthesis of PGE<sub>2</sub> was observed (control: 1.75 ± 0.1; NE 2.90 ± 0.3; p < 0.01). This increase in the synthesis was not accompanied by changes in the synthesis of any of the other three prostanoids. Prazosin, a well-known α<sub>1</sub>-receptor adrenoblocker at a dose of 10<sup>-5</sup> M did not modify the production of 6-keto-PGF<sub>1α</sub>, PGF2<sub>α</sub>, PGE<sub>2</sub> and TXB<sub>2</sub> but did induce a complete inhibition of the stimulation by NE of PGE<sub>2</sub> synthesis (NE: 2.85 ± 0.1; prazosin: 1.9 ± 0.09; p < 0.01). On the other hand, yohimbine, an α<sub>1</sub>-adrenoblocker did not modify the effect of NE on PGE<sub>2</sub> production. In summary, the results reported here demonstrated that sexual maturation involves the development of a mechanism by which NE stimulates PGE<sub>2</sub> production, an effect mediated through the α<sub>1</sub>-adrenoreceptor. The relationship of these results with the development of the positive feedback of estrogens on gonadotropin secretion during sexual maturation in the female rat is discussed.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1995
          1995
          09 April 2008
          : 62
          : 3
          : 226-230
          Affiliations
          Departamento de Fisiología, Facultad de Medicina, Universidad de Buenos Aires, y Cefybo (Conicet), Buenos Aires, Argentina
          Article
          127008 Neuroendocrinology 1995;62:226–230
          10.1159/000127008
          8538859
          © 1995 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: 5
          Categories
          Reproductive Physiology and Steroid Feedback

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