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      Implants of Estradiol Conjugated to Bovine Serum Albumin in the Male Rat Medial Preoptic Area Promote Copulatory Behavior

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          Abstract

          The expression of mating behavior in male rats is dependent on estrogen-responsive neurons in the medial preoptic area (MPO). Previous reports showed that mating is attenuated if the aromatization of testosterone to estradiol (E<sub>2</sub>) is blocked in the MPO and that mating is maintained by MPO E<sub>2</sub> implants. However, the mechanisms by which E<sub>2</sub> exerts its action are not fully understood. It had been thought that E<sub>2</sub> acted exclusively by binding to nuclear estrogen receptors to exert it effects; however, recent reports suggest that E<sub>2</sub> also binds to membrane-associated receptors activating downstream intracellular cascade responses. In this study, we aimed to determine if an action of E<sub>2</sub> at the cell surface is sufficient to support mating behavior. Therefore, either vehicle, E<sub>2</sub>, or E<sub>2</sub> conjugated to bovine serum albumin (BSA-E<sub>2</sub>: a complex of E<sub>2</sub> and a large protein that will not cross the plasma membrane, thereby restricting the action of E<sub>2</sub> to cell surface signaling) was chronically administered bilaterally to the MPO of castrated, dihydrotestosterone-treated male rats. Mating behavior was supported by MPO BSA-E<sub>2</sub> implants, suggesting that E<sub>2</sub> operates in the MPO via a cell surface mechanism to facilitate male rat mating behavior.

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          Cloning of a novel receptor expressed in rat prostate and ovary.

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            Interaction of oestrogen receptor with the regulatory subunit of phosphatidylinositol-3-OH kinase.

            Oestrogen produces diverse biological effects through binding to the oestrogen receptor (ER). The ER is a steroid hormone nuclear receptor, which, when bound to oestrogen, modulates the transcriptional activity of target genes. Controversy exists, however, concerning whether ER has a role outside the nucleus, particularly in mediating the cardiovascular protective effects of oestrogen. Here we show that the ER isoform, ER alpha, binds in a ligand-dependent manner to the p85alpha regulatory subunit of phosphatidylinositol-3-OH kinase (PI(3)K). Stimulation with oestrogen increases ER alpha-associated PI(3)K activity, leading to the activation of protein kinase B/Akt and endothelial nitric oxide synthase (eNOS). Recruitment and activation of PI(3)K by ligand-bound ER alpha are independent of gene transcription, do not involve phosphotyrosine adapter molecules or src-homology domains of p85alpha, and extend to other steroid hormone receptors. Mice treated with oestrogen show increased eNOS activity and decreased vascular leukocyte accumulation after ischaemia and reperfusion injury. This vascular protective effect of oestrogen was abolished in the presence of PI(3)K or eNOS inhibitors. Our findings define a physiologically important non-nuclear oestrogen-signalling pathway involving the direct interaction of ER alpha with PI(3)K.
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              Expression of c-fos protein in brain: metabolic mapping at the cellular level.

              The proto-oncogene c-fos is expressed in neurons in response to direct stimulation by growth factors and neurotransmitters. In order to determine whether the c-fos protein (Fos) and Fos-related proteins can be induced in response to polysynaptic activation, rat hindlimb motor/sensory cortex was stimulated electrically and Fos expression examined immunohistochemically. Three hours after the onset of stimulation, focal nuclear Fos staining was seen in motor and sensory thalamus, pontine nuclei, globus pallidus, and cerebellum. Moreover, 24-hour water deprivation resulted in Fos expression in paraventricular and supraoptic nuclei. Fos immunohistochemistry therefore provides a cellular method to label polysynaptically activated neurons and thereby map functional pathways.
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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2007
                November 2007
                27 August 2007
                : 86
                : 4
                : 249-259
                Affiliations
                Department of Biology, Georgia State University, Atlanta, Ga., USA
                Article
                107695 Neuroendocrinology 2007;86:249–259
                10.1159/000107695
                17726305
                ee79b0fd-4f09-4bd0-8ca7-9fdc6fc41788
                © 2007 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.

                History
                : 13 April 2006
                : 06 July 2007
                Page count
                Figures: 3, Tables: 1, References: 74, Pages: 11
                Categories
                GnRH, Gonadotropins, Gonadal Steroids and Reproduction

                Endocrinology & Diabetes,Neurology,Nutrition & Dietetics,Sexual medicine,Internal medicine,Pharmacology & Pharmaceutical medicine
                Immunocytochemistry,Estrogen receptor,Dihydrotestosterone,Sexual behavior

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