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      Estrogen Modulates α 1/β-Adrenoceptor- Induced Signaling and Melatonin Production in Female Rat Pinealocytes

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          Abstract

          Nocturnal rise in pineal melatonin output is due to the night-induced acceleration of noradrenergic transmission and α<sub>1</sub>- and β-adrenoceptor activation. In addition, in female animals, cyclic oscillations in circulating levels of sex steroid hormones are accompanied by changes in the rate of pineal melatonin secretion. To investigate whether estrogen directly affects pineal adrenoceptor responsiveness, pinealocytes from 21-day-old ovariectomized rats were exposed to physiological concentrations of 17β-estradiol (17β-E<sub>2</sub>) and treated with noradrenergic agonists. Direct exposure to 17β-E<sub>2</sub> reduced α<sub>1</sub>/β-adrenoceptor-induced stimulation of melatonin synthesis and release. This effect was mediated by an estrogen-dependent inhibition of both β-adrenoceptor-induced accumulation of cAMP and α<sub>1</sub>-adrenoceptor-induced phosphoinositide hydrolysis. Furthermore, estrogen reduced transient Ca<sup>2+</sup> signals elicited in single pinealocytes by α<sub>1</sub>-adrenoceptor activation or by potassium-induced depolarization. In the case of β-adrenoceptor responsiveness, neither forskolin- nor cholera toxin-induced accumulation of cAMP were affected by previous exposure to 17β-E<sub>2</sub>. This indicates that estrogen effects must be exerted upstream from adenylylcyclase activation, and independent of modifications in G protein expression, therefore suggesting changes in either adrenoceptor expression or receptor-effector coupling mechanisms. Since estrogen effects upon adrenoceptor responsiveness in pineal cells was not mimicked by 17β-E<sub>2</sub> coupled to bovine serum albumin and showed a latency of 48 h, this effect could be compatible with a genomic action mechanism. This is also consistent with the presence of two estrogen receptor proteins, α- and β-subtypes, in female rat pinealocytes under the present experimental conditions.

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          Most cited references 11

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          Switching of the coupling of the beta2-adrenergic receptor to different G proteins by protein kinase A.

          Many of the G-protein-coupled receptors for hormones that bind to the cell surface can signal to the interior of the cell through several different classes of G protein. For example, although most of the actions of the prototype beta2-adrenergic receptor are mediated through Gs proteins and the cyclic-AMP-dependent protein kinase (PKA) system, beta-adrenergic receptors can also couple to Gi proteins. Here we investigate the mechanism that controls the specificity of this coupling. We show that in HEK293 cells, stimulation of mitogen-activated protein (MAP) kinase by the beta2-adrenergic receptor is mediated by the betagamma subunits of pertussis-toxin-sensitive G proteins through a pathway involving the non-receptor tyrosine kinase c-Src and the G protein Ras. Activation of this pathway by the beta2-adrenergic receptor requires that the receptor be phosphorylated by PKA because it is blocked by H-89, an inhibitor of PKA. Additionally, a mutant of the receptor, which lacks the sites normally phosphorylated by PKA, can activate adenylyl cyclase, the enzyme that generates cAMP, but not MAP kinase. Our results demonstrate that a mechanism previously shown to mediate uncoupling of the beta2-adrenergic receptor from Gs and thus heterologous desensitization (PKA-mediated receptor phosphorylation), also serves to 'switch' coupling of this receptor from Gs to Gi and initiate a new set of signalling events.
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            Comparative distribution of estrogen receptor-? and -? mRNA in the rat central nervous system

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              Acute Activation of Maxi-K Channels (hSlo) by Estradiol Binding to the Subunit

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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2001
                February 2001
                23 February 2001
                : 73
                : 2
                : 111-122
                Affiliations
                aLaboratory of Cellular Neurobiology, Department of Physiology, University of La Laguna School of Medicine, Ofra, Sta. Cruz de Tenerife, bDepartment of Medical Physiology and Biophysics, University of Sevilla School of Medicine, Sevilla, cDepartment of Biostatistics, University Complutense of Madrid School of Medicine, Madrid, Spain; dDepartment of Psychiatry, Boston University Medical Center, Boston, Mass., USA
                Article
                54627 Neuroendocrinology 2001;73:111–122
                10.1159/000054627
                11244298
                © 2001 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: 6, References: 60, Pages: 12
                Categories
                Pineal Gland

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