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      Estrogen Receptor Expression in Laryngeal Muscle in Relation to Estrogen-Dependent Increases in Synapse Strength

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          Abstract

          In Xenopus laevis, the laryngeal neuromuscular synapse is the final effector for sexually differentiated song production. Females have stronger laryngeal synapses than males, and synapse strength is estrogen dependent. Estrogen-induced increases in synaptic strength require at least 3 weeks of exposure, suggesting that the hormone acts via a classical genomic mechanism involving the estrogen receptor (ER). The locus of the sex difference in synapse strength, determined using quantal analysis, is presynaptic, leading to the prediction that estrogen acts directly on vocal motor neurons. However, laryngeal motor neurons do not accumulate estrogen. Estrogen might instead affect motor neuron transmitter release via a retrograde signal from its target muscle. To test this hypothesis, we determined whether laryngeal muscle expresses ER. With RT-PCR using primers that recognize highly conserved domains of the ERα, mRNA products of the predicted size were amplified from laryngeal muscle as well as from other classical target tissues (forebrain and oviduct). Northern blots using a portion of the PCR product as primer revealed the same-sized band in oviduct and laryngeal muscle. Immunocytochemistry and Western blots confirmed the presence of ER protein in laryngeal muscle fibers and revealed several proteins in laryngeal muscle, brain and liver; among these was an approximately 66-kD protein – presumed to be full-length ER – that was the only one found in oviduct. Estrogen treatment of juveniles resulted in an upregulation of the 66-kD ER protein concomitant with an increase in quantal content. Taken together, these experiments strongly suggest that the ER is expressed by laryngeal muscle; this receptor could mediate estrogen-dependent changes in synaptic strength via retrograde signaling.

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          Most cited references 11

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          Functional domains of the human estrogen receptor.

          Two domains of the human estrogen receptor, responsible for hormone binding (region E) and tight nuclear binding (region C), are essential for the receptor to activate efficiently the transcription of estrogen-responsive genes. Region D, which joins the DNA- and hormone-binding domains, can be altered without affecting activation. Deletion of the N-terminal domain (region A/B) has no effect on activation of a reporter gene containing a vitellogenin estrogen-responsive element (ERE) and the HSV-tk promoter, whereas it severely impairs activation of the human pS2 gene promoter. Deletion of most or all of the hormone-binding domain leads to only about 5% constitutive transcriptional activity, yet these mutants appear to bind efficiently to an ERE in vivo. Apparently, region C recognizes the ERE of target genes, and the hormone-binding domain plays an essential role for efficient activation of transcription.
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            Behavioral effects of estrogen receptor gene disruption in male mice.

            Gonadal steroid hormones regulate sexually dimorphic development of brain functions and behaviors. Their nuclear receptors offer the opportunity to relate molecular events in neurons to simple instinctive mammalian behaviors. We have determined the role of estrogen receptor (ER) activation by endogenous estrogen in the development of male-typical behaviors by the use of transgenic estrogen-receptor-deficient (ERKO) mice. Surprisingly, in spite of the fact that they are infertile, ERKO mice showed normal motivation to mount females but they achieved less intromissions and virtually no ejaculations. Aggressive behaviors were dramatically reduced and male-typical offensive attacks were rarely displayed by ERKO males. Moreover, ER gene disruption demasculinized open-field behaviors. In the brain, despite the evident loss of functional ER protein, the androgen-dependent system appears to be normally present in ERKO mice. Together, these findings indicate that ER gene expression during development plays a major role in the organization of male-typical aggressive and emotional behaviors in addition to simple sexual behaviors.
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              Potentiation of developing synapses by postsynaptic release of neurotrophin-4.

               Xinming Wang,  M Poo (1997)
              The hypothesis that synaptic functions can be regulated by neurotrophins secreted from the postsynaptic cell was examined in Xenopus nerve-muscle cultures. Neuromuscular synapses formed on myocytes overexpressing neurotrophin-4 (M+ synapses) exhibited a higher level of spontaneous synaptic activity and enhanced evoked synaptic transmission as compared to those formed on normal control myocytes (M- synapses). The NT-4 effects involve a potentiation of presynaptic transmitter secretion as well as a lengthening of the mean burst duration of postsynaptic low conductance acetylcholine channels. Repetitive stimulation of either the presynaptic neuron or the postsynaptic myocyte led to a potentiation of synaptic transmission at M+ synapses. All potentiation effects of NT-4 overexpression were abolished by the extracellular presence of TrkB-IgG but not by the presence of TrkA-IgG, indicating that postsynaptic secretion of NT-4 was responsible for the synaptic modification.
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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2003
                August 2003
                20 August 2003
                : 78
                : 2
                : 72-80
                Affiliations
                Department of Biological Sciences, Columbia University, New York, N.Y., USA
                Article
                71962 Neuroendocrinology 2003;78:72–80
                10.1159/000071962
                12915759
                © 2003 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: 51, Pages: 9
                Categories
                Gonadal Steroids and Regulation of Reproductive Hormones

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