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      Estrogen Transiently Increases Delayed Rectifier, Voltage-Dependent Potassium Currents in Ovine Gonadotropes

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          Abstract

          Treatment of gonadotropes with estrogen (E) changes the electrophysiological response to gonadotropin-releasing hormone (GnRH) such that the cells are hyperpolarised immediately after stimulation with GnRH and then generate action potentials more frequently than non-E-treated cells. We investigated the role of K<sup>+</sup> current in this altered response to GnRH using cultures of ewe pituitary cells enriched for gonadotropes. K<sup>+</sup> current density was measured using nystatin-perforated whole-cell recordings in the voltage clamp mode. Treatment of cells with E for 16–20 h significantly (p < 0.01) increased the unit K<sup>+</sup> current to 180% of that in vehicle-treated cells. Outward current in these cells flows predominantly through voltage-dependent, delayed rectifier K<sup>+</sup> channels (I<sub>K</sub>), and E alters the magnitude of this current. The effect of E to increase the K<sup>+</sup> current was dose- and time-dependent and was maximal after 16–20 h. The unit K<sup>+</sup> current values returned to pre-treatment levels after 36 h of E treatment. Several cells were studied both before and after E treatment and the average effect of E on these cells was to increase the unit K<sup>+</sup> current by 90%. The time-course of the effect of E on K<sup>+</sup> current density is the same as the effect of E to increase LH release in vitro and in vivo. We conclude that the increase in K<sup>+</sup> current may be an important part of the mechanism whereby E acts on gonadotropes to facilitate the LH surge which triggers ovulation.

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          Most cited references 4

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          Apamin-sensitive potassium channels mediate agonist-induced oscillations of membrane potential in pituitary gonadotrophs

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            Cloned Ca(2+)-dependent K+ channel modulated by a functionally associated protein kinase.

            Calcium-dependent potassium (KCa) channels carry ionic currents that regulate important cellular functions. Like some other ion channels, KCa channels are modulated by protein phosphorylation. The recent cloning of complementary DNAs encoding Slo KCa channels has enabled KCa channel modulation to be investigated. We report here that protein phosphorylation modulates the activity of Drosophila Slo KCa channels expressed in Xenopus oocytes. Application of ATP-gamma S to detached membrane patches increases Slo channel activity by shifting channel voltage sensitivity. This modulation is blocked by a specific inhibitor of cyclic AMP-dependent protein kinase (PKA). Mutation of a single serine residue in the channel protein also blocks modulation by ATP-gamma S, demonstrating that phosphorylation of the Slo channel protein itself modulates channel activity. The results also indicate that KCa channels in oocyte membrane patches can be modulated by an endogenous PKA-like protein kinase which remains functionally associated with the channels in the detached patch.
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              Human growth hormone releasing factor (hGRF) modulates calcium currents in human growth hormone secreting adenoma cells

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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                1999
                April 1999
                21 April 1999
                : 69
                : 4
                : 254-260
                Affiliations
                Prince Henry’s Institute of Medical Research, Monash Medical Centre, Clayton, Vic., Australia
                Article
                54426 Neuroendocrinology 1999;69:254–260
                10.1159/000054426
                10207277
                © 1999 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: 43, Pages: 7
                Categories
                Reproductive Neuroendocrinology

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