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      Pituitary Growth Hormone Secretion in the Turbot, a Phylogenetically Recent Teleost, Is Regulated by a Species-Specific Pattern of Neuropeptides

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          Abstract

          In mammals, growth hormone (GH) is under a dual hypothalamic control exerted by growth hormone-releasing hormone (GHRH) and somatostatin (SRIH). We investigated GH release in a pleuronectiform teleost, the turbot (Psetta maxima), using a serum-free primary culture of dispersed pituitary cells. Cells released GH for up to 12 days in culture, indicating that turbot somatotropes do not require releasing hormone for their regulation. SRIH dose-dependently inhibited GH release up to a maximal inhibitory effect of 95%. None of the potential stimulators tested induced any change in basal GH release. Also, neither forskolin, an activator of adenylate cyclase, nor phorbol ester (TPA), an activator of protein kinase C, were able to modify GH release, suggesting that spontaneous basal release already represents the maximal secretory capacity of turbot somatotropes. In contrast, forskolin and TPA were able to increase GH release in the presence of SRIH. In this condition (coincubation with SRIH), pituitary adenylate cyclase-activating polypeptide (PACAP) stimulated GH release, whereas none of the other neuropeptides tested (GHRHs; sea bream or salmon or chicken II GnRHs; TRH; CRH) had any significant effect. These data indicate that inhibitory control by SRIH may be the basic control of GH production in teleosts and lower vertebrates, while PACAP may represent the ancestral growth hormone-releasing factor in teleosts, a role taken over in higher vertebrates by GHRH.

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          Most cited references 7

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          Hypothalamic and thyroidal regulation of growth hormone in tilapia.

          A radioimmunoassay (RIA) for recombinant tilapia growth hormone (GH) was established and validated. The ability of various hypothalamic factors to regulate GH secretion in the tilapia hybrid (Oreochromis niloticus x Oreochromis aureus) was studied. Somatostatin1-14 (SRIF1-14; 10-100 micrograms/kg) was found to reduce circulating GH levels in a dose-dependent manner. SRIF1-14 (0.1-1000 nM) inhibited GH release from perifused pituitary fragments (ED50 0.83 nM). Human growth hormone-releasing hormone fragment 1-29 (hGHRH1-29; 100 micrograms/kg) doubled circulating GH levels and modestly stimulated GH secretion in vitro. Carp growth hormone-releasing hormone (cGHRH) stimulated GH secretion in vitro to a similar degree at the same dose (1 microM). Injection of salmon gonadotropin-releasing hormone (sGnRH) superactive analog (10-100 micrograms/kg) increased plasma GH levels sixfold. sGnRH also stimulated GH release in vitro (ED50 142.56 nM). Dopamine (0.1-10 microM) and the D1 DA receptor agonist SKF 38393 increased GH secretion from perifused pituitary fragments dose-relatedly. Thyrotropin-releasing hormone (TRH) had no effect on GH secretion from perifused pituitary fragments, but increased plasma GH levels, as did bovine thyroid stimulating hormone (bTSH). The increased plasma GH in the bTSH-treated fish coincided with a dramatic increase in T4; however, TRH increased GH without changing T4 levels. T3 increased the synthesis of GH by isolated pituitaries (incorporation of [3H]leucine). SRIF1-14 seems to be a most potent hypothalamic regulator of GH secretion in tilapia; sGnRH and DA both increased GH secretion, although sGnRH elicited considerably greater responses at lower doses. Two forms of GHRH increased GH levels, although the unavailability of the homologous peptide prevented an accurate evaluation of its importance in regulating GH secretion. The thyroid axis (TRH, TSH, and T3) stimulates both synthesis and release of GH, although TRH did not appear to have a direct effect on the level of the pituitary.
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            Differential Management of Ca 2+ Oscillations by Anterior Pituitary Cells: A Comparative Overview

            Most electrical and ionic properties of anterior pituitary cells are common to all pituitary cell types; only gonadotropes exhibit a few cell specific features. Under basal conditions, the majority of pituitary cells in vitro, irrespective of their cell type, display spontaneous action potentials and [Ca 2+ ] i transients that result from rhythmic Ca 2+ entry through L-type Ca 2+ channels. The main function of these action potentials is to maintain cells in a readily activable responsive state. We propose to call this state a ‘pacemaker mode’, since it persists in the absence of extrinsic stimulation. When challenged by hypothalamic releasing hormones, cells exhibit two distinct response patterns: amplification of pacemaker activity or shift to internal Ca 2+ release mode. In the internal Ca 2+ release mode, [Ca 2+ ] i oscillations are not initiated by entry of external Ca 2+ , but by release of Ca 2+ from intracellular stores. In somatotropes and corticotropes, GHRH or CRH triggers the pacemaker mode in silent cells and amplifies it in spontaneously active cells. In contrast, in gonadotropes GnRH activates the internal Ca 2+ release mode in silent cells and switches already active cells from the pacemaker to the internal Ca 2+ release mode. Interestingly, homologous normal and tumoral cells display the same type of activity in vitro, in the absence or presence of hypothalamic hormones. Pacemaker and internal Ca 2+ release modes are likely to serve different purposes. Pacemaker activity allows long-lasting sequences of [Ca 2+ ] i oscillations (and thus sustained periods of secretion) that stop under the influence of hypothalamic inhibitory peptides. In contrast, the time during which cells can maintain internal Ca 2+ release mode depends upon the importance of intracellular Ca 2+ stores. This mode is thus more adapted to trigger secretory peaks of large amplitude and short duration. On the basis of these observations, theoretical models of pituitary cell activity can be proposed.
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              Growth hormone and gonadotropin secretion in the common carp (Cyprinus carpio L.): in vitro interactions of gonadotropin-releasing hormone, somatostatin, and the dopamine agonist apomorphine

               Lin,  XW Lin,  HR Lin (1993)
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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
                December 2001
                17 December 2001
                : 74
                : 6
                : 375-385
                Affiliations
                aLaboratoire de Physiologie Générale et Comparée, Muséum National d’Histoire Naturelle, UMR CNRS Paris, and bLaboratoire de Physiologie des Poissons, IFREMER, Station Ressources Vivantes, Plouzané, France; cDepartment of Zoology, The University of Hong Kong, China, dObservatoire Océanologique de Banyuls, Laboratoire Arago, Banyuls sur Mer, France
                Article
                54704 Neuroendocrinology 2001;74:375–385
                10.1159/000054704
                11752894
                © 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: 90, Pages: 11
                Categories
                Regulation of Prolactin and Growth Hormone

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