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      Effects of Amylin and Salmon Calcitonin on β-Endorphin-Induced Growth Hormone and Prolactin Secretion in the Rat

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          Abstract

          In this study we examined the possible interplay of amylin (AMY) and salmon calcitonin (sCT) in the central control of growth hormone (GH) and prolactin (PRL) secretion in male rats. For this purpose we first compared effects of central intracerebroventricular (i.c.v.) admininstration of various doses of AMY (2.5–2,500 ng/rat) and sCT (2.2–220 ng/rat) on β-endorphin (β-END, 0.5 µg/rat)-induced GH and PRL secretion. AMY and sCT dose-dependently inhibited β-END-induced GH secretion, whereas only sCT was able to inhibit β-END-induced PRL secretion. To examine whether the GH inhibitory effect of AMY was due to the possible cross-reactivity of AMY and sCT on the same receptors in the CNS, we pretreated some rats with the AMY antagonist (AMY<sub>8–37</sub>, 2.5 µg/rat, i.c.v.). AMY<sub>8–37</sub> significantly enhanced the GH-stimulatory action of β-END. AMY<sub>8–37</sub>, administered prior to AMY and sCT, significantly removed the inhibitory effect of both AMY and sCT on β-END-induced GH release, suggesting that both peptides mediate their response on GH through a common receptor. In vitro competition binding studies on rat hypothalamic membranes have shown that both AMY and sCT compete with [<sup>125</sup>I]rAMY binding with half inhibition (IC<sub>50</sub>) values of 3.6 × 10<sup>–11</sup> and 1.6 × 10<sup>–10</sup>  M, respectively. Binding of [<sup>125</sup>I]sCT was inhibited by sCT with an IC<sub>50</sub> of 1.09 × 10<sup>–10</sup> M and to a lesser extent by AMY with an IC<sub>50</sub> of 1.3 × 10<sup>–6</sup>  M. Thus it is possible that the two peptides recognize a common hypothalamic receptor but with different affinities (sCT > AMY). Overall these data indicate that AMY behaves as a mimic of sCT in the central control of GH secretion. The failure of AMY, at variance with sCT, to modify the PRL-releasing activity of β-END indicates that different receptor subtypes for sCT are involved in the endocrine effects of sCT and only those mediating the modulatory action of GH respond to AMY.

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          Most cited references 5

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          Localization of calcitonin binding sites in rat central nervous system: evidence of its neuroactivity.

          The distribution of calcitonin (CT) binding sites in serial sections of the rat brain and spinal cord has been examined by an 'in vitro' autoradiographic technique using a radioisotope-sensitive sheet film and [125]salmon CT. Autoradiograms of the diencephalic region had the highest grain density throughout the entire hypothalamus, with the exception of the nuclei ventromedialis, posterior and mammillaris, which were not labeled at all. In the brainstem, large amounts of grains were found in the ventrolateral division of the periaqueductal gray, in the locus coeruleus, in the nucleus tractus spinalis nervi trigemini and in the raphe obscurus, pallidus and magnus, while a widespread and lower grain density was observed in the reticular formation. In the spinal cord the labeling was discretely localized in laminae IV, V and VI of the dorsal horn. The observed distribution of CT binding sites is closely related to the neuroendocrine and analgesic effects of exogenous CT and reinforces the concept of a possible neuromodulatory role proposed for the peptide at brain level.
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            Biologically active salmon calcitonin-like peptide is present in rat brain

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              Amylin injection causes elevated plasma lactate and glucose in the rat

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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                1998
                September 1998
                18 September 1998
                : 68
                : 3
                : 220-228
                Affiliations
                Department of Pharmacology, Chemotherapy and Medical Toxicology, University of Milan, Italy
                Article
                54369 Neuroendocrinology 1998;68:220–228
                10.1159/000054369
                9734007
                © 1998 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: 7, References: 42, Pages: 9
                Categories
                Growth Hormone Regulation

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