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      Serotonin Receptor Subtypes Involved in the Elevation of Serum Corticosterone Concentration in Rats by Direct- and Indirect-Acting Serotonin Agonists

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          Abstract

          The serum corticosterone concentration in rats was increased by injection of quipazine, a relatively nonselective serotonin (5-hydroxytryptamine; 5-HT) agonist, or 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a serotonin agonist selective for the 5-HT<sup>1A</sup> subtype of receptor. The quipazine-induced increase in serum corticosterone was antagonized by 17 different serotonin antagonists; of these, MDL 11939, pirenperone, setoperone, mianserin, LY 281067, ketanserin, ritanserin and clozapine have relatively selective affinity for the 5-HT<sub>2</sub> subtype of receptor. The 8-OH-DPAT-induced increase in serum corticosterone was not antagonized by metergohne, the most potent antagonist of the quipazine effect, but was antagonized by pindolol or penbutolol, 5-HTIA receptor antagonists. Pindolol did not block the effect of quipazine. The results support earlier evidence that serum corticosterone concentration in rats can be increased by activation of either 5-HT<sub>1A</sub> or 5-HT<sub>1</sub> receptors. Indirect-acting serotonin agonists – fluoxetine, L-5-hydroxytryptophan and P<sup>-</sup>chloroamphetamine – also increased serum corticosterone concentrations. The increases elicited by those agents, which earlier had been reported not to be blocked by metergohne pretreatment, also were not blocked by pretreatment with pindolol or with the combination of metergohne and pindolol. Thus, an involvement of a specific serotonin receptor subtype in the actions of these indirect agonists has not been established.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1990
          1990
          03 April 2008
          : 52
          : 2
          : 206-211
          Affiliations
          Lilly Research Laboratories, Eli Lilly & Company, Lilly Corporate Center, Indianapolis, Ind., USA
          Article
          125586 Neuroendocrinology 1990;52:206–211
          10.1159/000125586
          2148812
          © 1990 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
          Pages: 6
          Categories
          Original Paper

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