Neuroendocrinology
Original Paper
Effects of Pituitary Beta-Endorphin Secretagogues on the Concentration of Beta-Endorphin in Rat Cerebrospinal Fluid: Evidence for a Role of Vasopressin in the Regulation of Brain Beta-Endorphin ReleaseBarna I. · Sweep C.G.J.F. · Veldhuis H.D. · Wiegant V.M. · De Wied D.Rudolf Magnus Institute, Department of Pharmacology, Medical Faculty, University of Utrecht, The Netherlands
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Article / Publication Details
Received: January 30, 1989
Accepted: June 05, 1989
Published online: April 03, 2008
Issue release date: 1990
Number of Print Pages: 7
Number of Figures: 0
Number of Tables: 0
ISSN: 0028-3835 (Print)
eISSN: 1423-0194 (Online)
For additional information: https://www.karger.com/NEN
Abstract
The concentration of β-endorphin-immunoreactivity (βE-IR) in cerebrospinal fluid (CSF) and plasma of rats was determined following intracerebroventricular (ICV) treatment of conscious animals with substances known to stimulate the release of βE and other pro-opiomelanocortin (POMC)-derived peptides at the level of the anterior and intermediate lobes of the pituitary. The β-adrenoceptor agoinst isoproterenol (ISO) did not influence the concentration of βE-IR in CSF collected 5–60 min after ICV administration of doses ranging from 3 to 30,000 pg/rat. Plasma βE-IR levels, however, were significantly increased 20 min following ICV injection of 30,000 pg ISO. ICV treatment of animals with ovine corticotropin-releasing factor (CRF; 30–30,000 pg/rat) also did not affect CSFlevels of βE-IR, whereas CRF in a dose of 30 pg significantly decreased, and in doses of 300–30,000 pg enhanced plasma βE-IR concentrations as determined by 20 min following treatments. ICV injection of arginine8-vasopressin (AVP) in doses of 10–1,000 pg/rat dose-dependently elevated the βE-IR concentration in CSF without affecting plasma βE-IR levels. This AVP-induced increase in CSF βE-IR was maximal 20–35 min and βE-IR levels had returned to basal 60 min following treatment. The data indicate that AVP and not ISO and CRF is a stimulator of CSF levels of βE-IR. As βE-IR in CSF likely originates from brain POMC neurons, these results suggest the hot vasopressin may be a physiological regulator of brain POMC activity, and may act as a releasing factor for POMC-derived peptides in the brain.
© 1990 S. Karger AG, Basel
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Article / Publication Details
Received: January 30, 1989
Accepted: June 05, 1989
Published online: April 03, 2008
Issue release date: 1990
Number of Print Pages: 7
Number of Figures: 0
Number of Tables: 0
ISSN: 0028-3835 (Print)
eISSN: 1423-0194 (Online)
For additional information: https://www.karger.com/NEN
Copyright / Drug Dosage / Disclaimer
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.
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