+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: found

      Use of 125I-Tyr 27 β-Endorphin for the Study of β-Endorphin Binding Sites in Rat Cortex

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          An iodine-labelled derivative of β-endorphin, <sup>125</sup>I-Tyr<sup>27</sup> β<sub>h</sub>-endorphin, was used in carrier-free form to study the binding of β-endorphin to brain opioid receptors. The experiments were carried out with rat cortex membranes in vitro under conditions that gave a high degree of naloxone reversible binding. β<sub>h</sub>-Endorphin and nonradioactive iodo-Tyr<sup>27</sup> β<sub>h</sub>-endorphin were found to be identical in their ability to inhibit the binding of <sup>l25</sup>I-Tyr<sup>27</sup> β<sub>h</sub>-endorphin. Competition experiments demonstrated the existence of binding sites with higher affinity for β-endorphin than for a variety of other opioids, including naturally occurring fragments of β-endorphin. The experiments show that <sup>125</sup>I-Tyr<sup>27</sup> β-endorphin possesses similar binding properties to the unmodified peptide and can be used with the advantages of iodine-<sup>125</sup> as an isotope for the investigation of β-endorphin receptors in brain. In experiments employing <sup>125</sup>I-Tyr<sup>27</sup> β-endorphin 1 -27 as the radioiodinated ligand, binding curves were obtained which showed that β-endorphin 1–31 was more potent than β-endorphin 1–27 in inhibiting the binding of the labelled 27 residue peptide. With both the 27 and 31 residue radioligands, magnesium ion enhanced the specific binding whereas sodium ion and guanylyl-imidodiphosphate had a strong inhibitory effect. The data indicate that β-endorphin 1–27 binds with reduced affinity to the same receptors as β-endorphin 1–31 and like the 31 residue peptide exhibits properties characteristic of an agonist.

          Related collections

          Author and article information

          S. Karger AG
          01 April 2008
          : 43
          : 6
          : 629-634
          aNational Institute for Medical Research, London; bAmersham International, Aylesbury, Bucks., UK
          124592 Neuroendocrinology 1986;43:629–634
          © 1986 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
          Original Paper


          Comment on this article