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

      Ibotenic Acid Lesions in the Bed Nucleus of the Stria terminalis Attenuate Conditioned Stress-Induced Increases in Prolactin, ACTH and Corticosterone

      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.


          The contribution of the bed nucleus of the stria terminalis (BST) to the expression of stress-induced increases in ACTH/corticosterone, prolactin and renin secretion was assessed. Neurons in the lateral part of the BST were destroyed with bilateral injections of the cell-selective neurotoxin ibotenic acid (1.5 µg in 0.1 µl of solution per side). Two weeks later, the rats were stressed using an immobilization or conditioned stress paradigm. Rats with lesions in the lateral part of the BST showed attenuated ACTH and corticosterone responses to conditioned stress. Bilateral ablation of lateral BST significantly reduced the prolactin secretory response to conditioned stress. The same lesions had no effect upon plasma increases in renin that occur in response to conditioned stress. Also, destruction of neurons in the BST did not affect immobilization-induced increases in ACTH, corticosterone, prolactin or renin. Previous studies have demonstrated that ibotenic acid lesions in the central amygdala reduce corticosterone and renin response to conditioned stress. Thus, both the BST and central amygdala are important for the adrenocortical response to conditioned stress. Neurons in the central nucleus of the amygdala are part of the circuitry that mediates renin responses to conditioned stress. Neurons in the BST are important for the full expression of prolactin responses to conditioned stress. The neuronal circuitry and stressor specificity in the mediation of prolactin, renin and ACTH/corticosterone responses are discussed.

          Related collections

          Author and article information

          S. Karger AG
          08 April 2008
          : 57
          : 3
          : 517-524
          Departments of aCell Biology, Neurobiology and Anatomy bPharmacology, Loyola Stritch School of Medicine, Maywood, Ill., cOregon Regional Primate Research Center, Beaverton, Oreg., USA
          126400 Neuroendocrinology 1993;57:517–524
          © 1992 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: 8
          Original Paper


          Comment on this article