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      Effects of Neurointermediate Pituitary Lobectomy on Humoral and Cell-Mediated Immune Responses in the Rat

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          Abstract

          Objective: Chronic stress is characterized by an increased activity of the hypothalamic-pituitary-adrenocortical axis and decreased humoral and cell-mediated immune responses. In the rat, corticosterone is the principal natural immune suppressor. Neurointermediate pituitary lobectomy () in rats induces diabetes insipidus and protracted increases in basal adrenocorticotropin and corticosterone plasma levels, a situation that resembles chronic stress. In this paper, we evaluated the effects of on humoral (hemagglutinin titers and footpad swelling to sheep red blood cells – SRBC) and cell-mediated immune responses (contact hypersensitivity to dinitrochlorobenzene). Methods: The studies were conducted on Wistar rats (body weight 150–200 g) 3 weeks after surgery. For comparisons, nonoperated control rats were used. Results: resulted in an increased water intake. Body weight gain and adrenal, thymus, and spleen weights were within the range of nonoperated controls. Eight days after SRBC immunizations a second SRBC injection into the footpad resulted in a decreased swelling response in rats. The hemagglutinin titers were also reduced in the rats. Conclusions: These results indicate that: (1) reduces humoral immune responses and decreases the cell-mediated immune response; (2) the immune alterations are most likely due to the increased activity of the hypothalamic-pituitary-adrenocortical axis induced by , and (3) animals constitute a valuable paradigm to study hypothalamic-pituitary-immune interactions.

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          Most cited references 2

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          Corticotropin-releasing hormone and pituitary-adrenocortical responses in chronically stressed rats.

          Brain corticotropin-releasing hormone (CRH) concentration and pituitary adreno-cortical responses were examined in chronically stressed rats: body restraint stress (6 h/day) for 4 or 5 weeks. Stressed rats showed a reduction in weight gain. CRH concentration in the median eminence and the rest of the hypothalamus were not different between control and chronically immobilized rats. The anterior pituitary adenocorticotropic hormone (ACTH) concentration was elevated in chronically stressed rats, whereas plasma ACTH and corticosterone levels did not differ from the control values. The median eminence CRH concentration was reduced to the same extent at 5 min after onset of ether exposure (1 min) in chronically immobilized rats and controls. However, plasma ACTH and corticosterone showed greater responses to ether stress in chronically immobilized rats than in control rats. Plasma ACTH and corticosterone responses to exogenous CRH were not different between control and chronically immobilized rats, while the response to arginine vasopressin (AVP) was significantly greater in chronically immobilized rats. These results suggest that chronic stress caused an increase in the ACTH-secreting mechanism and that pituitary hypersensitivity to vasopressin might at least be partly responsible for this.
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            Paradoxical responses of hypothalamic corticotropin-releasing factor (CRF) messenger ribonucleic acid (mRNA) and CRF-41 peptide and adenohypophysial proopiomelanocortin mRNA during chronic inflammatory stress

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              Author and article information

              Journal
              NIM
              Neuroimmunomodulation
              10.1159/issn.1021-7401
              Neuroimmunomodulation
              S. Karger AG
              1021-7401
              1423-0216
              2004
              July 2004
              09 July 2004
              : 11
              : 4
              : 233-240
              Affiliations
              aDepartamento de Fisiología y Farmacología, Centro de Ciencias Básicas, Universidad Autónoma de Aguascalientes, Aguascalientes, México; bDepartment of Laboratory Medicine and Pathobiology, St. Michael’s Hospital, University of Toronto, Toronto, Ont., and cDepartment of Immunology, Faculty of Medicine, University of Manitoba, Winnipeg, Man., Canada
              Article
              78441 Neuroimmunomodulation 2004;11:233–240
              10.1159/000078441
              15249729
              © 2004 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: 5, Tables: 2, References: 33, Pages: 8
              Categories
              Original Paper

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