The release of endogenous noradrenaline in the anterior hypothalamus was studied with microdialysis perfusion in freely moving rats that were subjected to immobilization stress. Experiments were carried out in sham-adrenalecto-mized and adrenalectomized rats that were first given drinking water containing corticosterone for 5 days following surgery and then switched to a corticosterone-free diet the day before stress application. One group of these adrenalectomized animals was injected with dexamethasone. Basal release of noradrenaline collected in 20-min fractions was similar in the three groups of animals and averaged 24 fmol. The recovery of the probe was about 10%. In sham-adrenalectomized rats application of 20-min immobilization stress increased noradrenaline release to 310% of baseline in the sample collected during stress application. A significant increase (+175% of baseline) was still observed in the next 20-min sample. Subsequent values were all identical to baseline. In adrenalectomized rats lacking exogenous corticosterone the stress-induced release of noradrenaline was prolonged with noradrenaline levels remaining elevated for 2 h after the onset of stress. The total noradrenaline release during this entire period was about 2.5 times higher in adrenalectomized than in sham-operated rats. However, the maximal increase during the period of immobilization was not significantly affected. Treatment with dexamethasone prevented the prolonged increase in noradrenaline release but did not affect the increase during the period of stress. While glucocorticoids do not appear to affect the increased release of NA in the anterior hypothalamus during the period of stress, they act to limit the duration of this activation after the application of stress. Our results show that glucocorticoids affect the stress-induced activation of the catecholaminergic systems innervating the anterior hypothalamus, i.e. the region of the paraventricular nucleus, and suggest that glucocorticoids exert on these systems a homeostatic, rather than a negative feedback, regulation during their stress-induced activation.

This content is only available via PDF.
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.
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.
You do not currently have access to this content.