Differential Effects of Rapid Eye Movement Sleep Deprivation and Immobilization Stress on Blood Lymphocyte Subsets in Rats

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Abstract

Objectives: There is growing evidence of the relationship between sleep and the immune response. Studies aimed at elucidating the function of rapid eye movement (REM) sleep have found it difficult to separate the effects due to REM sleep deprivation and the effects due to the stress produced by the deprivation procedure. It has been claimed that immobilization is the main stressor that the animals have to face during the deprivation process. In this study, we analyzed the effects of short-term (24 h) and long-term (240 h) REM sleep deprivation on the distribution of lymphocyte subsets in the peripheral blood of rats. In addition, these effects were compared with those obtained after both short- and long-term stress by immobilization. Methods: Lymphocyte population bearing surface markers such as CD5 (T cells), CD45RA (B cells), CD4 (T helper/inducer cells), CD8 (T suppressor/cytotoxic cells) and CD161 (NK cells) were analyzed using monoclonal antibodies. Lymphocyte subsets were assessed by flow cytometry. Results: Both short- and long-term REM sleep deprivation decreased the percentage of T lymphocytes and induced a significant increase in NK cells. Short-term immobilization induced only a significant increase in the percentage of B lymphocytes and a decrease in the percentage of T lymphocytes, while long-term immobilization did not elicit any change. Conclusion: The present results support the notion that REM sleep deprivation and immobilization stress each exert particular effects on the immune system. These data suggest that the characteristics of the immune response will depend on the nature of the behavioral manipulation.

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Sleep restriction alters the hypothalamic-pituitary-adrenal response to stress.

V F Turek, Sandra K M Drieszen-van der Cruijsen, M Koehl … (2002)

Chronic sleep restriction is an increasing problem in many countries and may have many, as yet unknown, consequences for health and well being. Studies in both humans and rats suggest that sleep deprivation may activate the hypothalamic-pituitary-adrenal (HPA) axis, one of the main neuroendocrine stress systems. However, few attempts have been made to examine how sleep loss affects the HPA axis response to subsequent stressors. Furthermore, most studies applied short-lasting total sleep deprivation and not restriction of sleep over a longer period of time, as often occurs in human society. Using the rat as our model species, we investigated: (i) the HPA axis activity during and after sleep deprivation and (ii) the effect of sleep loss on the subsequent HPA response to a novel stressor. In one experiment, rats were subjected to 48 h of sleep deprivation by placing them in slowly rotating wheels. Control rats were placed in nonrotating wheels. In a second experiment, rats were subjected to an 8-day sleep restriction protocol allowing 4 h of sleep each day. To test the effects of sleep loss on subsequent stress reactivity, rats were subjected to a 30-min restraint stress. Blood samples were taken at several time points and analysed for adrenocorticotropic hormone (ACTH) and corticosterone. The results show that ACTH and corticosterone concentrations were elevated during sleep deprivation but returned to baseline within 4 h of recovery. After 1 day of sleep restriction, the ACTH and corticosterone response to restraint stress did not differ between control and sleep deprived rats. However, after 48 h of total sleep deprivation and after 8 days of restricted sleep, the ACTH response to restraint was significantly reduced whereas the corticosterone response was unaffected. These results show that sleep loss not only is a mild activator of the HPA axis itself, but also affects the subsequent response to stress. Alterations in HPA axis regulation may gradually appear under conditions of long total sleep deprivation but also after repeated sleep curtailment.

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Immobilisation stress induces a paradoxical sleep rebound in rat.

C Rampin, R Cespuglio, N Chastrette … (1991)

An immobilisation stress (IS) of 2 h applied to rats at the beginning of the dark period (12 h), i.e. when the animals are more active, induces during the 10 consecutive h a significant rebound (+92%) of paradoxical sleep (PS) while slow-wave sleep state (SWS) is poorly affected. Two h of sleep deprivation, also applied at the beginning of the dark period and realized either by the platform technique or by maintaining the animals awake with gentle handling, do not affect significantly subsequent SWS and PS. Finally, when repetitive IS are inflicted to the animals (one IS of 2 h every 3 days) an attenuation of the PS rebound is observed. These data suggest that a qualitative aspect of the waking state as in an intense stressful situation might be the source of a hormonal process inducing a PS excess.

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Habituation to repeated stress is stressor specific.

G. Jean Kant, Terence Eggleston, Leigh Landman-Roberts … (1985)

Rats were exposed to 15 min of restraint or footshock or forced running in an activity wheel once a day for 10 days. Control groups were handled only. On the 11th day, rats from each stressor group and controls were exposed to 15 min of one stressor in a crossed design such that all combinations of one chronic stressor and one acute stressor were performed. Rats were sacrificed immediately following removal from their home cage or after 15 min stressor exposure on the 11th day and plasma corticosterone and prolactin and pituitary cyclic AMP levels were determined. There were no measured differences in these stress indices among groups of rats sacrificed immediately upon removal from their home cage on day 11 regardless of previous history on days 1 through 10. Plasma corticosterone and plasma prolactin and pituitary cyclic AMP levels were elevated in all rats exposed to any of the three stressors immediately prior to sacrifice as compared to all rats not exposed to stress immediately before sacrifice. However, plasma prolactin and pituitary cyclic AMP responses to each of the 3 stressors were attenuated in rats which had previous exposure to that specific stressor as compared to rats which had previous experience with a different or no stressor. We conclude that habituation results from behavioral experience with a particular stressor rather than biochemical adaptation resulting from repeated challenge to hormonal and neurochemical systems responsive to stress.

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Author and article information

Journal

Journal ID (publisher-id): NIM

Journal ID (nlm-ta): Neuroimmunomodulation

Journal ID (doi): 10.1159/issn.1021-7401

Title: Neuroimmunomodulation

Publisher: S. Karger AG

ISSN (Print): 1021-7401

ISSN (Electronic): 1423-0216

Publication date Subscription-year: 2004

Publication date (Print): July 2004

Publication date (Electronic): 09 July 2004

Volume: 11

Issue: 4

Pages: 261-267

Affiliations

^aDepartment of Reproductive Biology, and ^bDepartment of Health Sciences, Universidad Autónoma Metropolitana-Iztapalapa, Mexico City, Mexico

Article

Publisher ID: 78445 Other ID: Neuroimmunomodulation 2004;11:261–267

DOI: 10.1159/000078445

PubMed ID: 15249733

SO-VID: 98f93d16-d377-475f-bd99-2ee197490d9f

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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.

History

Date received : 03 March 2003

Date accepted : 30 September 2003

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Figures: 4, Tables: 1, References: 38, Pages: 7

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Differential Effects of Rapid Eye Movement Sleep Deprivation and Immobilization Stress on Blood Lymphocyte Subsets in Rats

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Karger: Endocrinology

Most cited references 18

Sleep restriction alters the hypothalamic-pituitary-adrenal response to stress.

Immobilisation stress induces a paradoxical sleep rebound in rat.

Habituation to repeated stress is stressor specific.

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