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38 - REM sleep in patients with depression

from Section V - Functional significance

Published online by Cambridge University Press:  07 September 2011

By
Axel Steiger  and
Harald Murck
Edited by
Birendra N. Mallick ,
S. R. Pandi-Perumal ,
Robert W. McCarley  and
Adrian R. Morrison
Axel Steiger
Affiliation:
Max Planck Institute of Psychiatry, Germany
Harald Murck
Affiliation:
Philipps-University of Marburg, Germany
Birendra N. Mallick
Affiliation:
Jawaharlal Nehru University
S. R. Pandi-Perumal
Affiliation:
Somnogen Canada Inc, Toronto
Robert W. McCarley
Affiliation:
Harvard University, Massachusetts
Adrian R. Morrison
Affiliation:
University of Pennsylvania
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Summary

Summary

Disinhibition of REM sleep is a characteristic finding in patients with major depression. REM disinhibition includes shortened REM latency, prolonged first REM periods, and increased REM density (measure of the frequency of rapid eye movements). REM latency, but not REM density, is influenced by age. REM-sleep changes appear to be closely related to the development and the course of depression. A relationship between REM-sleep changes before treatment and treatment outcome is suggested by several studies. REM density is elevated in healthy subjects who have a high genetic load for affective disorders. Most antidepressants suppress REM sleep in patients, normal controls, and laboratory animals. REM-sleep suppression appears to be a distinct hint for the antidepressive properties of a substance, whereas it is not absolutely required. REM-sleep variables during treatment with antidepressants appear to predict the course of the illness. The noradrenergic locus coeruleus and the serotonergic dorsal raphe nuclei, the cholinergic nuclei, and the nucleus of the solitary tract (NTS) are involved in sleep and mood regulation. Hyperaldosteronism has been demonstrated in major depression. Subchronic aldosterone administration can induce anxiety-like behavior. Because of the unusual presence within the brain of both mineralocorticoid receptors and 11-β hydroxysteroid dehydrogenase (11-β HSD), the NTS can act as the gate of the influence of peripheral aldosterone into the brain. Importantly, aldosterone secretion is closely related to the REM/non-REM cycle and is sensitive to sleep manipulations. Hypersecretion of corticotropin-releasing hormone (CRH), the key hormone of the hypothalamo–pituitary–adrenocortical system appears to participate in the pathophysiology of REM-sleep disinhibition. This is supported by increased time spent in REM sleep in mice overexpressing corticotropin-releasing hormone (CRH) in the brain. Furthermore CRH-receptor-type 1 antagonism seems to induce normalization of the REM-sleep changes related to the depression.

Type
Chapter
Information
Rapid Eye Movement Sleep
Regulation and Function
 , pp. 383 - 394
Publisher: Cambridge University Press
Print publication year: 2011

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