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21 - GABAergic modulation of REM sleep

from Section IV - Neuroanatomy and neurochemistry

Published online by Cambridge University Press:  07 September 2011

Giancarlo Vanini
Affiliation:
University of Michigan
Ralph Lydic
Affiliation:
University of Michigan
Helen A. Baghdoyan
Affiliation:
University of Michigan
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

Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the adult mammalian brain. GABA receptors are ubiquitous and are highly expressed in many brain areas modulating states of sleep and wakefulness. The consistent finding that drugs that enhance GABAergic transmission also enhance sleep supports the conclusion that endogenous GABA promotes sleep. The effects of GABA on sleep, however, vary as a function of brain region. GABAergic transmission in the pontine reticular formation, the tuberomammillary region of the posterior hypothalamus, and the ventrolateral part of the periaqueductal gray has been shown to promote wakefulness, non-rapid eye movement (NREM) sleep, or rapid eye movement (REM) sleep, respectively. The finding that hypothalamic GABA-containing neurons project to the dorsal raphe nucleus, locus coeruleus, and pontine reticular formation encourages future studies aiming to determine the extent to which these GABAergic neurons play a causal role in the generation and maintenance of REM sleep. Functional neuroanatomical studies have identified neural pathways that contribute to REM-sleep generation. Simultaneous, in vivo single-cell recordings of identified GABAergic neurons combined with direct measures of endogenous GABA offer a productive approach for gaining future insights.

Type
Chapter
Information
Rapid Eye Movement Sleep
Regulation and Function
, pp. 206 - 213
Publisher: Cambridge University Press
Print publication year: 2011

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