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Can J Anaesth. 2011 Feb;58(2):139-48. doi: 10.1007/s12630-010-9420-3. Epub 2010 Dec 18.

Sleep and general anesthesia.

Author information

1
Biophysics Section, Blackett Laboratory, Division of Cell and Molecular Biology, Imperial College, South Kensington, London, SW7 2AZ, UK. n.franks@imperial.ac.uk

Abstract

PURPOSE:

The mechanisms through which general anesthetics cause reversible loss of consciousness are characterized poorly. In this review, we examine the evidence that anesthetic-induced loss of consciousness may be caused by actions on the neuronal pathways that produce natural sleep.

PRINCIPAL FINDINGS:

It is clear that many general anesthetics produce effects in the brain (detected on electroencephalogram recordings) that are similar to those seen during non-rapid eye movement non-(REM) sleep. Gamma aminobutyric acid (GABA)ergic hypnogenic neurons are thought to be critical for generating non-REM sleep through their inhibitory projections to wake-active regions of the brain. The postsynaptic GABA(A) receptor is a major molecular target of many anesthetics and thus may be a point of convergence between natural sleep and anesthesia. Furthermore, we also present growing evidence in this review that modulating wake-active neurotransmitter (e.g., acetylcholine, histamine) release can impact on anesthesia, supporting the idea that this point of convergence is at the level of the brain arousal systems.

CONCLUSIONS:

While it is clear that general anesthetics can have effects at various points in the sleep-wake circuitry, it remains to be seen which points are true anesthetic targets. It will be challenging to separate non-specific effects on baseline arousal from a causal mechanism. Sophisticated experimental approaches are necessary to address basic mechanisms of sleep and anesthesia and should advance our understanding in both of these fields.

PMID:
21170623
DOI:
10.1007/s12630-010-9420-3
[Indexed for MEDLINE]
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