Research article summary (published 3 Aug 2009):

Cortical inhibition during burst suppression induced with isoflurane anesthesia.

Full Abstract

Isoflurane is a widely used anesthetic which safely and reversibly induces deep coma and associated burst suppression (BS) electroencephalographic patterns. Here we investigate possible underlying causes for the state of cortical hyperexcitability which was recently shown to be one of the characteristics of BS. Our hypothesis was that cortical inhibition is diminished during isoflurane-induced BS. Experiments were performed in vivo using intracellular recordings of cortical neurons to assess their responsiveness to stimulations of connected thalamic nuclei. We demonstrate that during BS EPSPs were diminished by 44%, whereas inhibitory potentials were completely suppressed. This finding was supported by additional results indicating that a decrease in neuronal input resistance normally found during inhibitory responses under low isoflurane conditions was abolished in the BS condition. Moreover, removal of inhibition occasionally revealed excitatory components which were absent during recordings before the induction of BS. We also show that the absence of inhibition during BS is not caused by a blockage of GABA receptors, since iontophoretically applied GABA shows receptor availability. Moreover, the concentration of extracellular chloride was increased during BS, as would be expected after reduced flow of chloride through GABA(A) receptors. Also inhibitory responses were reinstated by selective blockage of glial glutamate transporters with dihydrokainate. These results suggest that the lack of inhibition during BS is caused by reduced excitation, probably resulting from increased glial uptake of glutamate stimulated by isoflurane, which creates a diminished activation of cortical interneurons. Thus cortical hyperexcitability during BS is favored by suppressed inhibition.

Author information

Author/s: Ferron, Judy-Fay (JF); Kroeger, Daniel (D); Chever, Oana (O); Amzica, Florin (F);

Affiliation: Department of Stomatology, School of Medical Dentistry, Université de Montreal, Montreal, Quebec H3C 3J7, Canada.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience (J Neurosci), published in United States. (Language: eng)

Reference: 2009-Aug; vol 29 (issue 31) : pp 9850-60

Dates: Created 2009/08/06; Completed 2009/08/21;

PMID: 19657037, status: MEDLINE (last retrieval date: 8/21/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Amino Acid Transport System X-AG - antagonists & inhibitors; metabolism Anesthesia Anesthetics - pharmacology Animals Cats Central Nervous System Agents - pharmacology Cerebral Cortex - drug effects; physiology Chlorides - metabolism Electroencephalography Excitatory Postsynaptic Potentials - drug effects

Excitatory Postsynaptic Potentials - drug effects Extracellular Space - drug effects; metabolism Inhibitory Postsynaptic Potentials - drug effects Isoflurane - pharmacology Kainic Acid - analogs & derivatives; pharmacology Neural Pathways - drug effects; physiology Neuroglia - drug effects; physiology Neurons - drug effects; physiology Thalamus - drug effects; physiology gamma-Aminobutyric Acid - metabolism

Associated Chemicals: Amino Acid Transport System X-AG (0) ; Anesthetics (0) ; Central Nervous System Agents (0) ; Chlorides (0) ; Isoflurane (26675-46-7) ; Kainic Acid (487-79-6) ; dihydrokainic acid (52497-36-6) ; gamma-Aminobutyric Acid (56-12-2)

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