Department of Anesthesiology

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Sodium channels and the synaptic mechanisms of inhaled anaesthetics.

TitleSodium channels and the synaptic mechanisms of inhaled anaesthetics.
Publication TypeJournal Article
Year of Publication2009
AuthorsHemmings HC
JournalBr J Anaesth
Volume103
Issue1
Pagination61-9
Date Published2009 Jul
ISSN1471-6771
KeywordsAnesthetics, Inhalation, Humans, Ion Channel Gating, Neurotransmitter Agents, Sodium Channels, Synapses, Synaptic Transmission
Abstract

General anaesthetics act in an agent-specific manner on synaptic transmission in the central nervous system by enhancing inhibitory transmission and reducing excitatory transmission. The synaptic mechanisms of general anaesthetics involve both presynaptic effects on transmitter release and postsynaptic effects on receptor function. The halogenated volatile anaesthetics inhibit neuronal voltage-gated Na(+) channels at clinical concentrations. Reductions in neurotransmitter release by volatile anaesthetics involve inhibition of presynaptic action potentials as a result of Na(+) channel blockade. Although voltage-gated ion channels have been assumed to be insensitive to general anaesthetics, it is now evident that clinical concentrations of volatile anaesthetics inhibit Na(+) channels in isolated rat nerve terminals and neurons, as well as heterologously expressed mammalian Na(+) channel alpha subunits. Voltage-gated Na(+) channels have emerged as promising targets for some of the effects of the inhaled anaesthetics. Knowledge of the synaptic mechanisms of general anaesthetics is essential for optimization of anaesthetic techniques for advanced surgical procedures and for the development of improved anaesthetics.

DOI10.1093/bja/aep144
Alternate JournalBr J Anaesth
PubMed ID19508978
PubMed Central IDPMC2700013
Grant ListGM 58055 / GM / NIGMS NIH HHS / United States
R01 GM058055 / GM / NIGMS NIH HHS / United States