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BJA Advance Access originally published online on June 9, 2009
British Journal of Anaesthesia 2009 103(1):61-69; doi:10.1093/bja/aep144
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© The Author [2009]. Published by Oxford University Press on behalf of The Board of Directors of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournal.org

Sodium channels and the synaptic mechanisms of inhaled anaesthetics

H. C. Hemmings, Jr.1,2,*

1 Department of Anesthesiology
2 Department of Pharmacology, Weill Cornell Medical College, 1300 York Avenue, New York, NY 10021, USA

* E-mail: hchemmi{at}med.cornell.edu

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.

Keywords: anaesthetics volatile; anaesthetics volatile, halogenated hydrocarbons; nerve, neurotransmitters; pharmacology, anaesthetic action; pharmacology, neurotransmission


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