Abstract
1. General anesthetics at clinical concentrations are known to affect neurotransmitter-gated ion channels in postsynaptic membranes. 2. Volatile anesthetics suppress excitatory transmissions, whereas they potentiate inhibitory chloride currents evoked by GABA or glycine. Hexafluorodiethyl ether (a volatile convulsant) markedly depresses the GABA A response but not the glycine-evoked chloride current or the glutamate-induced excitatory response. 3. Molecular biology has revealed that GABA A receptor is a heteromeric pentamer composed of α, β, γ, δ, and/or ϱ subunits. In baculovirus-Sf9 expression system, the γ subunit was crucial for potentiation of the GABA-induced chloride current by volatile anesthetics. 4. Following sustained presence of GABA and high concentrations of isoflurane, simultaneous washout of both agents evoked a slowly decaying surge current, whose nature is controversial.
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