Modification of sodium and potassium channel gating kinetics by ether and halothane.

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Abstract
The effects of ether and halothane on the kinetics of Na and K currents were investigated in the crayfish [Procambarus clarkii] giant axon. Both general anesthetics produced a reversible, dose-dependent speeding up of Na current inactivation at all membrane potentials, with no change in the rising phase of the currents. Double-pulse inactivation experiments with ether showed faster inactivation, but the rate of recovery from inactivation at negative potentials was not affected. Ether shifted the midpoint of the steady-state fast inactivation curve in the hyperpolarizing direction and made the curve steeper. The activation of K currents was faster with ether present, with no change in the voltage dependence of steady-state K currents. Ether and halothane perturb the structure of lipid bilayer membranes; the alterations in Na and K channel gating kinetics are consistent with the hypothesis that the rates of the gating processes of the channels can be affected by the state of the lipids surrounding the channels, but a direct effect of ether and halothane on the protein part of the channels cannot be ruled out. Ether did not affect the capacitance of the axon membrane.