Abstract
I studied the role of the voltage-gated Na+ current, INaV, in mediating the effects of general anesthetics, using neuromuscular electrophysiology and computer simulations. Isoflurane-induced slowing of action potential propagation was enhanced in parats1, a hypomorphic mutant of the voltage-gated Na+ channel, providing a physiological correlate of behavioral hypersensitivity. Simulating anesthetic action as inhibition of voltage-dependent Na+ (INaV) slowed spike conduction. Fifty percent reduction of INaV, simulating a para mutation, enhanced the simulated effect of anesthetic. However, the simulated para mutation also enhanced the anesthetic effect when modeled as K+ currents.
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