Pentobarbital suppresses human brain sodium channels.

Ion channels, key components in neuronal signal transmission and processing, are likely to be important molecular sites of anesthetic action. Sodium channels from human brain tissue were incorporated into planar lipid bilayers in the presence of batrachotoxin and exposed to the anesthetic pentobarbital. This barbiturate, in a dose-dependent manner and at clinically relevant concentrations, reduced fractional channel open time independent of membrane potential, and interfered with the steady-state activation process.