Volatile anesthetics significantly suppress central and peripheral mammalian sodium channels.

1. Voltage-dependent sodium channels are important for neuronal signal propagation and integration. 2. Non-mammalian preparations, such as squid giant axon, have sodium channels which have been found to be insensitive to clinical anesthetic concentrations. 3. On the other hand, sodium channels from mammalian neurons are much more sensitive to block by volatile anesthetics. 4. Due to a significant hyperpolarizing shift in steady-state inactivation, IC50s for sodium channel block at potentials close to the resting membrane potential overlapped with clinical anesthetic concentrations. 5. Hence, sodium channels in mammalian neurons may be sensitive molecular targets of volatile anesthetics.