Background Previous studies have provided evidence that clinical levels of propofol alter the
functions of voltage-dependent sodium channels, thereby inhibiting synaptic release of
glutamate. However, most of these experiments were conducted in the presence of sodium-
channel activators, which alter channel inactivation. This study electrophysiologically
characterized the interactions of propofol with unmodified sodium channels. Methods
Sodium currents were measured using whole-cell patch-clamp recordings of rat brain IIa …