Skip to main content
. Author manuscript; available in PMC: 2009 Jul 1.
Published in final edited form as: J Pharmacol Exp Ther. 2008 Apr 23;326(1):270–277. doi: 10.1124/jpet.108.138370

Figure 1.

Figure 1

Inhibitory effects of ethanol (C2) (190 mM) and octanol (C8) (0.057 mM) on sodium channels at different holding potentials. (A) Traces of sodium currents evoked by a 50-ms depolarizing pulse to −20 mV from a holding potential of −90 mV (Vmax) and to −20 mV from a holding potential which induced half maximal current (V1/2), in the absence and presence of ethanol in an oocyte expressing Nav1.2. (B) Time course of ethanol effects on sodium currents of Nav1.2. Currents were elicited by 50-ms depolarizing pulses to −20 mV applied every 10 s from a V1/2 holding potential. The current is normalized to the initial values. Filled circles represent control and washout, and open circles represent currents during ethanol treatment. Ethanol was applied for 3 min. (C) Traces of sodium currents evoked by a 50-ms depolarizing pulse to −20 mV from Vmax and V1/2 in the absence and presence of octanol in an oocyte expressing Nav1.2. (D) Time course of octanol effects on sodium currents of Nav1.2. (E) Percent inhibition of sodium current by ethanol and octanol in oocytes expressing Nav1.2, Nav1.4, Nav1.6, and Nav1.8. Open columns indicate the effect at Vmax, and closed columns indicate the effect at V1/2. V1/2 value of Nav1.2, Nav1.4, Nav1.6, and Nav1.8 were 55.8 ± 0.5, 57.5 ± 2.0, 59.3 ± 0.4 and 43.9 ± 1.4 mV, respectively. Data are mean ± S.E.M. (n = 4–6). Differences between Vmax and V1/2 for each condition are indicated as *, p < 0.05; **, p < 0.01; and ***, p < 0.001 (one-way ANOVA).