PMC

A: Representative traces of inward currents in a TC neuron for control, 1 mM octanol, and washout in response to voltage steps from V_h of −100 mV to V_t −50 mV. B: Normalized peak amplitude (averaged data from 5 cells) is plotted against the time course, showing 10 min-long application of 1 mM octanol (horizontal bar) and consecutive washout. After washout, T-current reached only about 55% of control level. Inset: Same protocol (n = 5 cells) for application of 30 µM octanol (horizontal bar). Note stable current amplitudes during applications of octanol. For clarity, error bars have been omitted. C: Concentration-response relationship between percentage of peak current inhibition and escalating concentrations of octanol. Averaged data points (n = 22) were fitted with a Hill equation, giving an IC₅₀ = 287 ± 15 µM, slope = 1.84 ± 0.16, and nearly complete (90%) maximal current inhibition. For each concentration, statistical analysis was done separately: 30 µM octanol: 2.2 ± 4.3% inhibition, p = 0.25; 100 µM octanol: 10.0 ± 2.7%, p < 0.05; 300 µM octanol: 47.0 ± 5.7%, p < 0.0001; 1,000 µM octanol: 79.4 ± 5.0%, p < 0.0001; 2,000 µM octanol: 87.7 ± 5.6%, p < 0.0001.

A: Dose-response curves showing the effects of Octanol on the cycle frequency. The mean frequency of D-glutamate- and NMDA-induced motor activity patterns were reduced by Octanol concentrations >400 μM in a dose-dependent manner. B: Dose-response curves showing the effects of Octanol on the peak EMG amplitude for D-glutamate- and NMDA-induced activity. The amplitude of D-glutamate- and NMDA-induced activity was inhibited by Octanol concentrations >400 μM in a dose-dependent manner. C: Paired recordings from the flexor and extensor muscles showing the effects of Octanol on D-glutamate- (right) and NMDA-induced (left) motor activity patterns. Notice that the cycle frequency and EMG amplitude were reduced in the presence of 700 μM Octanol (lower pair of records) compared to the control saline (upper pair of records). Abbreviations, same as in .

Effect of the anesthetic octanol on the permeation rate. (Left) Permeation of R6G through DPPC/DPPG (95:5) LUV at 37.1°;C after the sudden addition of 1-octanol at the time indicated by the arrow. Permeation increases dramatically. (Center) Permeation in the absence and the presence of 3.5 mol % and 7 mol % octanol in the membrane at 37.6°C. (Right) Heat capacity profiles of the lipid LUV in the absence of octanol (see ) and in the presence of 7 mol % octanol. In the presence of octanol, the melting events occur at lower temperature. The solid circles indicate the permeation rates at 37.6°C in the absence of octanol and in the presence of 7 mol % octanol. The increase in permeability caused by octanol correlates nicely with the increase in heat capacity at 37.6°C.

Effects of ethanol (190 mM) and octanol (0.057 mM) on I–V curves of sodium currents in oocytes expressing Na_v1.2 and Na_v1.8. (A) Representative I_Na traces from oocytes expressing Na_v1.2 in the absence and presence of ethanol or octanol. Currents were elicited by 50-ms depolarizing steps between −80 and 50 mV in 10-m V increments from holding potentials of −90 mV. (B) Effects of ethanol and octanol on representative I–V curves elicited from V_max holding potential for Na_v1.2. (C) Effects of ethanol and octanol on representative I–V curves elicited from V_1/2 holding potential in oocytes expressing Na_v1.2. (D) Representative I_Na traces in oocytes expressing Na_v1.8 in the absence and presence of ethanol and octanol. (E) Effects of ethanol and octanol on representative I–V curves elicited from a V_max holding potential in oocyte expressing Na_v1.8. (F) Effects of ethanol and octanol on representative I–V curves elicited from a V_1/2 holding potential in oocyte expressing Na_v1.8.