Fig. 1. Tonic block of tetrodotoxin-sensitive Na⁺currents in ND7/23 cells by buprenorphine. (A ) Representative current traces of Na⁺channels in presence of increasing concentrations of buprenorphine (V^h= −140 mV). Currents were activated by 5 ms-long test pulses from −140 mV to 50 mV in intervals of 20 s. (B ) Concentration-dependent block of resting Na⁺channels examined at the holding potential (V^h= −140 mV) and of inactivated channels examined at the physiologic V^h−80 mV. Peak amplitudes of Na⁺currents at different drug concentrations were normalized with respect to the peak amplitude in control solution and plotted against the concentration of buprenorphine. The solid lines  are fits of the data with the Hill equation. (C ) Representative current traces of the voltage-dependent activation of Na⁺channels in ND7/23 in control solution and (D ) in presence of 30 μM. Cells were held at −140mV and currents were activated by depolarizing steps from −120 to 20 mV in steps of 10 mV. (E ) Shift of the voltage-dependent activation of Na⁺currents by buprenorphine at 3 and 30 μM. Currents were activated by 5 ms-long test pulses from −140 mV to −20 mV in steps of 10 mV. The conductance was calculated by the equation g^m= I^Na/(E  ^m–E  ^rev), where I^Nais the peak current, E  ^mis the amplitude of the voltage step, and E  ^revis the reversal potential. The solid lines  are fits by the Boltzmann function. (F ) Shift of steady-state inactivation of Na⁺currents by buprenorphine at 3 and 30 μM. Normalized currents of are plotted as a function of the conditioning prepulse potentials and the solid lines  are fits of the data with the Boltzmann function. 100 ms-long prepulses from −140 to 10 mV in steps of 10 mV were followed by a 5-ms long test pulse to 50 mV. Cells were held at −140 mV. Bupr. = buprenorphine.