Neuromuscular block produced by polymyxin B: interaction with end-plate channels.

The effect of polymyxin B on the amplitude and kinetics of miniature end-plate currents and acetylcholine-induced current fluctuations was studied in voltage-clamped fibers of the snake. Polymyxin B produced a voltage and concentration dependent reduction in both mean peak MEPC amplitude and the time constant of MEPC decay. A concomitant decrease in mean channel lifetime and single channel conductance indicated that a major mechanism for the neuromuscular block produced by polymyxin B is endplate channel blockade.