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Effects of procaine on ionic conductances of end-plate membranes.

The ionic mechanisms underlying the prolongation of the end-plate potential caused by application of procaine have been studied by means of voltage clamp techniques with the sartorius muscle fibers of the frog. The end-plate currents were recorded when the membrane was clamped at various potential levels in the muscle treated with glycerol to avoid contraction. Before application of procaine, the sodium component of the end-plate current measured at the equilibrium potential for potassium (-100 mV) was larger in peak amplitude and slower in decay than the potassium component measured at the equilibrium potential for sodium (+50 mV). The end-plate conductance was constant at the membrane potentials ranging from +50 to -100 mV but decreased slightly at inside more negative membrane potentials. The equilibrium potential for the end-plate current was estimated to be -4.2 mV on an average. Procaine (3.6 x 10-5 ∼ 3.6 x 10-4 M) suppressed the peak amplitudes of both sodium and potassium components of the end-plate current, the sodium current being slightly more affected than the potassium current. The equilibrium potential for the end-plate current was not significantly affected by procaine. The time course of the sodium current underwent marked changes by treatment with procaine; the time to peak was shortened, and the initial falling phase was accelerated and was followed by a very slow terminal phase. The current-voltage relation for the terminal current was different from that for the peak current. The time to peak potassium current was not affected by procaine, but the falling phase was slowed. The dose-response relations for the time parameters of the end-plate current are different from those for the peak amplitude, suggesting that different mechanisms are involved. The possibility of separate sodium and potassium ionic channels in the end-plate membrane is discussed.