Abstract

The effects of batrachotoxin (BTX) on isolated skeletal muscle preparations of the rat have been studied with intracellular micro-electrodes. At 37°C, BTX produced a complete depolarization of the muscle fiber and a block of its action potential. Concomitantly, a transient high-frequency discharge of miniature end-plate potentials and an increase in miniature end-plate potential and end-plate potential amplitudes was observed. Subsequently, the amplitude of miniature end-plate potentials and end-plate potentials decreased and there was failure of transmission. Micro-iontophoretic application of acetylcholine at end-plate regions of muscles treated with BTX revealed that the block of transmission was not postsynaptic, but presynaptic, in origin. Tetrodotoxin antagonized the effect of BTX on resting membrane potential and on spontaneous transmitter release. The reduction of the external sodium concentration to 5 mM also antagonized the depolarizing effect of BTX on the muscle membrane. Increasing the external calcium concentration to 15 mM delayed the onset of BTX effects, but did not completely reverse the depolarization previously induced by the poison. It is concluded that BTX produces these effects by selectively increasing sodium permeability, thus causing depolarization of the membrane and transiently increasing the spontaneous and stimulus-evoked transmiter release.