Effects of stannous chloride (SnCl2, 30-100 microM) on presynaptic currents recorded from frog neuromuscular junctions were investigated to confirm that increased calcium entry is involved in SnCl2-induced facilitation of the evoked transmitter release. After the potassium channel was blocked by tetraethylammonium (0.1 mM) and 3,4-diaminopyridine (10 microM), SnCl2 (0.1 mM) augmented the prolonged positive deflection of the presynaptic action potential ascribable to calcium inward current, which was thereafter suppressed by the addition of cadmium (0.1 mM). These results suggest that SnCl2 enhances the calcium inward current at the motor nerve terminals.