The effects of SnCl2 on potentials recorded extracellularly from motor nerve terminals of the bullfrog were studied to elucidate the mechanism of the SnCl2-induced facilitation of evoked transmitter release. Under conditions in which the muscle preparations were pretreated with d-tubocurarine and tetraethylammonium in a K+-free medium, SnCl2 (50 microM) augmented the prolonged positive deflection ascribed to the inward Ca2+ current, an effect which was reduced by addition of Cd2+. The results suggest that SnCl2 could increase Ca2+ entry into the nerve terminals.