By perineurial recording, the actions of toosendanin on three potassium currents and two calcium currents in the nerve terminal were observed in the intercostal nerve triangularis stein muscle of the mouse. Toosendanin partially blocked the voltage-dependent fast K+ current and irreversibly increased the voltage-dependent slow Ca2+ current. The increase in the Ca2+ current of the nerve terminal accounts for the facilitation of transmitter release and the antibotulismic effect of toosendanin.