Zinc ions block rectifier potassium channels and calcium activated potassium channels at the frog motor nerve endings.

The effect of Zn2+ on presynaptic currents was investigated on frog cutaneous pectoris nerve-muscle preparations. Nerve terminal spikes were recorded with extracellular electrodes placed in the perineurial sheaths of motor nerves. Zinc ions reversibly suppressed the component of the waveform associated with K+ currents--unmasking an inward current at the terminal--and induced repetitive firing when were applied to preparations perfused with calcium containing solutions. In experiments in which delayed rectifier channels were blocked by 3,4-diaminopyridine, Zn2+ caused a prolonged and reversible inward current associated with a slight decrease in the peak calcium current generated by 3,4-diaminopyridine. Zinc ions abolished the plateau calcium current produced by the simultaneous action of 3,4-diaminopyridine and tetraethylammonium. Finally, in all the preparations in which the exposure to Zn2+ was prolonged it was observed a dramatic and irreversible reduction of the presynaptic currents. These results suggest that Zn2+ has, at least, four different effects on presynaptic currents: (1) blockade of delayed rectifier potassium currents, (2) blockade of calcium-activated potassium currents, (3) blockade of calcium currents and (4) a delayed and irreversible disruption of all ionic conductances of the terminal.