The effects of zinc (Zn2+) on quantal acetylcholine release at the Torpedo nerve-electroplate junction were analysed by using loose patch electrodes designed to record evoked and spontaneous electroplate currents in a delimited area (electrode diameter of 10-15 microm) of the synaptic region. Zn2+ reduced the amplitude, prolonged the synaptic delay and slowed down the rising phase of all-or-none electroplate currents (EPCs) generated in response to activation of Na+ channels in a preterminal nerve branch. In graded EPCs (generated in response to direct activation of terminal Ca2+ channels), Zn2+ caused a reduction of quantal content but no change in the quantal size or in the minimum synaptic delay. The rise time of graded EPCs was prolonged but their half-decay time was not affected. Miniature EPCs (MEPCs) in control preparations had a widely distributed amplitude distribution but a homogeneous and rapid time course. Conversely, MEPCs in Zn2+-treated tissue exhibited a homogeneous and small amplitude, but a prolonged and more variable time course. Zn2+ at 1 mM caused, by itself, a high occurrence of MEPCs under conditions (flat-edged electrodes) when MEPCs are normally very infrequent. It is concluded that Zn2+ can both activate and inhibit the release mechanism and Zn2+-induced quanta exhibit an abnormal time course. The activation of the release process by Zn2+ or by Ca2+ may result in the production of quanta with different kinetics.