STIMULATION of the motor nerve, in addition to producing the synchronous, impulsive release of acetylcholine (ACh) that is recorded electrophysiologically as the endplate potential (e.p.p.)1, also elicits a delayed, asynchronous discharge of ACh quanta that appears as increases in miniature endplate potential (m.e.p.p.) frequencies2-4. The synchronous release of ACh is mediated by the movement of Ca2+ through specific conductance channels activated by depolarisation of the motor nerve ending (for reviews see refs 1, 5 and 6). Although asynchronous release is dependent in some fashion on extracellular (Ca2+) (ref. 4) there seems to be a controversy as to the precise nature of the ionic pathway responsible for this dependence. For example, although it has been suggested that asynchronous evoked release is mediated by residual Ca2+ that enters through the traditional Ca2+ conductance pathway3, results with Mg2+ have suggested the contrary4. Specifically, it has been shown that Mg2+, rather than antagonising the asynchronous release of ACh in Ca2+ solutions, (as would be expected if Ca 2+ moved through the same conductance pathway for both forms of release7-10), actually enhanced the asynchronous discharge of ACh quanta4. The present study investigated the effects of the conventional Ca2+ antagonists, Co2+ and Mg2+, on the asynchronous evoked release of ACh. The results demonstrate that after brief, repetitive stimulation, both ions competitively antagonise asynchronous ACh release in a manner similar to their respective antagonism of synchronous release7,10. We conclude that Ca2+ supports both dispersed and synchronous ACh release through the same conductance pathway.
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