Variability of quantal events in control solution and after cholinesterase blockade in frog

Amplitudes of miniature end-plate currents (AMEPCs) as well as their time constants of decay (TMEPCs) contribute to the amplitudes of miniature end-plate potentials and hence determine their mean values and variability. Larger mean amplitudes of miniature end-plate potentials observed after cholinesterase blockade result from both greater mean AMEPCs and greater mean TMEPCs. However, enhanced variability of amplitudes of miniature end-plate potentials is a result mainly of greater variability of TMEPCs. This occurs almost exclusively because the amplitude dependence of TMEPCs becomes markedly enhanced. Although the scatter of TMEPCs about TMEPC vs AMEPC curve is also larger, it does not contribute much to the increased variability of TMEPCs. The marked amplitude dependence of TMEPCs indicates that repetitive binding strongly depends on the quantal size--the number of acetylcholine molecules released per quantum, and suggests that if a quantum is the result of a release of several vesicles, then they should be released very close to each other. Marked amplitude dependence of TMEPCs also shows that, with cholinesterase inhibited, the quantal size can be estimated not only from AMEPCs, but also from TMEPCs. Greater scatter of TMEPCs from the TMEPC vs AMEPC curve is of more obscure origin and probably results because repetitive binding occurs over enlarged "critical areas" with more variable density of acetylcholine receptors.