Changes in miniature end-plate currents due to high potassium and calcium at the frog neuromuscular junction

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Abstract
Elevation of extracellular potassium concentration ([K+]0) in cutaneous pectoris neuromuscular junction from 2 to 20 mM slowly increased the variability of the amplitudes of miniature end‐plate currents (AMEPC‐s), (coefficient of variation of AMEPC‐s increased by 73%). Mean AMEPC‐s, however, decreased but not markedly (by 14%). Comparable MEPC changes were observed when [K+] was raised in the presence of choline chloride (50 μM), arguing that MEPC changes were not primarily due to a lower and less uniform vesicular filling. Channel kinetics were not altered by high [K+]O, since the time constant of decay of miniature end‐plate currents (TMEPC‐s) did not change. Acetylcholine clearance from the synaptic cleft, however, appeared to be faster in high [K+O since with cholinesterase blocked throughout, TMEPC‐s were shortened. The changes of spontaneous quantal discharge induced by high [K+]0] can be almost entirely explained by altered spatial distribution of vesicular release if, as recent reports suggest, at high [K+],0, exocytosis appears randomly not only at but also in between the active zones. However, relatively greater frequency of large MEPCs suggests that in high [K+]0 some, and possibly all, quanta are filled above normal levels. High [Ca2+]0 appears to counteract, although not always completely, all changes in spontaneous quantal secretion induced by high [K+]0. It is possible that high [Ca2+]0 reverses the changes in the spatial distribution of vesicular release induced by high [K+]0. However, high [Ca2+]0 also leads to other pre‐ and postsynaptic changes.