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

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 ( A MEPC ‐s ), (coefficient of variation of A MEPC ‐s increased by 73%). Mean A MEPC ‐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 ( T MEPC ‐s ) did not change. Acetylcholine clearance from the synaptic cleft, however, appeared to be faster in high [K + O since with cholinesterase blocked throughout, T MEPC ‐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 MEPC s suggests that in high [K + ] 0 some, and possibly all, quanta are filled above normal levels. High [Ca 2+ ] 0 appears to counteract, although not always completely, all changes in spontaneous quantal secretion induced by high [K + ] 0 . It is possible that high [Ca 2+ ] 0 reverses the changes in the spatial distribution of vesicular release induced by high [K + ] 0 . However, high [Ca 2+ ] 0 also leads to other pre‐ and postsynaptic changes.