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

@entity141 @entity1877 @entity934 @entity972
Elevation of extracellular @entity972 concentration ([K+]o) 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 @entity1877 (50 microM), 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. @entity934 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+]o can be almost entirely explained by altered spatial distribution of vesicular release if, as recent reports suggest, at high [K+]o, 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+]o some, and possibly all, quanta are filled above normal levels. High [ @entity141 ]o appears to counteract, although not always completely, all changes in spontaneous quantal secretion induced by high [K+]o. It is possible that high [ @entity141 ]o reverses the changes in the spatial distribution of vesicular release induced by high [K+]o. However, high [ @entity141 ]o also leads to other pre- and postsynaptic changes.
