ON THE POSSIBLE ORIGIN OF GIANT OR SLOW-RISING MINIATURE END-PLATE POTENTIALS AT THE NEUROMUSCULAR-JUNCTION

Giant or slow-rising miniature end-plate potentials (GMEPPs) caused by vesicular release of acetylcholine (ACh) occur at any time in about 5 0% of mouse diaphragm neuro muscular junctions, but generally at frequ encies less than 0.03 s(-1). Their frequency is, unlike that of miniat ure end-plate potentials (MEPPs), not affected by nerve terminal depol arization. Unlike MEPPs and stimulus-evoked end-plate potentials, GMEP Ps have a prolonged time-to-peak and show an increase in time-to-peak with amplitude, By using these differences in amplitude and time cours e, GMEPPs can be separated from MEPPs. In contrast to MEPPs, GMEPPs ar e not blocked by botulinum neurotoxin type A. GMEPPs have a greater te mperature sensitivity than MEPPs, disappearing at temperatures below 1 5 degrees C, Long-term paralysis by botulinum toxin and certain drugs which inhibit protein kinase C or affect actin filament polymerization (cytochalasins) enhance the frequency of GMEPPs. End-plate current re cordings show that similar postsynaptic ACh receptors are activated by MEPPs and GMEPPs, It is suggested that GMEPPs are not caused by mecha nisms involved in ''regulated'' neurotransmitter release but are gener ated by ''constitutive secretion''.