End-plate current recordings show that similar postsynaptic ACh receptors are activated by MEPPs and GMEPPs. 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. GMEPPs have a greater temperature sensitivity than MEPPs, disappearing at temperatures below 15☌. In contrast to MEPPs, GMEPPs are not blocked by botulinum neurotoxin type A. By using these differences in amplitude and time course, GMEPPs can be separated from MEPPs. Unlike MEPPs and stimulus-evoked end-plate potentials, GMEPPs have a prolonged time-to-peak and show an increase in time-to-peak with amplitude. Their frequency is, unlike that of miniature end-plate potentials (MEPPs), not affected by nerve terminal depolarization. Giant or slow-rising miniature end-plate potentials (GMEPPs) caused by vesicular release of acetylcholine (ACh) occur at any time in about 50% of mouse diaphragm neuro muscular junctions, but generally at frequencies less than 0.03 s −1.
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