Analysis of quantal acetylcholine noise at end‐plates of frog muscle during rapid transmitter secretion.

1. Using the theory of noise analysis an attempt was made to measure frequency and amplitude of miniature end-plate potentials (MEPPs) under conditions of vigorous transmitter release. Frog sartorius muscles were incubated in a depolarizing (32 mM-K+) medium which lacked Ca2+ to prevent transmitter release. Subsequently, when the membrane potential had become stable at about -40 mV, end-plates were superfused with 4 mM-Ca2+-containing medium for 1 min periods with 5 min intervals between the superfusions. 2. Most junctions ('fast' type) responded to Ca2+ with a relatively large, noisy depolarization (5.8-14.5 mV) which subsided rapidly during subsequent challenges with Ca2+. Other junctions ('slow' type) responded with only 1-1.6 mV depolarizations which were rather well sustained during the consecutive Ca2+ applications. 3. From the variance, E2, and the depolarization, V, caused by Ca2+ the frequency n and amplitude factor q of the MEPPs were calculated. Values of n were 3-4 x 10(4) and 0.1-1 x 10(4) s-1 in the fast- and slow-type junctions, respectively. The mean value of q was 0.16 mV; it remained more or less constant in the fast-type junctions, but tended to decline in the slow-type junctions. 4. As expected, cholinesterase inhibitors potentiated V and E2 as well as individual MEPPs. However, no advantage could be taken from this finding, since these drugs caused burst-like peaks superimposed on the voltage signal, precluding application of noise analysis. 5. The results strongly suggest that, at least in the fast-type junctions, K+ caused an extremely rapid depletion of the store of transmitter quanta, whose mean size did not change appreciably in the course of the experiment. However, in the slow-type junctions during prolonged incubation, it cannot be excluded that the gradual decline of q was due to the release of newly formed, unripe quanta.