title: Analysis of quantal acetylcholine noise at end-plates of frog muscle during rapid transmitter secretion.
abstract: 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.
authors.affiliation: Department of Pharmacology, University of Leiden, The Netherlands.
authors.forename: P C
authors.initials: PC
authors.lastname: Molenaar
authors.forename: B S
authors.initials: BS
authors.lastname: Oen
mesh_terms: D000109:Acetylcholine / Q000502:physiology*; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D066298:In Vitro Techniques; D009045:Motor Endplate / Q000502:physiology*; D009132:Muscles / Q000294:innervation*; D009469:Neuromuscular Junction / Q000502:physiology*; D011896:Rana temporaria; D013997:Time Factors
chemical_list: D002800:Cholinesterase Inhibitors; D000109:Acetylcholine; D002118:Calcium