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The Contribution of L-Type Calcium Channels to Acetylcholine Secretion in Frog and Mouse Neuromuscular Junctions with Active and Inactivated Voltage-Gated Potassium Channels

We report here experiments addressing the contribution of L-type Ca 2+ channels to evoked acetylcholine secretion from frog and mouse motor nerve endings with active and inactivated voltage-gated K + channels. These studies evaluated the effects of the specific L-type Ca 2+ channel blocker nitrendip...

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Published in:Neuroscience and behavioral physiology 2020-09, Vol.50 (7), p.920-927
Main Authors: Tsentsevitsky, A. N., Khuzakhmetova, V. F., Khaziev, E. F., Kovyazina, I. V.
Format: Article
Language:English
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Summary:We report here experiments addressing the contribution of L-type Ca 2+ channels to evoked acetylcholine secretion from frog and mouse motor nerve endings with active and inactivated voltage-gated K + channels. These studies evaluated the effects of the specific L-type Ca 2+ channel blocker nitrendipine on the quantum composition of endplate currents and the time course of the secretion of acetylcholine quanta in intact preparations and after preliminary blockade of voltage-gated K + channels with 4-aminopyridine (4-AP) in medium with depressed and physiological Ca 2+ levels. A fluorescence method was used to measure calcium transients reflecting the integral influx of Ca 2+ into nerve endings; computer modeling was applied to the processes underlying exocytosis in the presence of the two types of Ca 2+ channel (N and L) and with different durations of nerve ending action potentials. In frog synapses, L-type Ca 2+ channels were found to contribute to evoked acetylcholine secretion in the presence of active K + channels, but only in the presence of a depressed Ca 2+ level in the medium; on inactivation of voltage-gated K + channels, the contribution of L-type channels to the secretory process became less significant. At a physiological Ca 2+ level, the involvement of L-type channels in evoked acetylcholine secretion was apparent, as in mouse synapses, only in conditions of blockade of voltage-gated K + channels.
ISSN:0097-0549
1573-899X
DOI:10.1007/s11055-020-00986-z