The Contribution of L-Type Calcium Channels to Acetylcholine Secretion in Frog and Mouse Neuromuscular Junctions with Ac
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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 A. N. Tsentsevitsky,1,2 V. F. Khuzakhmetova,1,2 E. F. Khaziev,1,2 and I. V. Kovyazina1,2,3
Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 105, No. 10, pp. 1271–1282, October, 2019. Original article submitted June 24, 2019. Revised version received July 23, 2019. Accepted August 3, 2019. We report here experiments addressing the contribution of L-type Ca2+ 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 Ca2+ 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 Ca2+ levels. A fluorescence method was used to measure calcium transients reflecting the integral influx of Ca2+ into nerve endings; computer modeling was applied to the processes underlying exocytosis in the presence of the two types of Ca2+ channel (N and L) and with different durations of nerve ending action potentials. In frog synapses, L-type Ca2+ channels were found to contribute to evoked acetylcholine secretion in the presence of active K+ channels, but only in the presence of a depressed Ca2+ 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 Ca2+ 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. Keywords: neuromuscular synapse, potassium channel, calcium channel, acetylcholine.
The major presynaptic Ca2+ channels initiating neurosecretion in neuromuscular synapses are N-type channels (Cav2.2) in amphibia, and P/Q-type channels in mammalian synapses (Cav2.1) [1, 2]. Previous studies have shown that Ca2+ influx into nerve endings via L-type Ca2+ channels (Cav1.1) also makes a contribution to the process of evoked quantum acetylcholine (ACh) secretion in frog and mouse motor synapses [3–7]. Immunohistochemical analysis demonstrated the existence of L-type Ca2+ channels in neuromuscular contacts in rats (the Cav1.2 subtype) and frogs (Cav1.3 and Cav1.4) [8, 9].
Characteristic features of L-type Ca2+ channels are their high activation threshold, the long time period spent in the open state, Ca2+-dependent inactivation, and the fact that they are located remote from the zones at which synaptic vesicles are released [2]. The prolonged influx of Ca2+ through these channels may by due to the later release of transmitter quanta, apparent as an increase in the fraction of postsynaptic responses with longer synaptic delays [8, 9]. Some
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