Вклад кальциевых каналов L-типа в секрецию ацетилхолина в нервно-мышечных соединениях лягушки и мыши при активных и инактивированных потенциал-зависимых калиевых каналах

Abstract

In this work, the contribution of L-type Ca2+ channels to the evoked secretion of acetylcholine from the frog and mouse motor nerve endings with active and inactivated potential-dependent K+ channels was studied. The effects of the specific Ca2+ blocker of the L-type channels nitrendipine on the quantal content of endplate currents and the timing of acetylcholine quanta secretion in intact preparations and after the preliminary blockade of potential-activated K+ channels with 4-aminopyridine (4-AP) were evaluated under conditions of a decreased and physiological level of ambient Ca2+. Fluorescent measurement of calcium transient reflecting the integral input of Ca2+ into the nerve ending was performed as well as the computer simulation of the processes underlying exocytosis assuming the presence of two types of Ca2+ channels (N- and L-types) and varying duration of the nerve action potential. It was shown that in the frog synapses, L-type calcium channels contribute to the evoked secretion of acetylcholine at active K+ channels only under conditions of decreased Ca2+ level; after inactivation of potential-dependent K+ channels, the contribution of L-type channels to the secretory process becomes less significant. At the physiological level of ambient Ca2+, the involvement of L-type channels in the evoked acetylcholine secretion, as in mice synapses, is manifested only under conditions of inactivated potential-dependent K+ channels.