Methods of activation and the role of calcium/calmodulin-dependent protein kinase II in the regulation of acetylcholine secretion in the motor synapses of mice

Tarasova, E.O.; Gaydukov, A.E.; Balezina, O.P.

Авторы: Tarasova E.O., Gaydukov A.E., Balezina O.P.
Журнал: Neurochemical Journal
Том: 9
Номер: 2
Год издания: 2015
Издательство: Maik Nauka/Interperiodica Publishing
Местоположение издательства: Russian Federation
Первая страница: 101
Последняя страница: 107
DOI: 10.1134/s1819712415020099
Аннотация: In electrophysiological studies of neuromuscular junctions of mice, it was demonstrated that evoked release of mediator triggered by calcium influx via P/Q-calcium channels in the terminals remains unchanged in the presence of KN-62, a blocker of calcium/calmodulin-dependent protein kinase II(CaMKII). Disinhibition of L-type calcium channels by blockage of phosphatase calcineurin with cyclosporine A (CsA) causes an increase in the quantal content of endplate potentials (EPP’s QC), which can be prevented by the L-type calcium channel blocker nitrendipine, as well as by preliminary inhibition of CaMKII with KN-62. Thus, the acetylcholine (ACh) release is enhanced with involvement of activated CaMKII only after disinhibition of L-type calcium channels. When disinhibition of L-type calcium channels was induced by suppression of calcium-activated BK-type potassium channels with paxilline, an increase in EPP’s QC was also observed. The conclusion was drawn that in motor synapses of mice, calcium influx via P/Q-type calcium channels cannot provide selective activation of CaMKII to facilitate transmission. However, disinhibition of L-type calcium channels results in the activation of CaMKII, which is accompanied by a persistent increase in evoked ACh release.
Добавил в систему: Гайдуков Александр Евгеньевич

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Methods of activation and the role of calcium/calmodulin-dependent protein kinase II in the regulation of acetylcholine secretion in the motor synapses of miceстатья

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