Mechanism of inhibition of acetylcholine secretion in newly formed mouse synapses involving Ca2+-dependent kinases and voltage-gated K+-channels.

Autor: Bogatcheva PO; Department of Human and Animal Physiology, Biological Faculty, M. V. Lomonosov Moscow State University, Russia. untergang@inbox.ru, Ezhova EV, Balezina OP
Jazyk: English; Russian
Zdroj: Bulletin of experimental biology and medicine [Bull Exp Biol Med] 2010 Aug; Vol. 149 (2), pp. 170-3.
DOI: 10.1007/s10517-010-0899-y
Abstrakt: Nifedipine, a blocker of L-type Ca(2+)-channels, increased quantal content of endplate potentials in newly formed nerve-muscle synapses, while R 24571 (calmodulin inhibitor) and KN 62 (inhibitor of calmodulin-dependent kinase II) did not change it. KN 62 suppressed the increase in quantal content of endplate potentials evoked by nifedipine. Similar to nifedipine, chelerythrine and bisindolylmaleimide I (blockers of protein kinase C) increased quantal content of endplate potentials. In the presence of chelerythrine, nifedipine lost its ability to facilitate secretion of neurotransmitter. 4-Aminopyridine, a blocker of voltage-gated potassium channels, increased quantal content of endplate potentials. In the presence of chelerythrine, 4-aminopyridine induced no additional increase in the quantal content of endplate potentials. In its turn, chelerythrine induced no extra facilitation of secretion in the presence of 4-aminopyridine. It is hypothesized that Ca(2+)-dependent inhibition of secretion results from suppression of calmodulin-dependent kinase II and activation of protein kinase C, which potentiates the work of voltage-gated K(+)-channels.
Databáze: MEDLINE
Externí odkaz: