Calmodulin inhibitor W-7 did not cause changes in the quantal content of postsynaptic endplate potentials (EPP) in newly formed synapses, but prevented facilitation of acetylcholine secretion induced by L-type Ca2+ channels blocker nitrendipine. CaMKII inhibitor KN-62 produced similar effect and suppressed the increase in EPP quantal content caused by blockade of L-type Ca2+ channels. Phosphatase PP2A inhibitor okadaic acid significantly facilitated secretion in newly formed synapses; the effect was completely blocked by KN-62. In mature synapses, okadaic acid had no effect on transmitter secretion. KN-62 increased EPP quantal content. We hypothesize that CaMKII produced different effects on acetylcholine secretion in mature and immature synapses depending on specificity of calcium signaling and PP2A phosphatase activity.
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Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 154, No. 9, pp. 294-298, September, 2012
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Bogatcheva, P.O., Balezina, O.P. Multidirectional Effects of Calmodulin Kinase II on Transmitter Release in Mature and Newly Formed Mouse Motor Synapses. Bull Exp Biol Med 154, 316–319 (2013). https://doi.org/10.1007/s10517-013-1940-8
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DOI: https://doi.org/10.1007/s10517-013-1940-8