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Oppositely directed activity of CaMK II in regulation of neurotransmitter secretion in mature and immature mouse neuromuscular junctions is described. In immature junctions, the latent ability of CaMK II to increase neurotransmitter release is suppressed by calcium influx through L-type Ca2+-channels and activity of Ca2+-sensitive serine-threonine phosphatase PP2A. It is suggested, that Ca2+-dependent inhibition of CaMK II activity in immature junctions may be one of the mechanisms of elimination of redundant synaptic contacts, which takes place during reinnervation and synaptic maturation in skeletal muscle fibers.