Activity-dependent regulation of synaptic vesicle exocytosis and presynaptic short-term plasticity

Abstract

Neuronal firing activity controls protein function and dynamically remodels synaptic efficacy. Exocytosis is triggered and regulated by Ca²+ which enters through voltage-gated Ca²+(CaV) channels and diffuses into the presynaptic terminal accompanying action potential firings. Residual Ca²+ is sensed by Ca²+-binding proteins; among other potential actions, it mediates time- and space-dependent synaptic facilitation and depression via effects on Ca(V)2 channel gating and vesicle replenishment in the readily releasable pool (RRP). Mitochondria are also associated with short-term synaptic plasticity due to a sufficient ATP supply for vesicle mobilization into the RRP. Mitochondria-deficient synapses with impaired anterograde transport of mitochondria in neuronal processes show defects in presynaptic short-term plasticity.