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Synaptic efficacy is remodeled by neuronal firing activity at the presynaptic terminal. Presynaptic activity-dependent changes in transmitter release induce postsynaptic plasticity, including morphological change in spine, gene transcription, and protein synthesis and trafficking. The presynaptic transmitter release is triggered and regulated by Ca 2+ , which enters through voltage-gated Ca 2+  (Ca V ) channels and diffuses into the presynaptic terminal accompanying action potential firings. Residual Ca 2+  is sensed by Ca 2+ -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). Calmodulin, a Ca 2+ -sensor protein with an EF-hand motif that binds Ca 2+ , interacts with Ca V 2 channels and autoreceptors in modulation of SNARE-mediated exocytosis.

Ca2+/Calmodulin and Presynaptic Short-Term Plasticity

Ca²⁺/Calmodulin and Presynaptic Short-Term Plasticity