Voltage-gated calcium channels (VGCCs), especially Cav2.1 and Cav2.2, are the major mediators of Ca2+ influx at the presynaptic membrane in response to neuron excitation, thereby exerting a predominant control on synaptic transmission. To guarantee the timely and precise release of neurotransmitters at synapses, the activity of presynaptic VGCCs is tightly regulated by a variety of factors, including auxiliary subunits, membrane potential, G protein-coupled receptors (GPCRs), calmodulin (CaM), Ca2+-binding proteins (CaBP), protein kinases, various interacting proteins, alternative splicing events, and genetic variations.
Keywords: Alternative splicing; Ca2+-binding protein; CaBP; Calmodulin; Channelopathy; G protein-coupled receptor; GPCR; PIP2; Phosphatidylinositol 4,5-bisphosphate; Protein kinase; Voltage-gated Ca2+ channel.
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