L-type calcium channel

L-type calcium channels (Ca_V1) convert membrane depolarization into Ca²⁺ influx in excitable cells, supporting contraction, secretion, gene expression, neuronal excitability, synaptic plasticity, and sensory synaptic transmission^[1][2]. Mechanistically, Ca²⁺ entry through these channels activates calpain, CaMKs, calcineurin, and MAPKs, linking localized Ca²⁺ signals to fast responses such as muscle contraction and longer-term transcriptional regulation^[3]. In skeletal muscle, Ca_V1.1 directly supports excitation-contraction coupling by acting as the voltage sensor for RyR1, and loss of STAC3 disrupts this coupling and prevents contraction^[4]. In disease-relevant models, Ca_V1.3 loss impairs pacemaking and atrioventricular conduction, while Ca_V1.2 mutations are associated with inherited cardiac arrhythmia syndromes^[5][6]. Compared with Ca_V2 channels that primarily initiate fast synaptic transmission and Ca_V3 channels that support repetitive firing, Ca_V1 channels preferentially regulate contraction, secretion, gene expression, and specialized sensory transmission^[1]. For experimental applications, dihydropyridine sensitivity enables isoform-specific studies, and Ca_V1.1e currents increase with Bay K 8644 and decrease with nifedipine^[7][8].