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Voltage-gated calcium channel subunit alpha-1H (CaV3.2) is a low-voltage-activated (T-type) calcium channel encoded by the CACNA1H gene, widely expressed in the central and peripheral nervous systems as well as heart and other tissues[1][3][5]. CaV3.2 channels conduct small, transient calcium influx at subthreshold membrane potentials, modulating neuronal excitability, pacemaker activity, neurotransmitter release, muscle contraction, cell proliferation, and apoptosis[4][5][6]. Dysfunction or dysregulation of CaV3.2 is associated with neurological diseases such as epilepsy, neuropathic pain, and potentially psychiatric and cardiovascular disorders[1][2][5]. CaV3.2 can be selectively blocked or modulated by certain small molecules or ions, making it a validated therapeutic target for pain, epilepsy, and related conditions[1][4][10]. Widespread physiological roles mean selective modulation and safety remain key challenges for drug development[5].
Channel blockade, leading to inhibition of low-voltage-activated calcium influx and reduced neuronal excitability Modulation of channel phosphorylation state to alter channel gating[2][5]
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