T-type calcium channel subunit alpha-1H (Cav3.2)

T-type calcium channel subunit alpha-1H (Cav3.2) is a voltage-gated, low voltage-activated calcium channel expressed broadly in the central and peripheral nervous systems, heart, and other tissues. It is encoded by the gene CACNA1H and forms the ion-conducting pore of the channel. Cav3.2 channels are distinguished by their ability to open near resting membrane potentials, allowing them to play vital roles in regulating neuronal excitability, pacemaker activity, hormone secretion, and pain signaling. Cav3.2 is highly phosphorylated in vivo, and its function is modulated by kinases and phosphatases. Dysfunction or dysregulation of Cav3.2 has been linked to neurological and cardiovascular diseases, especially neuropathic pain and absence epilepsy. Pharmacological inhibition of Cav3.2 is a promising therapeutic strategy for pain and epilepsy, but safety concerns exist due to its widespread physiological roles[1][2][3][5][7].

Other names

Cav3.2T-type calcium channel alpha-1H subunitVoltage-dependent T-type calcium channel subunit alpha-1HCACNA1H (gene name)Low voltage-activated calcium channel Cav3.2TTCC Cav3.2

Blockade of calcium influx via the Cav3.2 channel, leading to reduced neuronal excitability and inhibited action potential firing (analgesia, anticonvulsant action)[5][3]. Allosteric inhibition via binding to central cavity or fenestrations of the channel pore (state-dependent block)[5].