Voltage-dependent T-type calcium channel subunit alpha-1G (Cav3.1) (Cav3.1)

The Voltage-dependent T-type calcium channel subunit alpha-1G, commonly known as Cav3.1, is a pore-forming protein that facilitates the influx of calcium ions into cells at low membrane potentials. It is a critical regulator of neuronal excitability, particularly within the thalamocortical circuit, where it supports rhythmic burst firing and oscillatory activity. In addition to its role in the central nervous system, Cav3.1 contributes to cardiac pacemaking in the sinoatrial and atrioventricular nodes. Its unique low-voltage activation threshold allows it to modulate cellular responses near the resting membrane potential. Dysregulation of Cav3.1 is linked to several neurological conditions, most notably childhood absence epilepsy and essential tremor, where aberrant burst firing occurs. Mutations in the encoding gene, CACNA1G, have been identified as the cause of spinocerebellar ataxia type 42 (SCA42). Furthermore, altered expression of this channel has been observed in various cancers, such as prostate and colorectal cancer, where it may influence cell proliferation or act as a tumor suppressor. Therapeutic targeting of Cav3.1 involves small-molecule inhibitors, including traditional antiepileptics like ethosuximide and novel selective blockers like suvecaltamide, which are being investigated for movement disorders.

Other names

CACNA1GCav3.1Calcium voltage-gated channel subunit alpha1 GNystagmus 6NYS6Alpha-1G subunitCaV3.1c

Blockade of T-type calcium currents, inhibition of low-threshold calcium spikes, and suppression of neuronal burst firing.