Voltage-gated T-type calcium channel (CaV3) (CaV3)

Voltage-gated T-type calcium channels (CaV3) are a subfamily of low-voltage-activated (LVA) ion channels that open in response to small membrane depolarizations near the resting potential (Perez-Reyes, 2003). They consist of three primary isoforms—CaV3.1, CaV3.2, and CaV3.3—which are encoded by the CACNA1G, CACNA1H, and CACNA1I genes, respectively (UniProt Consortium, 2024). These channels are essential for regulating neuronal burst firing, cardiac pacemaking, and hormone secretion, making them vital for normal physiological rhythms (IUPHAR/BPS Guide to Pharmacology, 2024). Pathological overactivity or mutations in CaV3 channels are implicated in several conditions, most notably absence epilepsy, neuropathic pain, and certain sleep disorders (Zamponi et al., 2015). In the thalamus, CaV3.1 and CaV3.3 are critical for generating the rhythmic oscillations seen in sleep and absence seizures, while CaV3.2 is a major contributor to pain signaling in peripheral sensory neurons (Cribbs et al., 1998). Therapeutic intervention typically involves small-molecule blockers that stabilize the channel in an inactivated state or physically plug the pore to reduce hyperexcitability (Zamponi et al., 2015). While older drugs like ethosuximide are standard for epilepsy, newer selective CaV3 inhibitors are being developed to treat chronic pain and tremors with fewer side effects (IUPHAR/BPS Guide to Pharmacology, 2024).

Other names

T-type calcium channelLow-voltage-activated calcium channelLVA calcium channelVoltage-dependent T-type calcium channelCaV3.1CaV3.2CaV3.3

Inhibition of low-voltage-activated calcium currents to reduce neuronal hyperexcitability and regulate rhythmic firing patterns (Perez-Reyes, 2003; Zamponi et al., 2015).