T-type voltage-gated calcium channel (Cav3) (Cav3)

T-type voltage-gated calcium channels (Cav3) are low-voltage-activated (LVA) channels that open at relatively negative membrane potentials, playing a pivotal role in regulating cellular excitability and rhythmic firing (Perez-Reyes, 2003, PMID: 12514117). These channels are composed of three distinct alpha-1 subunits—Cav3.1, Cav3.2, and Cav3.3—which are widely expressed in the central nervous system, heart, and endocrine tissues (UniProt: O43497, O95180, Q9P0X4). In the brain, they facilitate the burst firing of thalamocortical neurons, a process essential for sleep and sensory processing, but also implicated in the generation of absence seizures (Chemin et al., 2002, PMID: 11834179). In the cardiovascular system, they contribute to the pacemaker activity of the sinoatrial node and are involved in vascular smooth muscle contraction (Vassort et al., 2006, PMID: 16461348). Pharmacologically, T-type channels are targeted by anticonvulsants like ethosuximide and zonisamide, which reduce calcium influx to stabilize neuronal activity (StatPearls, 2023). Beyond epilepsy, these channels are significant therapeutic targets for neuropathic pain, where Cav3.2 is particularly relevant, and for certain cancers where they promote cell cycle progression (Bourinet et al., 2016, PMID: 26860474). Safety concerns for T-type channel blockers often include cardiovascular effects such as bradycardia and central nervous system side effects like sedation or dizziness (Iftinca & Zamponi, 2009, PMID: 19244257).

Other names

Low-voltage-activated calcium channelLVA calcium channelCav3.1Cav3.2Cav3.3Voltage-dependent T-type calcium channel

Inhibition of low-voltage-activated calcium currents to reduce repetitive firing and stabilize membrane potential (Perez-Reyes, 2003, PMID: 12514117).