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CaV3.2 is a voltage-sensitive, low-voltage activated (LVA) calcium channel that gives rise to T-type calcium currents. It is the primary pore-forming α1 subunit of the T-type calcium channels and is encoded by the CACNA1H gene. These channels are essential for mediating transient (T-type) inward Ca²⁺ currents in response to small depolarizations near resting membrane potential. Dysfunction or altered regulation/expression of Cav3.2 has been implicated in neurological disorders like absence epilepsy, neuropathic pain syndromes, and cardiac arrhythmias. Recent studies suggest that targeting Cav3.2 may have therapeutic potential for cerebral ischemia/reperfusion injury.
Inhibition of T-type calcium channels
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