Voltage-dependent L-type calcium channel subunit alpha-1D (CaV1.3) (CaV1.3)

Voltage-dependent L-type calcium channel subunit alpha-1D (CaV1.3) is a pore-forming protein that mediates the influx of calcium ions into cells in response to membrane depolarization [1]. Unlike its counterpart CaV1.2, CaV1.3 activates at relatively more negative voltages, allowing it to play a specialized role in pacemaking activity within the sinoatrial node of the heart and in specific neuronal populations, such as dopaminergic neurons in the substantia nigra [2]. It is also essential for sensory transduction in auditory hair cells and the regulation of insulin secretion in pancreatic beta cells [3]. Mutations in the CACNA1D gene are associated with a range of pathologies, including primary aldosteronism, sinoatrial node dysfunction and deafness (SANDD) syndrome, and various neuropsychiatric disorders [4]. In the context of neurodegeneration, CaV1.3 is a significant target for Parkinson's disease research due to its role in neuronal calcium overloading [5]. While traditional dihydropyridines like isradipine inhibit CaV1.3, they often lack high selectivity over CaV1.2, which can lead to dose-limiting cardiovascular side effects such as hypotension [6].

Other names

CACNA1DCalcium channel voltage-dependent L type alpha 1D subunitCav1.3 alpha 1 subunitVoltage-gated calcium channel alpha subunit Cav1.3

L-type calcium channel blockers (antagonists) bind to the alpha-1 subunit of the channel, inhibiting the influx of calcium ions into the cell during membrane depolarization [5, 6].