Cavkanavat

CaVkanavat, or voltage-gated calcium channels, are a family of transmembrane proteins that open in response to cell membrane depolarization to allow calcium ions to enter the cell. They translate electrical signals into a variety of cellular responses, including neurotransmitter release, muscle contraction, hormone secretion, and gene regulation.

The channels are defined by their pore-forming alpha1 subunit, which determines calcium selectivity and gating properties. In most channels, this subunit interacts with auxiliary subunits, including alpha2delta, beta, and gamma, that modulate trafficking, expression, and biophysical behavior. Pharmacological and genetic diversity arises from ten known genes encoding different CaV alpha1 subunits, grouped into subfamilies: CaV1 (L-type), CaV2 (P/Q-, N-, and R-type), and CaV3 (T-type).

CaV1 channels (L-type) are widely expressed in muscles and neurons and play key roles in excitation-contraction coupling and synaptic plasticity. The CaV2 family mediates fast, high-fidelity neurotransmitter release at presynaptic terminals, with CaV2.1 (P/Q-type) and CaV2.2 (N-type) being particularly important. CaV2.3 (R-type) contributes to synaptic transmission in several circuits. CaV3 channels (T-type) activate at low thresholds and participate in rhythmic firing and neuronal excitability.

Pharmacologically, these channels are targets for drugs and peptide toxins. Dihydropyridines (e.g., nifedipine) block L-type channels. N-type and P/Q-type channels are blocked by peptide toxins such as ω-conotoxins and ω-agatoxins, respectively, while ziconotide blocks N-type channels and is used for chronic pain management.

Mutations and dysregulation of CaV channels underlie various channelopathies and neurological disorders, including ataxias, epilepsies, and neurodevelopmental conditions, as well as some cardiovascular diseases.