Anti-NaV1.7 (SCN9A) Antibody

Voltage-gated sodium channels (Na_V) are essential for the generation of action potentials and for cell excitability.¹ Na_v channels are activated in response to depolarization and selectively allow flow of Na⁺ ions. To date, nine Na_v α subunits have been cloned and named Na_V1.1-Na_V1.9.^4-5  The Na_V channels are classified into two groups according to their sensitivity to Tetrodotoxin (TTX): TTX-sensitive (Na_V1.1, Na_V1.2, Na_V1.3, Na_V1.4, Na_V1.6 and Na_V1.7)  and TTX-resistant (Na_V1.5, Na_V1.8 and Na_V1.9).^2-3 Mammalian sodium channels are heterotrimers, composed of a central, pore-forming α subunit and two auxiliary β subunits. Expression of the α subunit isoform is developmentally regulated and tissue specific. Sodium channels in the adult central nervous system and heart contain β₁ through β₄ subunits, whereas sodium channels in adult skeletal muscle have only the β₁ subunit.^6-8
 
Na_V1.7 is predominantly expressed in dorsal root ganglions (DRG) of the peripheral nervous system. Dominant gain of function mutations in the Na_V1.7 gene are associated with erythermalgia (a rare autosomal disease characterized by sporadic burning pain accompanied by redness and heat in the extremities).^9-11 Loss, or function mutations in Na_V1.7 channels, leads to complete ablation of pain perception in humans.¹¹  These  recent findings highlight the role of this Na_V isoform and the subset of DRG neurons that express this channel in physiological pain sensation.