- Peptide CSQWPPSDSAFE, corresponding to amino acid residues 277-288 of rat NaV1.3 (Accession P08104). 3rd extracellular loop, domain I.
- Rat newborn brain and rat brain lysates (1:200-1:1000).
- Western blot analysis of rat newborn brain lysates (lanes 1 and 3), rat adult brain membranes (lane 2):1,2. Anti-SCN3A (NaV1.3) (extracellular) Antibody (#ASC-023), (1:200).
3. Anti-SCN3A (NaV1.3) (extracellular) Antibody, preincubated with SCN3A/Nav1.3 (extracellular) Blocking Peptide (#BLP-SC023).
- Transfected HEK 293 cells expressing rat NaV1.3.
Voltage-gated sodium channels (NaV) are essential for the generation of action potentials and for cell excitability.1 NaV channels are activated in response to depolarization and selectively allow flow of Na+ ions. To date, nine NaV α subunits have been cloned and named NaV1.1-NaV1.9.4-5 The NaV channels are classified into two groups according to their sensitivity to Tetrodotoxin (TTX): TTX-sensitive (NaV1.1, NaV1.2, NaV1.3, NaV1.4, NaV1.6 and NaV1.7) and TTX-resistant (NaV1.5, NaV1.8 and NaV1.9).2-3
Mammalian sodium channels are heterotrimers, composed of a central, pore-forming α subunit and two auxiliary β subunits. The 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.6,7
NaV1.3, also known as SCN3A, is highly expressed in embryonic sensory neurons and CNS, but its level dramatically decreases in adult rodents.8 Up-regulation of NaV1.3 channel expression was described in injured neurons and injured spinal cord.9-11