Overview
- Peptide (C)HLEGNHRADGDRFP, corresponding to amino acid residues 511-524 rat NaV1.3 (Accession P08104). Intracellular, loop between domains I and II.
- Rat newborn brain membranes (1:200). Addition of 0.1-0.5% Tween-20 to the primary antibody solution is recommended. Mouse membrane lysate (see Kim, D.Y. et al. (2011) J. Biol. Chem. 286, 8106.).
- Western blot analysis of rat newborn brain membranes:1. Anti-SCN3A (NaV1.3) Antibody (#ASC-004), (1:200).
2. Anti-SCN3A (NaV1.3) Antibody, preincubated with SCN3A/Nav1.3 Blocking Peptide (#BLP-SC004).
- CNahIII-12 cells expressing human NaV1.3 and β1 subunit. (Meadows, L.S. et al. (2002) J. Neurosci. 22, 10669.).
- Rat embryo DRG frozen section.
- Rat DRG primary culture (fixed and permeabilized) (1:200).
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