No abstract

channel b-subunit genes revealed a mutation in the SCN2B gene, which we have functionally tested. Current-clamp analysis revealed that this mutant b2 subunit rendered small-diameter dorsal root ganglion (DRG) neurons hyperexcitable compared to DRG neurons expressing the wild-type b2 subunit. Additionally, b-subunits are known to increase sodium current density and alter biophysical properties of sodium channels. Voltageclamp analysis of small DRG neurons expressing the variant b2 subunit showed increased total sodium current density. As b-subunits can interact with all Na v channels, we subsequently investigated the effect of this mutation on TTXsensitive vs. TTX-resistant sodium channels. Results of this analysis and on the effect of the expression of the mutant b-subunit on gating properties of sodium channels will be presented.