Fig 1: Nax is responsible for sodium sensitivity in stellate ganglia neurons. (A) Single-cell RNA-sequencing highlighted expression of the Nax encoding gene SCN7A (Yellow, with red box) at a transcript level in the stellate ganglia sympathetic neurons. These data are shown against expression of other ion channel encoding genes, SCN1A-SCN3A (Nav) (Red), KCNQ5 (Kv) (Green) and CACNA1B (Cav) (Blue). Here expression level indicates normalized count data. Here the count data per cell is divided by the total number of counts within that cell, multiplied by a scale factor and then natural-log transformed. (B) Immunohistochemistry highlights protein expression of Nax in tyrosine hydroxylase positive stellate ganglia neurons. Cultured stellate ganglia cells were co-labelled for Nax (Red), the sympathetic neuron marker, tyrosine hydroxylase (Green), and the nuclear stain Hoescht 33342 (Blue). (C) Knockdown of SCN7A significantly reduced the depolarization induced by an additional 30 mM NaCl, compared to GAPDH RNA knockdown (-2.87 ± 1.04 mV; n = 11–12; One-tailed unpaired t-test; p = 0.006) knockdown of a scrambled RNA control (–3.091 ± 0.8674 mV; n = 7–12; One-tailed unpaired t-test; p = 0.0012). (D) Knockdown of SCN7A caused a non-significant decrease in the increase in firing rate following 170 mM [NaCl]o (4.5–0 Hz; n = 8–10; One-tailed Mann Whitney test; p = 0.06). Similarly, SCN7A knockdown reduced the firing rate induced by 170 mM [NaCl]o when compared to a scrambled RNA knockdown control (4 Hz–0 Hz; n = 10; One-tailed Mann-Whitney test; p = 0.04).