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. 2020 Sep 16;6(38):eabb8828. doi: 10.1126/sciadv.abb8828

Fig. 4. ExTxA delays fast inactivation of voltage-gated sodium channels in sensory neurons.

Fig. 4

(A and B) ExTxA (50 nM) delays fast inactivation of voltage-gated Na+ current in DRG neurons. (A) Representative Na+ current trace and (B) total sustained current (40 ms from peak current), normalized to peak, from DRG neurons (n = 8). (C) Effect of ExTxA on sustained current is reversed by removal of external Na+ and addition of TTX (1 μM) (n = 5). (D) Effect of ExTxA (green symbols) on the conductance-voltage (GV) curve of Na+ current compared to control (white symbols). Circles, channel activation; squares, steady-state inactivation (n = 3). (E) Concentration-dependent effects of ExTxA, MoTxA, and PA1b on Na+ current inactivation (n = 4 to 7 cells). (F) Effect of ExTxA (1 μM) on sustained current is not reversible with repeated wash steps. Black arrow, peptide addition; gray arrows, washout steps (n = 4; 35 min). (G) Co-administration of TTX (1 μM) or the NaV1.7-selective inhibitor Pn3a (1 μM) with ExTxA by the intraplantar route significantly decreases in vivo nocifensive responses. n = 5 per group. Data are presented as means ± SEM; *P < 0.05.