The increase of pRII intensity induced by KCl is independent of NaV, TRPA1, TRPV1, or ionomycin-induced calcium influx . (A) Time course of pRII intensity in lidocaine-pretreated (2, 20, and 200 µM; 10 min) rat DRG neurons stimulated with KCl (40 mM). (B) Dose–response curve of pRII intensities in DRG neurons of WT, TRPA1, TRPV1, and TRPA1/V1 double-knockout mice exposed to KCl (0–80 mM, EC₅₀ = 10 mM) for 3 min. (C) Calcium imaging (FLIPR Calcium 5 dye) showing calcium influx evoked by ionomycin (2 or 5 µM) followed by KCl (40 mM). Values in are means ± SEM; n = 4; >1,000 neurons/condition. (D) Time course of pRII intensities in DRG neurons stimulated with ionomycin (2 or 5 µM) versus KCl (40 mM). Data in A, B, and D are means ± SEM; n = 3–4 independent experiments; >2,000 neurons/condition; two-way ANOVA with Bonferroni’s test; *, P < 0.05; **, P < 0.01; ***, P < 0.001 indicate significance levels between baseline and stimulated conditions. Calcium imaging data in C are means ± SEM; n = 4 independent experiments with a total of >500 analyzed neurons/condition.