Fig. 3
From: Sensory TRP channels contribute differentially to skin inflammation and persistent itch

Genetic ablation of TRPA1/TRPV1 abolishes SADBE-induced activation of DRG. a–d Representative time-lapse traces show that SADBE-induced a robust [Ca2+]i response in 56.7% of wt (317/558, a), 40.2% of Trpa1 −/− (220/547, b), 59.5% of Trpv1 −/− (334/561, c), and 0% of Trpa1 −/−/Trpv1 −/− dKO (0/509, d) DRG neurons. n = 5 coverslips for each genotype; e–h Representative traces show that SADBE-induced depolarization of membrane potential and action potential firing in DRG neurons isolated from wt (e), Trpa1 −/− (f), Trpv1 −/− (g) and Trpa1 −/−/Trpv1 −/− dKO (h) mice, n = 5 for each genotype; (i) Percentages of DRG neurons responding to SADBE, AITC, capsaicin and KCl in neurons isolated from wt, Trpa1 −/−, Trpv1 −/− and Trpa1 −/−/Trpv1 −/− dKO mice in live-cell Ca2+ imaging assays. Data are presented as mean ± SEM; (j) Quantification of SADBE-induced depolarization of membrane potentials of DRG neurons isolated from wt, Trpa1 −/−, Trpv1 −/− and Trpa1 −/−/Trpv1 −/− dKO mice. Data are presented as mean ± SEM. Asterisks indicate statistical significance. ****p < 0.0001, ANOVA