Fig. 5: CXCL5 depolarizes and excites mouse nociceptive DRG neurons via CXCR2 and TRPA1-dependent mechanism.
A, B Summary of the No. of action potentials (AP) elicited by injecting different amounts of currents into small-sized DRG neurons (capacitance<42 pF) under the vehicle- (panel A) or CXCL5 (100 nM)-treated condition (panel B). *p < 0.05, **p < 0.01 vs. control group. C Representative AP firing traces from vehicle (0.1% PBS)-treated DRG neuron. D Summary of the number of APs triggered by a vehicle. E Representative AP firing traces recorded from CXCL5-challenged DRG neuron. F Summary of the No. of APs triggered by CXCL5. G, I Representative AP firing traces from CXCL5-challenged DRG neuron pretreated with SB225002 (100 nM, panel G) or HC030031 (100 μM, panel I). H and J Summary of the number of APs triggered by CXCL5 under SB225002 (panel H) or HC030031 (panel J) pretreated condition. K, M Representative AP firing traces triggered by CXCL5 from Cxcr2−/− (panel K) and Trpa1−/− (panel M) mice. L and N Summary of the No. of APs triggered by CXCL5 from Cxcr2−/− (panel L) and Trpa1−/− (panel N) mice. O Summary of depolarization of membrane potential in DRG neurons caused by CXCL5 in different groups. **p < 0.01 vs. Veh group. ##p < 0.01 vs. control group. NS: no significance. One-way ANOVA with Bonferroni’s post hoc test for panel (O). Student’s paired t-test (two-tailed) was for others. Data are shown as mean ± SEM. The n number, exact p-value, and statistical results are provided in the Source Data file.
