Fig. 4

AnxA1 deletion sensitizes capsaicin induced TRPV1 responses. Representative traces show the injected currents induced repetitive action potentials in control (a) and AnxA1^−/− (b) DRG neurons. c Quantification of action potential frequencies in control and AnxA1-deficient DRG neurons after different currents injection (20, 100, and 200 pA). (AnxA1^−/− versus control group, ****P < 0.0001, Two-way ANOVA repeated measures with Tukey’s multiple comparisons test. Control group, n = 10; AnxA1^−/− group, n = 8). Representative traces of d 10 μM capsaicin-gated currents, g 100 μM mustard oil-gated currents, j 100 μM menthol-gated currents and h 10 μM ATP-gated currents at -70 mV in control (black trace) and AnxA1^−/− (red trace) DRG neurons. Quantification of average current density after capsaicin e (AnxA1^−/− versus control group, ***P < 0.001, Student’s t-test, n = 8 neurons in WT group and n = 8 neurons in AnxA1^−/− group from 3 cultures, respectively), mustard oil (h) (AnxA1^−/− versus control group, P = 0.61, Student’s t-test, n = 10 neurons from 3 cultures in each group), and menthol (k) (AnxA1^−/− versus control group, P = 0.94, Student’s t-test, n = 9 neurons from 3 cultures in each group), application measured at the current peak between control and AnxA1^−/− group. Time constants Tau of capsaicin (f), mustard oil (i), and menthol (l)-induced activation and deactivation at -70 mV in control and AnxA1-deficient DRG neurons (AnxA1^−/− versus control group, capsaicin: P = 0.81, P = 0.55; mustard oil: P = 0.79, P = 0.87; menthol: P = 0.99, P = 0.59,  Student’s t-test). All data are represented as mean ± SD