Fig. 8
From: TRPV1 SUMOylation regulates nociceptive signaling in models of inflammatory pain
SUMOylation had no effect on capsaicin- and proton-evoked and the voltage dependence of TRPV1 channel activation in DRG neurons. a, b Representative whole-cell currents at −60 mV evoked by varying concentrations of capsaicin (Cap) as indicated in DRG neurons isolated from control (a) and SENP1 cKO mice, respectively. Holding potentials = −60 mV. c Concentration responses to capsaicin for control and SENP1 cKO DRG neurons. Data were fitted with Hill equation, which yielded: control, EC50 = 0.91 ± 0.01 μM, and nH = 2.40 ± 0.15 (n = 8); SENP1 cKO, EC50 = 0.87 ± 0.02 μM and nH = 2.68 ± 0.28 (n = 10). d, e Representative whole-cell currents at −60 mV in responses to bath solutions of varying pH as indicated in control and SENP1 cKO DRG neurons, respectively. The cell was also stimulated with 10 μM Cap and then pH 5.5 combined with 10 μM capsazepine (Cpz) to confirm that the currents were mediated by TRPV1. f Dose responses to pH for control and SENP1 cKO TRPV1-positive DRG neurons. Data were fitted with Hill equation, which yielded: control, pH0.5 = 5.9 ± 0.1, nH = 5.3 ± 2.4 (n = 8); SENP1 cKO, pH0.5 = 5.8 ± 0.1, nH = 5.6 ± 3.2 (n = 7). g–l Representative whole-cell currents elicited by the voltage step protocol shown in the inset in g for control (g–i) and SENP1 cKO (j–l) DRG neurons. The cell was exposed to 0.3 μM Cap combined with 10 mM TEA-Cl and 1 μM TTX (g and j) or 0.3 μM Cap combined with 10 mM TEA-Cl, 1 μM TTX, and 10 μM Cpz (h and k), in order to isolate the net TRPV1-mediated currents through subtraction (i and l). I–V (m) and G–V (n) relationships of TRPV1 for control and SENP1 cKO DRG neurons. Data in n were fitted with Boltzmann equation, which yielded: control V1/2 = 56.9 ± 2.6 mV, and slope factor = 26.2 ± 2.3; SENP1 cKO, V1/2 = 65.4 ± 1.1 mV, and slope factor = 25.2 ± 1.0
