Effects of TRPV1 gene knockout on function of voltage-gated Na
currents recorded in bladder sensory neurons. (A) Current–voltage (I-V) relationship of total Na+ current recorded in bladder dorsal root ganglia (DRG) neurons after intracolonic 2,4,6-trinitrobenzene sulfonic acid (TNBS) treatment in wild-type (WT) mice. *P ≤0.05 when compared to vehicle group. (B) Current–voltage (I-V) relationship of total Na+ current recorded in bladder sensory neurons isolated from transient receptor potential vanilloid 1 knockout (TRPV−/−) animals. (C) Voltage dependence of steady-state activation and inactivation of total Na+ current recorded in bladder DRG neurons from WT mice. The steady-state activation of voltage-gated sodium channels (VGSC) was assessed by a three-pulse protocol with a negative pre-pulse to −110 mV and a series of short pulses of 10 ms duration from −110 mV to +70 mV to activate Na+ currents. The amplitude of steady-state inactivation was measured at 0 mV after 150 ms depolarizing pulses ranging from −100 mV to 70 mV. (D) Activation and inactivation kinetics of total Na+ current recorded in lumbosacral bladder neurons isolated from TRPV1 KO mice.