Fig. 5
Potentiation of proton-evoked currents and spikes by the activation of PAR2 in rat DRG neurons. The a current traces and b bar graphs show that I pH 6.6 was enhanced by PAR2-AP (10−5 M) or trypsin (10−5 M) pre-applied alone for 1 min in rat DRG neurons. This enhancing effect of PAR2-AP was inhibited by FSLLRY-NH2 (10−5 M), a selective PAR2 antagonist. Also, this proton-induced current could be completely blocked by 2 μM APETx2, an ASIC3 inhibitor. Currents were evoked by extracellular application of a pH 6.6 solution for 5 s in the presence of capsazepine (10 μM) to block proton-induced TRPV1 activation. DRG neurons with membrane potential clamped at −60 mV. The c spike recordings and d bar graphs show that pretreatment of PAR2-AP (10−5 M, for 1 min) increased the acidosis-induced number of action potentials in DRG neurons. The spikes were not evoked by pH 6.6 acidic solution in the presence of 2 μM APETx2. Action potentials were evoked by pH 6.6 acidic solution for 5 s with current clamp recording in the presence of capsazepine (10 μM) to block proton-induced TRPV1 activation. The acidosis-evoked action potentials recovered to control condition after washout of PAR2-AP. *P < 0.05, paired t test, compared with pH 6.6 column alone; #P < 0.05, paired t test, compared with PAR2-AP + pH 6.6 column, n = 9 in each column