Figure 6.

Effect of prokineticin 2 on proton-evoked membrane excitability of rat dorsal root ganglia neurons. (A) Original current and membrane potential recordings from the same DRG neuron. Left panel: voltage-clamp recording of current induced by a pH 6.0 acid stimulus in the presence of the TRPV1 inhibitor capsazepine (10 μm). Holding potential was −60 mV. Right panel: current-clamp recording (I = 0 pA) of the depolarization evoked by the pH 6.0 acid stimulus from the same neuron as the left panel in the presence of capsazepine (10 μM) to block TRPV1 and TTX (1 μM) to block Na⁺ channel-mediated action potentials. The pretreatment of PK2 (1 nM) enhanced the acid-induced membrane depolarization. No action potential was triggered by the membrane depolarization in the neuron. (B) Original current and spiking recordings from the same DRG neuron. Left panel: a pH 5.5 acid stimulus induced an inward current with voltage-clamp recording. Right panel: the pH 5.5 acid stimulus produced a cell spiking with current-clamp recording in the same neuron in the presence of the TRPV1 inhibitor capsazepine (10 μM). The pretreatment with PK2 (1 nM) increased the acid-induced spiking activity. (C and D) Bar graphs show the effect of PK2 on membrane potential depolarization produced by pH 6.0 and the number of spiking produced by pH 5.5. After a 20 min washout of PK2, the acid-evoked depolarization and spiking recovered to control condition. *P <0.05, paired t-test, compared with pH alone, n = 6 in each column. DRG: dorsal ganglia root; PK2: prokineticin 2; TRPV1: transient receptor potential vanilloid receptor-1; TTX: tetrodotoxin.