Intracellular mechanisms underlying the potentiation of proton-gated currents by prokineticin 2 signaling. (A) The first line of current traces show that PK2 still enhanced proton-gated currents after re-patch with normal internal solution on the same neuron. The second line of current traces show the effect of intracellular dialysis of GF109203X, a PKC inhibitor, on the PK2-induced potentiation of proton-gated currents. The third line of traces were taken from neurons treated with PICK1 inhibitor FSC-231. GF109203X (2 μM) and FSC-231 (50 μM) was included in the recording pipette for intracellular dialysis. Proton-gated currents were elicited by application of pH 5.5 for 5 s durations. PK2 (1 nM) was pre-applied to external solution for 1 min. Arrow represents re-patch clamp and intracellular dialysis. The bar graph in (B) shows the percentage increases in the IpH5.5 induced by PK2 (10-9 M) with recording pipettes filled with the normal internal solution (n = 7), GF109203X (n = 8) or FSC-231 (n = 8) containing internal solution in the second patch experiments. Intracellular dialysis of GF109203X or FSC-231 abolished the enhancing effect of PK2 on IpH5.5. *P <0.05, **P <0.01, post hoc Bonferroni’s test, compared with normal internal solution. PICK1: protein interacting with C-kinase 1; PK2: prokineticin 2.