Figure 2.

Gα_q Is Essential for BK-Induced Inhibition of TRPM8-Dependent Firing Responses in DRG Neurons

(A–C) Representative firing responses elicited by WS-12 (1 μM) or capsaicin (Cap, 0.5 μM) (C) in WT DRG neurons before and after vehicle (A) or BK (1 μM, 1 min) (B and C). (B) and (C) indicate the same neuron.

(D–F) Example firing responses evoked by WS-12 or capsaicin (F) in DRG neurons lacking Gα_q before and after vehicle (D) or BK (E and F). (E) and (F) indicate the same neuron.

(G) Scatterplot of ratio of action potentials (APs) induced by WS-12 after and before BK in experiments similar to those in (A)–(D). ^∗∗p = 0.00588; NS, p = 0.107.

(H) Summary of ratio of firing responses evoked by capsaicin after and before BK from experiments similar to those in (C) and (F).

(I) Example currents evoked by capsaicin (100 nM, 5 s) in a Gα_q null DRG neuron. The gap indicates BK treatment (1 μM, 1 min).

(J) Collective results of sensitization fold caused by BK from experiments similar to those in (I). The sensitization was abolished by U73122 (2.5 μM). The number of experiments is denoted above each bar.

All data indicate mean ± SEM. ^∗∗p < 0.01; ^∗∗∗p < 0.001; NS, not significant.