Upregulation of TRPC6 in DRG neurons contributed to mechanical allodynia induced by 3 chemotherapeutics. (A) The hind paw withdraw threshold of rats was obviously reduced following oxaliplatin, paclitaxel, or bortezomib treatment (n = 12 in each group; *P < .05, **P < .01 vs the vehicle group). (B) The heatmap of PCR array showed the relative mRNA expression of 84 ion channels in DRG following chemotherapeutics treatment (n = 4 in each group). (C–F) The levels of TRPC6 mRNA (C) and protein (D–F) in DRG were significantly upregulated following chemotherapeutics treatment (n = 4 in each group; **P < .01 vs the vehicle group). (G–I) The immunofluorescence staining showed the colocalization of TRPC6 (red) with NF200 (a marker for A-type neurons, green) and IB4 (a marker for C-type neurons), but not GFAP (a marker for satellite glial cells, green) in DRG (n = 4 in each group), scale bar = 100 μm. (J–L) Intrathecal injection of TRPC6 siRNA for 10 consecutive days obviously relieved the mechanical allodynia in rats treated with oxaliplatin, paclitaxel, or bortezomib (n = 12 in each group; *P < .05, **P < .01 vs the vehicle group; #P < .05, ##P < .01 vs the chemotherapeutics group). BTZ, Bortezomib; Oxal, Oxaliplatin; Pacl, Paclitaxel; Veh, Vehicle.