One possible mechanism involves P2X3 receptors,ATP-gated ion channels that mediate pain signaling and central sensitization.,−, ,  After nerve injury, both GPR151 and P2X3 are upregulated in nociceptiveC-fiber DRG neurons. Overexpression of GPR151 significantly enhanced P2X3-mediated calcium elevationand dorsal root ganglion excitability. Conversely, DRG-specific deletion of GPR151 inhibitsP2X3 function, reducing calcium elevation, DRG neuronal hyperexcitability,and CSF1 expression. Here, GPR151 is linked to injury.