The aim of the present study is to characterize the role of endogenous ATP leaked from damaged cells in a rat model of postoperative pain using behavioural and immunocytochemical approaches. We found that systemic (i.v.) and local (incision area) administration of a P2 receptor antagonist, pyridoxal-phosphate-6-azophenyl-2′,4′-disulphonic acid (PPADS) before surgery significantly attenuated mechanical allodynia caused by an incision of the plantar surface of the hindpaw. Furthermore, PPADS significantly reduced the incision-evoked c-Fos protein expression, a marker of neuronal activity, in the dorsal horn of the spinal cord. The present findings suggest that excitatory signaling by endogenous ATP leaked from damaged cells via PPADS-sensitive P2 receptors is necessary for the induction of the postoperative pain characterized by mechanical allodynia.
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