Abstract
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.
Original language | English |
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Pages (from-to) | 1701-1704 |
Number of pages | 4 |
Journal | NeuroReport |
Volume | 12 |
Issue number | 8 |
DOIs | |
Publication status | Published - Jun 13 2001 |
All Science Journal Classification (ASJC) codes
- Neuroscience(all)