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The aim of this study was to understand some molecular and electrophysiological mechanisms of neuropathic pain after chronic constriction of the saphenous nerve (CCS) in mice. After surgery, CCS mice displayed significant allodynia and hyperalgesia, which were sensitive to acute systemic injection of morphine (4 mg\/kg), gabapentin (50 mg\/kg), amitriptyline (10 mg\/kg), and the cannabinoid agonist WIN 55,212\u20102 (5 mg\/kg). These behavioral changes were accompanied after surgery by an increase of c\u2010Fos expression and by an overexpression of \u03bc\u2010opioid and cannabinoid CB<jats:sub>1<\/jats:sub>and CB<jats:sub>2<\/jats:sub>receptors in the spinal cord and the dorsal hind paw skin. In combination with the skin\u2010nerve preparation, this model showed a decrease in functional receptive fields downstream to the injury and the apparition of A\u2010fiber ectopic discharges. In conclusion, CCS injury induced behavioral, molecular, and electrophysiological rearrangements that might help us in better understanding the peripheral mechanisms of neuropathic pain. This model takes advantage of the possible use in the future of genetically modified mice and of an exclusively sensory nerve for a comprehensive study of peripheral mechanisms of neuropathic pain. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.20821","type":"journal-article","created":{"date-parts":[[2006,3,1]],"date-time":"2006-03-01T22:16:58Z","timestamp":1141251418000},"page":"1310-1322","source":"Crossref","is-referenced-by-count":54,"title":["Characterization of chronic constriction of the saphenous nerve, a model of neuropathic pain in mice showing rapid molecular and electrophysiological 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