• Eun J Lim, Hye J Jeon, Gwi Y Yang, Min K Lee, Jin S Ju, Seung R Han, and Dong K Ahn.
• Department of Oral Physiology and BrainKorea 21, School of Dentistry, Kyungpook National University, Daegu (700-412), South Korea.
• Prog. Neuropsychopharmacol. Biol. Psychiatry. 2007 Aug 15;31(6):1322-9.

AbstractThe present study investigated the role of mitogen-activated protein kinase (MAPK) in orofacial neuropathic pain following chronic constriction injury of the infraorbital nerve (ION-CCI). Experiments were carried out on male Sprague-Dawley rats weighing between 200 and 230 g. The ION was separated from adhering tissue, and two ligatures (5-0 chromic gut) were tied loosely around it. We examined the air-puff thresholds (mechanical allodynia), scores of pinprick (mechanical hyperalgesia), and face grooming frequency for acetone application (hypersensitivity for cold stimulation) - 3, 3, 6, 9, 12, 15, 20, 25, 30, and 40 days after surgery. ION-CCI produced mechanical allodynia, hyperalgesia, and cold hypersensitivity. We investigated whether administration of MAPKs inhibitors blocks ION-CCI-induced mechanical allodynia. Intracisternal administration with PD98059 or SB203580, a MEK inhibitor or a p38 MAPK inhibitor, respectively, significantly inhibited ION-CCI-induced mechanical allodynia in the orofacial area. These results indicate that the ION-CCI produced behavioral alterations in the orofacial area and those central MAPKs pathways contribute to orofacial neuropathic pain. Our findings suggest that MAPKs inhibitors have a potential role in treatment for orofacial neuropathic pain.

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