REGULATION OF GENE EXPRESSION AND NEUROFUNCTION UNDER OROFACIAL PAIN

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We examined change in gene expression in the rat nervous system with experimental mononeuropathy.1) Pain modelWe used Chronic Constriction Injury model and Chung model, Zeltzer model, Crush model. Allodynia and Hyperalgesia examined by Pain Behavior Test, von Frey filaments and Planter foot test. Furthermore, we used a rat model of facial paralysis.2) Involvement of glutamate receptors on Neuropathic painIn order to clarify the functional role of glutamate receptors on the gracile nucleus neurons involved in nerve injury-induced hyperalgesia, pharmacological, electro-physiological and in situ hybridization technic were rats with experimental mononeuropathy. CNQX, AMPA type receptor antagonists significantly depressed the responses to mechanical stimuli. The responses to noxious stimuli were much more strongly affected by CNQX as compared with those to innocuous stimuli. In contrast, we observed only slight modulation of neuronal activity of wide dynamic range neurons in the gracile nucleus following NMDA antagonists, MR-801 and AP-5, applications. These suggest that AMPA receptors would be dominantly involved in the hyperexcitability of WDR neurons in gracile nucleus, and may be related to the hyperalgesia observed following peripheral nerve injury.