REGULATION OF GENE EXPRESSION AND NEUROFUNCTION UNDER OROFACIAL PAIN

1）疼痛模型采用Chronic Constriction Injury模型、Chung模型、Zeltzer模型、Crush模型。通过疼痛行为试验、von Frey细丝和足底试验检测异常性疼痛和痛觉过敏。2）谷氨酸受体参与神经病理性痛的研究为了阐明谷氨酸受体在薄束核神经元参与神经损伤性痛敏中的功能作用，采用药理学、电生理学和原位杂交技术对实验性单神经病大鼠进行了研究。CNQX、AMPA型受体拮抗剂显着抑制对机械刺激的反应。CNQX对伤害性刺激的反应比对无害性刺激的反应更强烈。与此相反，我们观察到只有轻微的调制的神经元活动的宽动态范围的神经元在薄束核NMDA拮抗剂，MR-801和AP-5，应用程序。提示AMPA受体参与了薄束核WDR神经元的过度兴奋，并可能与周围神经损伤后的痛敏有关。

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.