神经病理性疼痛严重影响人类的生存质量，目前仍未有效解决。研究表明，卫星胶质细胞的神经免疫功能与疼痛密切相关。它分泌炎症因子介导DRG神经元痛觉敏化。然而其免疫激活的具体机制尚不明确，且单纯干预炎症因子治疗神经病理性疼痛时间窗短，疗效差。前期研究发现Wnt信号通路的关键分子β-catenin在SNL大鼠DRG卫星胶质细胞中表达减少，而鞘内注射Wnt通路特异性激动剂增加了卫星胶质细胞β-catenin表达，并缓解了SNL大鼠的痛敏症状。由此我们推测：β-catenin可能是卫星胶质细胞介导神经免疫反应的关键分子，并通过调控多种炎症分子的表达影响神经元的敏化，介导了神经病理性疼痛的发生。本研究拟用SNL大鼠模型、形态学、分子生物学等技术，研究其对动物行为学、卫星胶质细胞激活及其介导的DRG神经元痛觉敏化的影响，旨在为神经病理性疼痛的治疗提供新的靶点。

The treatment for neuropathic pain is a worldwide difficulty which is still lack of effective solution. Recent studies indicate that the development of neuropathic pain involves not only neuronal pathways, but also glial cells. Glial cells can release immunologic and inflammatory factors triggered by noxious stimuli, inflammation, or damage to the peripheral nerve injury. The stimulation of immune response can change the neuronal plasiticity and finally result in neuralgia. Then, satellite glial cells in dorsal root ganglia was reported to play an indispensable role in neuropathic pain mechanism. From our primary work, we found β-catenin was down expressed in satellite gial cells in SNL modal of rats. And intrathecal injection Wnt agonist can reduce pain for SNL rats. Howerver, there are few study on β-catenin regulating neuropathic pain. We spectulate that satellite cell β-catenin is a key molecular for inducing neuropathic pain, which regulate the neuroimmune disorder in the interface between glial cell and neuron. This study is to clarify the intracellular function of β-catenin in inducing neuropathic pain and we hope to determine whether or not satellite cell β-catenin can be a target of regulating neuronal plasiticity. So a lot of studies in behavioral work, electrophysiology and molecular biology research need be supported. And the outcome will bring a lot of benefits for new drugs research and clinical therapy.