糖尿病神经痛（DNP）是糖尿病最常见的并发症之一，发病率高，严重影响患者生存质量。脊髓背角小胶质细胞P2X4受体在DNP发生机制中起着重要作用。我们前期研究发现在DNP大鼠脊髓背角小胶质细胞阳性表达增多，低频电针能有效抑制其表达，但电针对小胶质细胞内信号通路的干预机制尚不清楚。研究表明BDNF/TrkB-KCC2通路参与糖尿病神经痛，初步研究表明脊髓背角小胶质细胞P2X4介导BDNF/TrkB-KCC2通路调控参与神经痛。本项目拟采用DNP大鼠模型，观察DNP大鼠痛行为、脊髓背角小胶质细胞P2X4受体、BDNF、TrkB、KCC2表达变化及低频电针对其的干预作用，并运用相关拮抗剂或激动剂开展验证实验，明确基于脊髓背角小胶质细胞P2X4受体介导BDNF/TrkB-KCC2通路的调控机制和低频电针的干预机制，将为电针治疗DNP的机理阐释提供科学基础。

Diabetic neuropathic pain (DNP) is one of the most common complications of diabetes, and severely affects the patients’ life quality. Studies show that P2X4 receptor of microglia in spinal dorsal cord horn plays an important role in its mechanisms. We previously found that microglia in spinal dorsal cord horn was increased in DNP rats, and low frequency electroacupuncture could effectively downregulated, but the mechanism is unclear. Studies show that BDNF/TrkB-KCC2 signal pathway participate in diabetic neuropathic pain, and initial studies show that microglia P2X4 receptor regulated BDNF/TrkB-KCC2 signal pathway. The project is to adopt a rat model with DNP, the behavior of pain sensitization, microglia P2X4 receptor in spinal dorsal cord horn expression and activation, activation of BDNF/TrkB-KCC2 pathway, as well as the effects of low frequency electroacupuncture on these processes were studied, and agonist or inhibitor were applied, together to clear the mechanism of low frequency electroacupuncture on intervention on diabetic neuropathic pain based on its regulation of P2X4 receptor in microglia of spinal cord dorsal horn through BDNF/TrkB-KCC2 pathway. These will provide a scientific foundation for the elucidation of the mechanism underlying electroacupuncture treatment for DNP.