炎性痛和神经病理痛是最常见的病理性疼痛，发生机制各异但可能存在交叉。TRPV1和P2X3是引起外周痛敏化的关键受体，在不同病理痛发生时的相关性不明确。对外周痛敏化的干预可能是电针镇痛的关键机制之一。拟通过建立CFA致大鼠炎性痛模型和SNI致大鼠神经病理痛模型，并采用不同频率（2、100、2/100Hz）电针处理，通过检测mRNA表达和总蛋白/膜蛋白表达/磷酸化水平，和运用全细胞膜片钳、siRNA、免疫共沉淀共表达等技术，观察不同病理痛时大鼠背根神经节（DRG）TRPV1和P2X3受体的活化及其相互关系、和不同频率电针刺激的调控效应。结合特异性激动剂/抑制剂，进一步验证优效（频）电针对不同病理痛大鼠DRG TRPV1和P2X3活化与交互作用的调控。初步揭示不同病理痛时外周敏化关键受体的活化与内在关系，明确干预外周敏化的电针镇痛新原理，为针灸临床基于外周敏化受体调控效应的治疗新策略提供依据。

Inflammatory pain and neuropathic pain are the most commonly-seen pathological pains. The pathogenesis differs but may be related each other. TRPV1 and P2X3 are considered the crucial receptors in peripheral sensitization of pain, and their interrelation is not unclear during the onset of pathological pains. Mediating peripheral pain sensitization may be one of the key mechanisms of EA analgesia. By establishing the CFA-induced inflammatory pain model and the SNI-induced neuropathic pain model of rats, and applying electroacupuncture (EA) treatment with different frequencies (2 Hz, 100 Hz, and 2/100 Hz), the study is to observe transient receptor potential vanilloid 1 (TRPV1) and P2X3 activations and cross-relation in dorsal root ganglion (DRG) of inflammatory pain or neuropathic pain rats, and the regulatory effect of different frequency EA, by measuring expressions of mRNA, total protein/membrane protein and phosphorylation level, and using techniques of whole cell patch clamp, siRNA and immune coprecipitation. We are going to further verify the regulatory mechanisms of EA on TRPV1 and P2X3 by using specific inhibitors/agonists. The present project is likely to initially reveal the intrinsic relationship between TRPV1 and P2X3 in peripheral sensitization of different pathological pain, and elucidate the new mechanism of EA analgesia, and finally will provide scientific evidence of novel strategy of EA analgesia in clinic based on regulating the key receptors in peripheral pain sensitization.