腰椎间盘突出症（LDH）是神经根性疼痛(RP)的主要病因，外周敏感化作为RP产生的机制已得到深入研究，中枢敏感化是否参与了RP的发生发展尚不清楚。申请人早期研究发现酪氨酸家族激酶（SFKs）活化是脊髓背角突触传递效率长时程增强（LTP），即中枢敏感化产生的重要原因。最近又发现LDH大鼠脊髓背角突触后电位出现LTP，并与疼痛的产生时程高度正相关；脊髓SFKs活化介导的中枢敏感化可能参与LDH诱导的痛觉过敏；细胞和整体实验提示TNF-α剂量依赖性的上调p-SFKs表达。提示：TNF-α可能通过上调脊髓SFKs参与了LDH诱导的中枢敏感化和RP。本研究拟从在体和离体水平，研究脊髓背角SFKs及其家族成员在LDH诱导的中枢敏感化和RP中的作用；探讨 TNF-α及其下游信号通路上调SFKs从而引起中枢敏感化和疼痛的机制，以期为治疗RP提供新的靶点和策略。

Lumbar disc herniation (LDH) is a major cause of radicular pain (RP). The role of peripheral sensitization in this process has been intensively studied. However, whether central sensitization is involved in RP is still unclear. We have reported that the activation of Src-family kinases (SFKs) is vital for inducing long term potentiation (LTP) of spinal synaptic transimission which represents central sensitization. Recently, we found LTP of spinal postsynaptic potential was highly positively correlated with the time course of pain in rats with LDH. Central sensitization that mediated by activation of spinal SFKs may be involved in LDH induced hyperalgesia. Cell and integral experiments showed TNF-α increased p-SFKs expression in a dose dependent manner. Therefore, TNF-α may be involved in LDH induced central sensitization and RP by up-regulating spinal SFKs. In the present study, from the level of in vivo and in vitro, we will examine the role of SFKs and its’ family members in LDH induced central sensitization and RP, then discuss the mechanism of TNF-α and downstream signal pathways up-regulating SFKs, inducing central sensitization and pain, thus explore new targets and strategies for RP treatment.