中文摘要：

目的研究外周组织损伤对脊髓背角AMPA受体突触表达的影响及其分子调节机制。方法小鼠足底皮下注射完全弗氏佐剂（CFA），建立炎性疼痛模型；24h后分离L4～IJ5脊髓背角，提取“富含突触后致密质（PSD）”的亚细胞结构，免疫印迹法检测AMPA受体GluR2亚基突触表达的变化，并观察cAMP依赖性蛋白激酶（PKA）在调节GluR2突触含量中的作用。结果CFA在引发痛觉超敏的同时，脊髓背角GluR2的突触含量明显升高。虽然PKA抑制剂H一89并不影响正常小鼠的痛阈及GluR2的突触含量，但H一89却能有效缓解炎性痛觉超敏，同时完全翻转CFA诱发的GluR2亚基在突触中的过量表达。结论外周组织损伤通过激活脊髓PKA，明显提高AMPA受体GluR2亚基在脊髓突触中的含量，可能是慢性炎性疼痛形成的重要机制。

英文摘要：

Aim To investigate the effects of peripheral tissue injury on the synaptic contents of AMPA receptor in spinal dorsal horn and its underlying molecular mechanisms. Methods Complete Freund＇ s Adjuvant （CFA） was injected into the plantar surface of mouse hindpaws to induce inflammatory pain. 24 h later, PSD-enriched fraction was isolated from L4-L5 spinal dorsal horn for immunoblotting analysis of the synaptic content of GluR2. The role of cAMP-dependent protein kinase （PKA） in the regula also investigated. Results tion of synaptic GluR2 was CFA simultaneously in- duced the mechanical allodynia and the increase in the synaptic amount of GluR2 in spinal dorsal horn. A1-though PKA inhibitor H-89 generated minimal effects on the Paw Withdrawal Threshold and synaptic GluR2 amount in intact mice, it dramatically repressed GluR2 synaptic concentration in inflamed mice, which was co- incident with the alleviation of allodynia. Conclusion Peripheral tissue injury evokes aberrant increase in the synaptic contents of AMPA receptor GluR.2 subunits in spinal dorsal horn via PKA signaling closely involved in the induction of chronic ry pain. , which is inflammato-