【摘要】 目的分析戊四氮(PTZ)点燃慢性癫痫模型SD大鼠脑组织酪氨酸激酶受体B(TrKB)及谷氨酸转运体1(GLT-1)的表达变化,为进一步研究胶质细胞BDNF/TrkB信号通路与GLT-1的相关性提供实验依据,为癫痫的防治提供靶位线索。方法 SD大鼠40只随机分成模型组(30只)及对照组(10只),采用PTZ点燃法制作慢性癫痫大鼠模型。运用Western技术分析SD大鼠PTZ点燃后7天海马及颞叶皮层TrkB和GLT-1的蛋白表达、采用免疫荧光双标法分析SD大鼠PTZ点燃后7天海马及颞叶皮层GFAP/TrkB双标阳性细胞的表达,并与对照组进行比较。结果 SD大鼠慢性癫痫发作后,海马及颞叶皮层TrkB和GLT-1蛋白的表达均明显上调、GFAP/TrkB双标阳性细胞平均光密度值较对照组明显增高(P<0.05)。结论 PTZ点燃慢性癫痫SD大鼠海马及颞叶皮层脑组织TrkB表达上调与GLT-1表达异常之间可能存在内在联系,BDNF/TrkB信号通路可能通过改变PTZ点燃慢性癫痫SD大鼠胶质细胞中GLT-1的生物效应来影响或参与癫痫过程。更多还原

【Abstract】 Objective To analyze the expressions of TrkB and GLT-1 in the brain of pentylenetetrazol(PTZ)kindling model of chronic epilepsy in rats,and provide evidence for correlation between the BDNF/TrkB pathway and GLT-1 and clues for the prevention and treatment targets of epilepsy.Methods 40 Sprague-Dawley(SD)rats were randomly classified as model(30)and control(10)groups,respectively.Western blotting was used for analyzing the expression of TrkB and GLT-1,and double immunofluorescence staining was used for detecting the cells positive for both glial fibrillary acidic protein(GFAP)and TrkB in the hippocampus and temporal cortex 7days after establishing the kindling model.Results Compared with the control group,protein level expression of TrkB and GLT-1,and mean optical density(OD)value of the cells positive for both GFAP and TrkB in the hippocampus and temporal cortex were significantly increased after the onset of epilepsy(P<0.05).Conclusion The BDNF/TrkB pathway may participate in epileptogenesis through modulating the biological effect of GLT-1 in the glial cells of PTZ kindling rats,though the specific mechanism requires further investigation.更多还原