摘要
目的：探讨实验性癫痫大鼠齿状回中微管相关蛋白-2(MAP-2)的变化及其在癫痫MFs出芽和突触重建中的意义。方法：建立海马快速电点燃模型,运用免疫组化方法研究齿状回中MAP-2在点燃不同阶段的动态变化，并结合尼氏染色和电镜观察阐明MAP-2的变化特点，探讨其原因及意义。结果：齿状回分子层颗粒细胞树突的MAP-2的免疫反应性于点燃后3天明显增强，至14天达到高峰(P<0.01)，20～30天降至对照水平（P<0.01） 。MAP-2的增加与齿门神经元的变性之间存在指数曲线相关关系（R2=0.9362）。电镜下，分子层神经元树突内的微管于点燃后3天增多，14天明显增多，至30天已有崩解。还可见轴突分支出芽，神经末梢与树突形成多个突触。结论：MAP-2的过度表达在癫痫大鼠苔纤维出芽和突触重建过程中发挥了重要作用，而大量受损的齿门神经元对抑制性细胞广泛的去神经支配可能是其过度表达的启动因素。
Objective: To investigate the changes of microtubule-associated protein- 2 (MAP2) in epileptic dentate gyrus and the significance in epilepsy. Methods: Alterations in MAP2-immunoreactivity(MAP2-IR) in the kindling model of epilepsy were investigated in rats with survival times ranging from three to thirty days. Nissl staining and electron microscopic studies were also used to explore more deeply. Results: MAP2-IR was obviously enhanced in the dendrites of granule cells three days after kindling and remained enhanced up to fourteen days (P<0.01). It was returned to control patterns twenty to thirty days after kindling (P<0.01). Nissl staining demonstrated an exponential curve correlation between the enhancement of MAP-2 and degeneration of hilar neurons (R2=0.9362). Electron microscopic studies showed that microtubules of dendrite in the dentate molecule was increased three days after kindling and obviously increased fourteen days after kindling, but it was decreased thirty days later. Sprouting of dentate granule cell axons and synaptic contacts between nerve terminal and dendrite were discovered. Conclusion: It suggests that the overexpression of MAP-2 via the formation of microtubules may play an important role in the sprouting of mossy fibers in epileptic rats，and the extensive denervation of inhibitory cells by many damaged hilar neurons may trigger a process that leads to overexpression of MAP-2.
出处
《重庆医科大学学报》
CAS
CSCD
2002年第4期379-382,共4页
Journal of Chongqing Medical University
关键词
癫痫
大鼠
齿状回
微管相关蛋白-2
临床意义
Epilepsy
Microtubule-associated protein-2 (MAP-2)
Dentate gyrus
Kindling
