突触囊泡蛋白在ALS转基因鼠海马的表达变化

目的为了为揭示肌萎缩脊髓侧索硬化症（amyotrophic lateral sclerosis，ALS）认知功能障碍的机制提供依据，观察不同年龄ALS转基因小鼠海马中突触囊泡蛋白（synaptophysin，Syp）的表达情况。方法取95d、108d和122dALS转基因鼠海马，应用免疫荧光、Westernblot、RT-PCR技术检测Syp在海马中的表达变化。结果与同窝野生型鼠比较，Syp蛋白和mRNA表达水平在95d龄ALS转基因鼠海马中无明显变化，在108d与122d龄ALS转基因鼠海马中明显降低。结论Syp在ALS转基因鼠海马中表达减少表明，突触可塑性降低是ALS学习记忆能力下降的重要病理学基础。

Expression of Synaptophysin in the hippocampus of ALS transgenic mice

Objective To provide evidence for uncovering the underlying mechanism of cognitive im- pairment in amyotrophic lateral sclerosis （ALS）, we observed the change of the expression of synapto- physin （Syp） in the hippocampus of ALS transgenic mice at different ages. Methods The expression of Syp protein and mRNA in the hippocampus of ALS transgenic mice was detected by immunohistochemistry, western blot or RT-PCR at the ages of 95d, 108d and 122d. Results Immunofluorescence and Western blot showed that the expression of Syp protein was significantly decreased in ALS transgenic mice at the ages of 108d and 122d, compared with wild-type mice at the same ages. Consistently, the mRNA level of Syp de- tected by RT-PCR in ALS transgenic mice at the ages of 108d and 122d was also significantly lower than that wild-type mice at the same ages. There was no obvious change in the expression of Syp at both protein and mRNA level at the age of 95d. Conclusion The decrease of Syp expression in the hippocampus of ALS transgenic mice suggests that the decrease of synaptic plasticity may be the important pathological basis of cognitive impairment in ALS.