外周神经损伤降低背侧海马的突触可塑性导致短期记忆障碍  

The mouse model of spared nerve injury reduces the Schaffer-CA1 synaptic plasticity in dorsal hippocampus

作　　者：文君健 韩霜 蒋斌[1] WENJun-jian;HAN Shuang;JIANG Bin(Guangdong Province Key Laboratory of Brain Function and Disease,Zhongshan School of Medicine,Sun Yat-sen University,Guangzhou,Guangdong Province 510080,China)

机构地区：[1]中山大学中山医学院广东省脑功能与脑疾病研究重点实验室,广东广州510080

出　　处：《解剖学研究》2022年第2期118-122,共5页Anatomy Research

基　　金：国家自然科学基金面上项目(81870869)。

摘　　要：目的探讨保留性神经损伤(SNI)模型对小鼠背侧海马Schaffer-CA1的突触可塑性及短期记忆功能的影响。方法比较了Sham组和SNI组小鼠的新物体识别记忆(NOR)。用全细胞细胞内记录的方法记录了背侧海马Schaffer侧支到锥体细胞的LTP并比较Sham和SNI模型小鼠背侧海马的N-甲基-D-天冬氨酸受体电流(NMDAR current);用Western blot的方法比较了Sham组和SNI组小鼠背侧海马BDNF的蛋白表达量。结果与Sham组相比,SNI组小鼠新物体识别指数、背侧海马Schaffer-CA1的LTP幅度、NMDAR电流和BDNF的蛋白表达量均有下降(均P<0.05)。结论SNI导致了背侧海马NMDAR依赖的Schaffer-CA1突触可塑性降低,可能导致短期记忆功能受损。Objective To investigate the effects of spared nerve injury on short-term memory and the underlying mechanisms.Methods The novel object recognition(NOR)were tested;To induce LTP from Schaffer to CA1 pyramidal cells and NMDAR current in the dorsal hippocampus by whole-cell recording and to examine the expression of brain-derived neurotrophic factor(BDNF)in the dorsal hippocampus between Sham and SNI mice.Results Compared to the Sham group,the NOR index,dorsal Schaffer-CA1 LTP,NMDAR current,and the expression of BDNF in the dorsal hippocampus decreased significantly(P<0.05).Conclusion SNI surgery induced memory deficit via the impairment in NMDAR-dependent Schaffer-CA1 synaptic plasticity in the dorsal hippocampus.

关 键 词：保留性神经损伤模型 短期记忆 海马 脑源性神经营养因子 新物体识别记忆 

分 类 号：R745[医药卫生—神经病学与精神病学]