癫痫对幼年小鼠大脑皮质和海马神经元突起及突触的影响  

Effects of epilepsy on neuronal processes and synapses in the cerebral cortex and hippocampus of young mice

作　　者：邓同兴[1] 王敏丽[2] 常成 江丽[1] 范文娟[1] DENG Tongxing;WANG Minli;CHANG Cheng;JIANG Li;FAN Wenjuan(Department of Human Anatomy,Luohe Medical College,Luohe 462002;Department of Pediatrics,the Second Affiliated Hospital of Luohe Medical College,Luohe 462300;Department of Human Anatomy,School of Basic Medical Sciences,Zhengzhou University,Zhengzhou 450001,China)

机构地区：[1]漯河医学高等专科学校解剖教研室,漯河462002 [2]漯河医学高等专科学校第二附属医院儿科,漯河462300 [3]郑州大学基础医学院人体解剖学系,郑州450001

出　　处：《神经解剖学杂志》2024年第4期478-484,共7页Chinese Journal of Neuroanatomy

基　　金：河南省科技攻关项目(242102310088);河南省自然科学基金(222300420246);漯河医学高等专科学校创新创业发展能力提升工程项目(2020-LYZKYZD002,2021LYZTDXM009)。

摘　　要：目的:探讨癫痫持续状态(SE)对幼年小鼠大脑皮质和海马区神经元突起及突触的影响。方法:利用腹腔注射氯化锂和匹罗卡品方法制备幼年SE小鼠模型,用Morris水迷宫实验检测小鼠行为学变化,免疫荧光染色法观察小鼠大脑皮质和海马区神经元轴突、树突及突触连接形态学变化,透射电镜观察小鼠海马区锥体神经元突触的超微结构变化。结果:小鼠Ⅳ级以上发作率为80%,死亡率为25%。SE小鼠逃逸潜伏期延长(P<0.05),探寻平台路程轨迹明显延长且复杂化,且目标象限停留时间和穿越平台次数均明显减少(P<0.05)。两组小鼠大脑皮质和海马区均发现轴突神经丝标记蛋白SMI312和微管相关蛋白2(MAP2)阳性表达,且SE组轴突神经丝和神经元树突长短不一,排列比较密集散乱。SE组小鼠大脑海马区突触素(SYP)阳性表达增多,且SYP阳性斑点数量明显增加(P<0.01)。SE组突触囊泡数量增加,且突触后致密带(PSD)厚度明显降低(P<0.01)。结论:SE可能导致幼年小鼠大脑皮质和海马区突触急性损伤,诱发突触囊泡循环障碍,进而引起轴突和树突网络广泛的破坏和紊乱,突触发生反应性或代偿性重建。Objective:To explore the effects of status epilepticus(SE)on neuronal processes and synapses in the cerebral cortex and hippocampus of young mice.Methods:The young mice of SE model was established by intraperitoneal injection of lithium chloride and pilocarpine.Morris water maze test was used to detect the behavioral changes in the mice.Immunofluorescence staining was used to observe the morphological changes of axons,dendrites and synaptic connections of neurons in the cerebral cortex and hippocampus of mice,and the ultrastructural changes of synapses of pyramidal neurons in the mouse hippocampus were observed with transmission electron microscopy.Results:The seizure rate of grade IV and above in mice was 80%,and the mortality rate was 25%.The escape latency of SE mice was prolonged(P<0.05),the trajectory of exploring the platform was significantly longer and more complicated,and the time spent in the target quadrant and the number of crossing the platform were significantly reduced(P<0.05).Positive expression of axonal neurofilament marker protein SMI312 and microtubule-associated protein 2(MAP2)were found in the cerebral cortex and hippocampus of both groups,and the axonal neurofilaments and neuronal dendrites in the SE group were of different lengths and arranged densely and scatteredly.The positive expression of synaptophysin(SYP)and the number of positive spots increased significantly in in the hippocampus of SE group(P<0.01).The number of synaptic vesicles in the SE group increased significantly,and the postsynaptic density(PSD)thickness decreased significantly(P<0.01).Conclusion:SE might lead to acute injury of synapses in the cerebral cortex and hippocampal area of young mice,induce synaptic vesicle circulation disorders,and then cause widespread destruction and disorder of the axon and dendrite networks,the reactive or compensatory reconstruction of synaptic.

关 键 词：癫痫持续状态 海马 突触 突触囊泡 突触重建 小鼠 

分 类 号：R742.1[医药卫生—神经病学与精神病学]