慢性应激对大鼠海马CA3区锥体细胞顶树突细胞骨架的效应及其机制研究  

Effects of chronic stress on cytoskeleton of dendrites in rat hippocampal CA3 neurons and its relevant mechanism

作　　者：金海燕[1] 刘少文[2] 杨权[2] 

机构地区：[1]广东省人民医院,广州广东省精神卫生研究所510120 [2]汕头大学精神卫生中心

出　　处：《中华精神科杂志》2007年第2期117-119,共3页Chinese Journal of Psychiatry

摘　　要：目的探讨慢性强迫游泳应激对大鼠海马 CA3区锥体细胞顶树突细胞骨架的效应及可能的机制。方法将16只雄性 Sprague-Dawley 大鼠(2月龄),随机分为对照组和应激组(强迫游泳,20 min/d,共4周),每组8只。用常规透射电镜观察两组大鼠海马 CA3区锥体细胞顶树突细胞骨架,用免疫组织化学方法定量测定锥体细胞内磷酸化微管相关蛋白2(MAP2)表达水平。结果 (1)海马 CA3区锥体细胞顶树突内细胞骨架的变化:对照组纵切面显示微管排列整齐、连续,呈平行状;横切面显示环状微管完整、规则,分布均匀;线粒体嵴清晰。应激组纵切面显示微管断裂,平行微管间距离变宽;横切面显示微管环不完整,单体分布不均匀;线粒体嵴模糊,偶见空泡样变性。(2)海马CA3区锥体细胞磷酸化 MAP2的表达:应激组大鼠平均灰度值(145.0±4.4)低于对照组(149.3±1.8)(P<0.05),表达的阳性细胞数[(40.36±1.36)个/视野]少于对照组[(42.73±1.56)个/视野;P<0.01]。结论慢性强迫游泳应激可导致大鼠海马 CA3区锥体细胞顶树突内细胞骨架的损害,这一效应可能通过增加磷酸化 MAP2的表达实现。Objective To explore the effects and mechanism of chronic stress on cytoskeleton of dendrites in the rat hippacampal CA3 neurons. Methods Sixteen male Sprague-Dawley rats were randomly divided into two groups （8 in each）, one was given 4-week forced-swimming to make stress model, The ultrastructure of dendritic microtubules was observed by using an electron-microscope. The level of phosphorylated MAP2 in rat hippocampal CA3 pyramidal neurons was detected with immunohistochemistry method. Results The destroyed changes of cytoskeleton were observed in hippocampal CA3 pyramidal neuronal dendrites in the stress group. The average gray degree of phosphorylated MAP2 in hippocampal CA3 pyramidal neurons was significantly lower in the stress group （145.0 ± 4.4 ）than that in control group （ 149. 3 ± 1.8） ; and the number of neurons （40. 36 ± 1.36 ） was significantly less than that of control group （42. 73 ± 1.56）. Conclusion It is suggested that chronic stress could damage the cytoskeleton of dendrites in rat hippocampal CA3 pyramidal neurons through enhancing level of phosphorylation of MAP2.

关 键 词：应激 海马 细胞骨架 微管相关蛋白质类 

分 类 号：R363[医药卫生—病理学]