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作 者:吕丹丹[1] 尹洁[1] 穆继英[1] 景玉宏[1]
机构地区:[1]兰州大学基础医学院人体解剖与组织胚胎学研究所,甘肃兰州730000
出 处:《中国老年学杂志》2012年第2期300-302,共3页Chinese Journal of Gerontology
基 金:国家自然科学基金资助项目(No.30872731);兰州大学中央高校基本科研业务费(Lzujbky-2009093)
摘 要:目的探讨代谢异常导致的海马区树突棘变化与认知功能障碍的关系。方法通过水迷宫实验检测动物学习记忆变化,通过Gol-gi-Cox染色结合体视学半定量技术分析海马CA1区锥体细胞树突棘密度变化。结果 2型糖尿病(T2DM)小鼠在一个月出现胰岛素抵抗,并伴随持续的高血糖及高胆固醇血症。2个月出现学习记忆能力下降(P<0.05),随时间延长而加重,4个月后海马CA1区锥体细胞树突棘密度显著下降(P<0.01)。结论研究结果表明T2DM持续高血糖,高血脂可能直接导致海马区神经细胞树突棘丢失,突触可塑性下降,从而出现认知功能障碍。Objective To explore the roles of dendritical spine of pyramid cell in hippocampus on impairment of cognition under the condition of untreated-diabetes mellitus. Methods Learning and memory were tested by Morris water maze, and dendritical spines were ob- served by Golgi-Cox-staining. Stereologieal methods were used to quantitate the density of dendritical spine. Results The diabetic mice presented the insensitivity of insulin in fast at one month, accompanied the last hyperglycemia and hyperlipidemia. Diabetes caused the de- cline of cognition at two or four months in diabetic mice( P 〈 0. 05 ). Density of dendritical spine of hippocampus was significantly decreased in diabetic mice compared with that of control group ( P 〈 0. 01 ). Conclusions Persistent high glucose and cholesterol in diabetic mice can lead to the lose of dendritical soine of hipoocampus and the decreasin~ of svnaptie plasticity, which can result in the impairment of memory.
分 类 号:R322.81[医药卫生—人体解剖和组织胚胎学] R749.16[医药卫生—基础医学]
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