慢性酒精中毒小鼠小脑的超微结构实验研究  

Experimental Study on Cerebellar Ultrastructure in Mice of Chronic Ethanol Intoxication

作　　者：童林艳[1] 李小凤[1] 

机构地区：[1]重庆医科大学附属第二医院神经内科,重庆400010

出　　处：《世界科技研究与发展》2010年第6期847-849,共3页World Sci-Tech R&D

基　　金：重庆市科委自然科学基金计划资助项目(2007BB5312)

摘　　要：目的探讨慢性酒精中毒导致神经系统损伤的机制。方法建立小鼠慢性酒精中毒动物模型,观察动物行为学的改变,测量血浆酒精浓度,通过透射电镜了解小脑的超微结构变化。结果酒精处理组的血浆酒精浓度为101.4±20.5mg/dL,与对照组和配对对照组比较,酒精处理组小鼠行动欠灵活,小脑线粒体形状多样、大小多变、数量增加和平均横断面面积显著减小;突触的数量减少、突触后膜致密物质厚度变薄、突触活性区长度变短及突触间隙宽度变宽,突触前结构内附着于突触的囊泡较多。结论酒精对线粒体和突触结构、功能的损害可能是慢性酒精中毒的神经系统损伤机制之一。Objective To explore the mechanisms how ethanol leads to injuries of central nervous system. Methods Chronic ethanol intoxication model of mice with chronic ethanol intoxication is built up. Behavioral changes are observed. Ethanol concentrations in plasma are measured. Cerebellar ultrastructure is found out by transmission electron microscope. Results The plasma ethanol concentrations of ethanol treatment group are 101.4± 20. 5 mg/dL. The mice in chronic ethanol intoxication are ataxic. Mitochondria in cerebellum differs greatly in shape and size. The number and mean transverse area of mitochondria increases and decreases significantly, respectively. There are more synapses, thicker postsynaptic densities and shorter synaptic active areas, wider synaptic space and more vesicles attached to the synapses, compared with mice in control and pair control group. Conclusion It is suggested that disturbance of the structure and function of mitochondria and synapses is one of the mechanisms of central nervous system injuries of chronic intoxication.

关 键 词：小鼠 慢性酒精中毒 小脑 超微结构 线粒体 突触 

分 类 号：R595.6[医药卫生—内科学]