摘要
目的 探讨亚急性乙醇中毒导致小鼠记忆障碍的脑内突触机制。方法 用新鲜配制体积分数为 3 0 %的乙醇溶液按 10ml kg剂量分别灌胃染毒 1、7和 2 8d ,用Y 迷宫检测小鼠分辨学习记忆行为的变化 ,用紫外分光光度计和荧光分光光度计分别检测脑组织超氧化物歧化酶 (SOD)、脂褐素生化指标 ;用电镜和计算机图像分析仪观测小鼠海马CA3区GrayⅠ型突触界面结构参数的变化。结果 一次性乙醇染毒对小鼠学习记忆无影响 ;连续 7d乙醇染毒 ,使小鼠Y 迷宫分辨学习能力下降 ,3 0min记忆保持率下降 ,但 2 4h记忆无明显变化 ,脑SOD活性下降 ,海马突触界面结构无明显变化 ;连续 2 8d乙醇染毒 ,小鼠学习和记忆均明显减退 ,脑组织SOD的活性显著降低 ,脂褐素积累增加 ;同时海马突触后致密物质 (PSD)厚度显著减小 ,突触间隙显著增宽。结论 亚急性乙醇中毒致小鼠学习记忆功能障碍与其降低脑组织抗氧化能力 。
Objective To study impairment of learning\|memory induced by subacute adiministration of alcohol in mice,probe into its possible mechanism of action.Methods The mice were induced by adiministration of 30% alcohol (10 ml\5kg -1 )for 1,7 and 28 days,respectively.Thirty minites after the last treatment,learning\|memory behavior was tested by using Y\|maze.Then the activity of SOD,the content of lipofuscin were measured with Uv\|photospectrometer and Fluorospectrophometer analysis system,and the structure of Gray Ⅰ synaptic interface in CA\-3 area of hippocampus was quantitatively analyzed by electronic microscope and computer image processing appliance.Results Adiministration of alcohol for 28 days caused impairment of learning and memory in mice,declined SOD activity,increased level of lipofuscin,thinned the thickness of post\|synaptic density(PSD)significantly,and widened the width of the synaptic cleft in hippocampus CA\-3 area,but had no significant effect on learning\|memory when alcohol was given only one time.Adiministration of alcohol for 7 days impaired discriminating learing behavior in Y\|maze,and attenuated remarkablely memory retention in 30 mineters and SOD activity.Conclusion subacute adiministration of alcohol could cause learning and memory impairment in mice,decline of the antioxidase activity of brain and a pathological alteration of synaptic interface structure of hippocampus in the mice might be involved in the effects.
出处
《卫生毒理学杂志》
CAS
CSCD
北大核心
2002年第4期203-205,共3页
Journal of Health Toxicology
基金
浙江省分析测试基金项目 (0 1 2 0 8)
