东莨菪碱所致记忆障碍的脑内突触机制

THE SYNAPTIC MECHANISM OF SCOPOLAMINE-INDUCED MEMORY DYSFUNCTION IN THE BRAIN

研究问题是东莨菪碱所致记忆障碍的脑内突触机制。在东莨菪碱所致记忆障碍模型上定量分析了小鼠海马ＣＡ３区ＧｒａｙＩ突触界面结构多数的变化，并以３Ｈ－Ｌｅｕ为标记物进行同位素示踪，观察了东莨菪碱对小鼠海马突触体摄取３Ｈ－Ｌｅｕ的影响。结果表明，抗胆碱能药物东莨菪碱能引起小鼠海马ＣＡ３区突触后致密物质极显著变薄，另外，东莨菪碱还能显著降低海马突触体对３Ｈ－Ｌｅｕ的摄取。提示东莨菪碱所致记忆障碍的脑内突触机制可能与其引起脑内胆碱能神经系统突触体内蛋白质合成能力下降，继而导致突触界面结构参数的改变有关。

In this study the synaptic mechanism of scopolamine-induced memory dysfunctionwas investigated in the brain,the changes of the structure parameters of Gray Isynaptic interface in the hippocampal CA3 area were quantitatively analyzed in micemodel of scopolamine-induced memory dysfunction,and the effect of scopolamine onthe incorporation of3 H-Leu into hippocampal symaptosomes was observed.The resultsshowed that scopolamine could induce the thickness of post-synaptic density (PSD)thinned down significantly(P<0.01),and reduced the incorporation of 3 H-Leu intohippocampal symaptosomes apparently (p<0.001).These results suggested that thescopolamine-included memory dysfunction may be based on the decrease ofsynaptosomal protein syntheses of cholinergic system,and the changes of the synapticstructural parameters in the brain.