论文部分内容阅读
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。
The research problem is the brain synaptic mechanism of scopolamine-induced memory impairment. Quantitative analysis of GrayI synaptic interface structure in mouse hippocampal CA3 region was quantitatively analyzed by scopolamine-induced memory impairment model. 3H-Leu was used as isotope tracer to observe the effect of scopolamine on the uptake of mouse hippocampal synaptosomes 3H -Leu effect. The results show that the anticholinergic scopolamine can cause the post-synaptic densification of hippocampal CA3 region significantly thinning, in addition, scopolamine can significantly reduce the 3H-Leu uptake of hippocampal synaptosomes. Suggesting that scopolamine-induced memory impairment in the brain synaptic mechanism may be related to its ability to cause brain synaptic cholinergic synaptic body protein synthesis decreased, which led to changes in the structure parameters of the synaptic interface.