miR-132调控神经环路-突触可塑性与改善卒中后痴呆的机制研究

发布时间：2018-03-14 00:24

本文选题：miR-调控神经环路　切入点：突触可塑性　出处：《中风与神经疾病杂志》2017年12期 　论文类型：期刊论文

【摘要】：目的分析卒中后痴呆大鼠模型脑内和外周血中的miR-132的表达以及其对模型行为学的影响,并探讨其可能的机制。方法选取48只大鼠,建立卒中后痴呆的大鼠模型,实验分为4组,其中一组为模型组,另外3组为对照组,然后分别对4组大鼠的行为进行检测,探究miR-132对卒中后痴呆大鼠的影响及其可能的作用机制。结果水迷宫实验提示miR-132对卒中后痴呆大鼠的行为学有改善作用,同时大鼠旷野试验行为检测结果提示agomir-132组的大鼠垂直得分及水平得分均高于模型组(P0.05),说明miR-132可改善卒中后痴呆相关的额叶-皮质下神经环路的突触可塑性,从而改善PSD小鼠认知功能;agomir-132+Grin2A组的大鼠垂直得分以及水平得分均明显低于其阴性对照(agomir-132+vector)和agomir-132组(P0.05),并且agomir132+Grin2A组糖水消耗百分比明显低于其阴性对照和agomir-132组(P0.05),表明Grin2A参与了miR-132对卒中后痴呆大鼠的治疗作用,Grin2A基因的表达可以抑制miR-132调控突触可塑性。结论 miR-132通过改善额叶-皮质环路突触的可塑性,改善卒中后大鼠的认知功能,Grin2A可以阻断miR-132对卒中后痴呆大鼠行为学的改善作用。
[Abstract]:Objective to analyze the expression of miR-132 in the brain and peripheral blood of rats with dementia after stroke and its effect on the behavior of the model, and to explore the possible mechanism. Methods 48 rats were selected to establish the model of dementia after stroke, and the rats were divided into 4 groups. One group was the model group and the other three groups were the control group. To explore the effect of miR-132 on poststroke dementia rats and its possible mechanism. Results the water maze experiment showed that miR-132 could improve the behavior of poststroke dementia rats. At the same time, the results of field test showed that the vertical and horizontal scores of agomir-132 group were higher than that of model group (P 0.05), indicating that miR-132 could improve the synaptic plasticity of the frontal lobe-subcortical nerve loop associated with poststroke dementia. Therefore, the vertical and horizontal scores of rats in the group of improving cognitive function of PSD mice were significantly lower than those of the negative control group (P0.05) and the agomir-132 group, and the percentage of sugar water consumption in the agomir132 Grin2A group was significantly lower than that in the negative control group and the agomir-132 group, indicating that the percentage of sugar water consumption in the agomir132 Grin2A group was significantly lower than that in the negative control group and the agomir-132 group. Grin2A is involved in the therapeutic effect of miR-132 on poststroke dementia rats. The expression of Grin 2A gene can inhibit the regulation of synaptic plasticity by miR-132. Conclusion miR-132 can improve the plasticity of synapses in frontal lobe and cortical loop. Improving the cognitive function of poststroke rats could block the effect of miR-132 on the behavior of poststroke dementia rats.
【作者单位】：南京鼓楼医院集团宿迁市人民医院神经内科;南京鼓楼医院神经内科;
【分类号】：R743.3

【相似文献】