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先天性巨细胞病毒感染对大鼠海马齿状回突触可塑性的影响。

Effects of congenital HCMV infection on synaptic plasticity in dentate gyrus (DG) of rat hippocampus.

机构信息

Department of Neurology, Southern Medical University, Guangzhou, 510515, China.

出版信息

Brain Res. 2011 May 10;1389:27-34. doi: 10.1016/j.brainres.2011.03.007. Epub 2011 Mar 9.

DOI:10.1016/j.brainres.2011.03.007
PMID:21396925
Abstract

This study was carried out to investigate whether the congenital HCMV infection affect the induction and maintenance of LTP /DP. Rat models of Sprague-Dawley rats congenitally infected by HCMV were made. Field excitatory postsynaptic potentials (EPSPs) were recorded in the hippocampal slices of offspring rats (50-65days) to study alterations of LTP /DP in area dentate gyrus (DG) of the hippocampus after congenital infection. The Ca(2+) and mRNA level of calmodulin (CaM) in the hippocampus neurons of the experiment group (congenital infected by HCMV) and the control group were measured;The input/output (I/O) curves of the EPSP slope PS amplitude in area DG in experiment group were significantly depressed when compared to control group (P<0.05). LTP of the EPSP slope and PS amplitude in area DG of the hippocampus was 137±4% (EPSP) and 225±11% (PS) in control rats and 115±9% (EPSP) and 163±7% (PS) in experiment rats (EPSP: F=25.29,P<0.05;PS: F=74.33 P<0.05, two-way ANOVA with Tukey test); DP of the EPSP slope and PS amplitude was 86±3% (EPSP) and 85±2% (PS) in control rats and 94±5% (EPSP) and 93±4% (PS) in congenitally infected rats (EPSP: F=5.62, P<0.05;PS: F=4.22, P<0.05, two-way ANOVA with Tukey test) . At the same time, intracellular [Ca(2+)] and mRNA level of CaM in the hippocampus neurons of the experiment group were significantly increased than that of in the controls ([Ca(2+)]: P<0.01;CaM mRNA: P<0.01) . The results demonstrate that congenital HCMV infection could reduce the range of synaptic plasticity in the Sprague-Dawley rats, which may trigger the dysfunction of learning and memory through disrupting the calcium balance.

摘要

本研究旨在探讨先天性 HCMV 感染是否会影响 LTP/DP 的诱导和维持。通过建立先天性感染 HCMV 的 Sprague-Dawley 大鼠模型,在其子代大鼠(50-65 日龄)海马切片中记录场兴奋性突触后电位(EPSP),以研究先天性感染后海马齿状回(DG)区 LTP/DP 的变化。测量实验组(先天性感染 HCMV)和对照组海马神经元中的 Ca(2+)和钙调蛋白(CaM)mRNA 水平;实验组(感染 HCMV)的 EPSP 斜率 PS 幅度在 DG 区的输入/输出(I/O)曲线明显低于对照组(P<0.05)。对照组大鼠海马 DG 区 EPSP 斜率和 PS 幅度的 LTP 分别为 137±4%(EPSP)和 225±11%(PS),实验组大鼠分别为 115±9%(EPSP)和 163±7%(PS)(EPSP:F=25.29,P<0.05;PS:F=74.33,P<0.05,双向方差分析加 Tukey 检验);对照组大鼠 EPSP 斜率和 PS 幅度的 DP 分别为 86±3%(EPSP)和 85±2%(PS),实验组大鼠分别为 94±5%(EPSP)和 93±4%(PS)(EPSP:F=5.62,P<0.05;PS:F=4.22,P<0.05,双向方差分析加 Tukey 检验)。同时,实验组海马神经元内的 [Ca(2+)]和 CaM mRNA 水平明显高于对照组([Ca(2+)]:P<0.01;CaM mRNA:P<0.01)。结果表明,先天性 HCMV 感染可减少 Sprague-Dawley 大鼠突触可塑性范围,可能通过破坏钙平衡导致学习记忆功能障碍。

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