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在实验性缺血再灌注损伤后,突触后密度蛋白(PSD)-95 在海马 CA1 区的表达明显减少。

Postsynaptic density protein (PSD)-95 expression is markedly decreased in the hippocampal CA1 region after experimental ischemia-reperfusion injury.

机构信息

Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea.

出版信息

J Neurol Sci. 2013 Jul 15;330(1-2):111-6. doi: 10.1016/j.jns.2013.04.023. Epub 2013 May 16.

DOI:10.1016/j.jns.2013.04.023
PMID:23684672
Abstract

Synaptic plasticity is important for functional recovery after cerebral ischemic injury. In the present study, we investigated chronological change in the immunoreactivity of PSD-95, a kind of postsynaptic density protein, in the hippocampus proper (CA1-3 regions) after 5 min of transient cerebral ischemia in gerbils. PSD-95 immunoreactivity was observed in MAP-2-immunoreactive dendrites in the CA1-3 regions of the sham group. The PSD-95 immunoreactivity was shown as beaded structure in the MAP-2-immunoreactive dendrites. However, PSD-95 immunoreactivity began to be dramatically decreased in MAP-2-immunoreactive dendrites in the CA1 region, not CA2-3 region, at early time after ischemia-reperfusion. At 5 days after ischemia-reperfusion, MAP-2 immunoreactivity almost disappeared in the ischemic CA1 region, and PSD-95 immunoreactivity was much lower than that in the sham group. In brief, PSD-95 immunoreactivity in the CA1 dendrites was markedly decreased at early time after ischemia-reperfusion. We suggest that decreased PSD-95 immunoreactivity in the ischemic CA1 region may lead to a deficit of postsynaptic plasticity in the brain.

摘要

突触可塑性对于脑缺血损伤后的功能恢复很重要。在本研究中,我们研究了沙土鼠短暂脑缺血 5 分钟后海马区(CA1-3 区)中 PSD-95(一种突触后密度蛋白)免疫反应性的时间变化。PSD-95 免疫反应性存在于假手术组 CA1-3 区的 MAP-2 免疫反应性树突中。PSD-95 免疫反应性表现为 MAP-2 免疫反应性树突中的珠状结构。然而,在缺血再灌注后早期,CA1 区而非 CA2-3 区的 MAP-2 免疫反应性树突中 PSD-95 免疫反应性开始显著减少。缺血再灌注后 5 天,缺血 CA1 区的 MAP-2 免疫反应性几乎消失,PSD-95 免疫反应性明显低于假手术组。总之,缺血再灌注后早期 CA1 树突中的 PSD-95 免疫反应性明显降低。我们认为缺血 CA1 区 PSD-95 免疫反应性的降低可能导致大脑突触后可塑性的缺失。

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