Neuroprotective effects of GluR6 antisense oligodeoxynucleotides on transient brain is chemia/reperfusion-induced neuronal death in rat hippocampal CA1 region

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	Neuroprotective effects of GluR6 antisense oligodeoxynucleotides on transient brain is chemia/reperfusion-induced neuronal death in rat hippocampal CA1 region
	Pei, DS ; Guan, QH ; Sun, YF ; Zhang, QX ; Xu, TL(徐天乐) ; Zhang, GY
刊名	JOURNAL OF NEUROSCIENCE RESEARCH
	2005
卷号	82 期号:5 页码:642-649
关键词	cerebral ischemia glutamate receptor 6 (GluR6) mixed lineage kinase-3 (MLK3) postsynaptic density protein 95 (PSD-95) POSTSYNAPTIC DENSITY PROTEIN-95 GLUTAMATE RECEPTORS FOREBRAIN ISCHEMIA CEREBRAL-ISCHEMIA MAP KINASES KAINATE ACTIVATION MICE JNK3 APOPTOSIS
ISSN号	0360-4012
通讯作者	Zhang, GY (reprint author), Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, 84 W Huai Hai Rd, Xuzhou 221002, Jiangsu, Peoples R China,gyzhang@xzmc.edu.cn
英文摘要	To investigate whether the kainate (KA) receptors subunit GluR6 is involved in the neuronal cell death induced by cerebral ischemia followed by reperfusion, the antisense oligodeoxynucleotides (ODNs) of GluR6 were used to suppress the expression of GluR6 by intracerebroventricular infusion once per day for 3 days before ischemia. Transient brain ischemia was induced by four-vessel occlusion in Sprague-Dawley rats. The effects of GluR6 antisense ODNs on the phosphorylation of MLK3 and JNK and the interactions of MLK3 and PSD-95 with GluR6 were examined by immunoprecipitation and immunoblotting. Our results show that GluR6 antisense ODNs can knock down the expression of GluR6 and suppress the assembly of the GluR6. PSD-95. MLK3 signaling module and, therefore, inhibit JNK activation and phosphoralation of c-jun. On the other hand, the GluR6 antisense ODNs also show a protective role against neuronal cell death induced by cerebral ischemia/reperfusion. Administration of GluR6 antisense ODNs once per day for 3 days before cerebral ischemia significantly decreased neuronal degeneration. In conclusion, our results demonstrate that kainate receptor subunit GluR6 plays an important role in neuronal death induced by cerebral ischemia followed by reperfusion. (c) 2005 Wiley-Liss, Inc.
学科主题	Neurosciences & Neurology
收录类别	SCI
语种	英语
公开日期	2012-07-23
内容类型	期刊论文
源URL	[http://ir.sibs.ac.cn/handle/331001/1862]
专题	上海神经科学研究所_神经所(总)
推荐引用方式 GB/T 7714	Pei, DS,Guan, QH,Sun, YF,et al. Neuroprotective effects of GluR6 antisense oligodeoxynucleotides on transient brain is chemia/reperfusion-induced neuronal death in rat hippocampal CA1 region[J]. JOURNAL OF NEUROSCIENCE RESEARCH,2005,82(5):642-649.
APA	Pei, DS,Guan, QH,Sun, YF,Zhang, QX,Xu, TL,&Zhang, GY.(2005).Neuroprotective effects of GluR6 antisense oligodeoxynucleotides on transient brain is chemia/reperfusion-induced neuronal death in rat hippocampal CA1 region.JOURNAL OF NEUROSCIENCE RESEARCH,82(5),642-649.
MLA	Pei, DS,et al."Neuroprotective effects of GluR6 antisense oligodeoxynucleotides on transient brain is chemia/reperfusion-induced neuronal death in rat hippocampal CA1 region".JOURNAL OF NEUROSCIENCE RESEARCH 82.5(2005):642-649.