Up-regulation of syntaxin1 in ischemic cortex after permanent focal ischemia in rats

被引:11
|
作者
Cao, Fang [1 ]
Hata, Ryuji [1 ]
Zhu, Pengxiang [1 ]
Niinobe, Michinobu [2 ]
Sakanaka, Masahiro [1 ]
机构
[1] Ehime Univ, Grad Sch Med, Dept Funct Histol, Toon, Ehime 7910295, Japan
[2] Osaka Univ, Inst Prot Res, Div Regulat Macromol Funct, Suita, Osaka 5650871, Japan
关键词
SNARE; Cerebral ischemia; Synaptotagmin; SYNAPTOTAGMIN-I; CA2+ SENSOR; MICROGLIA; DEATH; TERMINALS; RELEASE; FUSION; DAMAGE; NMDA; AMPA;
D O I
10.1016/j.brainres.2009.03.047
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Syntaxin1 and synaptotagmin are located in the pre-synaptic terminals and play central roles in Ca2+-triggered neurotransmitter release. Because excessive synaptic transmission has been implicated in neuronal cell death after ischemia, we investigated the effects of cerebral ischemia on the levels of these proteins using a rat permanent focal ischemia model. Western blot analysis revealed that the protein level of syntaxin1 was significantly up-regulated in the ischemic core cortex and peri-ischemic cortex at 1 day after ischemia, while the protein level of synaptotagmin was not. Immunohistochemical analysis revealed that the protein level of syntaxin1 was markedly up-regulated in the ischemic areas where immunoreaction for MAP2 was lost. Furthermore, we showed that resident microglial cells were quite vulnerable to ischemia. Our data provide novel insights into the molecular mechanism of cerebral ischemia at the pre-synaptic terminals. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码:52 / 61
页数:10
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