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pubmed-article:19344701pubmed:abstractTextSyntaxin1 and synaptotagmin are located in the pre-synaptic terminals and play central roles in Ca(2+)-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.lld:pubmed
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pubmed-article:19344701pubmed:dateRevised2011-11-17lld:pubmed
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pubmed-article:19344701pubmed:articleTitleUp-regulation of syntaxin1 in ischemic cortex after permanent focal ischemia in rats.lld:pubmed
pubmed-article:19344701pubmed:affiliationDepartment of Functional Histology, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime 791-0295, Japan.lld:pubmed
pubmed-article:19344701pubmed:publicationTypeJournal Articlelld:pubmed
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