Up-regulation of syntaxin1 in ischemic cortex after permanent focal ischemia in rats
Abstract 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 th...
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| Veröffentlicht in: | Brain research 2009-05, Vol.1272, p.52-61 |
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| creator | Cao, Fang Hata, Ryuji Zhu, Pengxiang Niinobe, Michinobu Sakanaka, Masahiro |
| description | Abstract 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. |
| doi_str_mv | 10.1016/j.brainres.2009.03.047 |
| format | Article |
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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.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2009.03.047</identifier><identifier>PMID: 19344701</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Analysis of Variance ; Animals ; Biological and medical sciences ; Calcium-Binding Proteins - metabolism ; Cerebral Cortex - metabolism ; Cerebral Cortex - physiopathology ; Cerebral ischemia ; Disease Models, Animal ; Glial Fibrillary Acidic Protein - metabolism ; Infarction, Middle Cerebral Artery - pathology ; Male ; Medical sciences ; Microfilament Proteins ; Microtubule-Associated Proteins - metabolism ; Neurology ; Rats ; Rats, Inbred SHR ; SNARE ; Synaptotagmin ; Synaptotagmins - metabolism ; Syntaxin 1 - metabolism ; Up-Regulation - physiology ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Brain research, 2009-05, Vol.1272, p.52-61</ispartof><rights>Elsevier B.V.</rights><rights>2009 Elsevier B.V.</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-53f4fe90b165403e33cd3f4be8cc0596d5c08b23faace7a19786a44e7d4fd1f53</citedby><cites>FETCH-LOGICAL-c482t-53f4fe90b165403e33cd3f4be8cc0596d5c08b23faace7a19786a44e7d4fd1f53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.brainres.2009.03.047$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27911,27912,45982</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21532892$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19344701$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cao, Fang</creatorcontrib><creatorcontrib>Hata, Ryuji</creatorcontrib><creatorcontrib>Zhu, Pengxiang</creatorcontrib><creatorcontrib>Niinobe, Michinobu</creatorcontrib><creatorcontrib>Sakanaka, Masahiro</creatorcontrib><title>Up-regulation of syntaxin1 in ischemic cortex after permanent focal ischemia in rats</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Abstract 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.</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium-Binding Proteins - metabolism</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cerebral Cortex - physiopathology</subject><subject>Cerebral ischemia</subject><subject>Disease Models, Animal</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>Infarction, Middle Cerebral Artery - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microfilament Proteins</subject><subject>Microtubule-Associated Proteins - metabolism</subject><subject>Neurology</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>SNARE</subject><subject>Synaptotagmin</subject><subject>Synaptotagmins - metabolism</subject><subject>Syntaxin 1 - metabolism</subject><subject>Up-Regulation - physiology</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkstu1DAUQK0K1E4fv1BlA7uE60eceINAFRSkSixo15bjXIOHxBnspOr8PY5mChKbrixb576OLyHXFCoKVL7bVl00PkRMFQNQFfAKRHNCNrRtWCmZgFdkAwCybJXiZ-Q8pW2-cq7glJxRxYVogG7I_cOujPhjGczsp1BMrkj7MJsnH2jhQ-GT_Ymjt4Wd4oxPhXEzxmKHcTQBw1y4yZrhmTJrRDRzuiSvnRkSXh3PC_Lw-dP9zZfy7tvt15uPd6UVLZvLmjvhUEFHZS2AI-e2z08dttZCrWRfW2g7xp0xFhtDVdNKIwQ2vXA9dTW_IG8PeXdx-r1gmvWYW8FhyM1NS9KyYRJUnvolkEHd0FrIDMoDaOOUUkSnd9GPJu41Bb2K11v9LF6v4jVwncXnwOtjhaUbsf8XdjSdgTdHwKTszEUTrE9_OUZrzlrFMvfhwGEW9-gx6mQ9Bou9j2hn3U_-5V7e_5fCDj74XPUX7jFtpyWG_C2a6sQ06O_rmqxbsqqStFH8Dz2euiQ</recordid><startdate>20090526</startdate><enddate>20090526</enddate><creator>Cao, Fang</creator><creator>Hata, Ryuji</creator><creator>Zhu, Pengxiang</creator><creator>Niinobe, Michinobu</creator><creator>Sakanaka, Masahiro</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20090526</creationdate><title>Up-regulation of syntaxin1 in ischemic cortex after permanent focal ischemia in rats</title><author>Cao, Fang ; Hata, Ryuji ; Zhu, Pengxiang ; Niinobe, Michinobu ; Sakanaka, Masahiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-53f4fe90b165403e33cd3f4be8cc0596d5c08b23faace7a19786a44e7d4fd1f53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Calcium-Binding Proteins - metabolism</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cerebral Cortex - physiopathology</topic><topic>Cerebral ischemia</topic><topic>Disease Models, Animal</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>Infarction, Middle Cerebral Artery - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microfilament Proteins</topic><topic>Microtubule-Associated Proteins - metabolism</topic><topic>Neurology</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>SNARE</topic><topic>Synaptotagmin</topic><topic>Synaptotagmins - metabolism</topic><topic>Syntaxin 1 - metabolism</topic><topic>Up-Regulation - physiology</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cao, Fang</creatorcontrib><creatorcontrib>Hata, Ryuji</creatorcontrib><creatorcontrib>Zhu, Pengxiang</creatorcontrib><creatorcontrib>Niinobe, Michinobu</creatorcontrib><creatorcontrib>Sakanaka, Masahiro</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cao, Fang</au><au>Hata, Ryuji</au><au>Zhu, Pengxiang</au><au>Niinobe, Michinobu</au><au>Sakanaka, Masahiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Up-regulation of syntaxin1 in ischemic cortex after permanent focal ischemia in rats</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2009-05-26</date><risdate>2009</risdate><volume>1272</volume><spage>52</spage><epage>61</epage><pages>52-61</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Abstract 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.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>19344701</pmid><doi>10.1016/j.brainres.2009.03.047</doi><tpages>10</tpages></addata></record> |
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| subjects | Analysis of Variance Animals Biological and medical sciences Calcium-Binding Proteins - metabolism Cerebral Cortex - metabolism Cerebral Cortex - physiopathology Cerebral ischemia Disease Models, Animal Glial Fibrillary Acidic Protein - metabolism Infarction, Middle Cerebral Artery - pathology Male Medical sciences Microfilament Proteins Microtubule-Associated Proteins - metabolism Neurology Rats Rats, Inbred SHR SNARE Synaptotagmin Synaptotagmins - metabolism Syntaxin 1 - metabolism Up-Regulation - physiology Vascular diseases and vascular malformations of the nervous system |
| title | Up-regulation of syntaxin1 in ischemic cortex after permanent focal ischemia in rats |
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