mGluR1 antagonist decreases tyrosine phosphorylation of NMDA receptor and attenuates infarct size after transient focal cerebral ischemia
The contribution of metabotropic glutamate receptors to brain injury after in vivo cerebral ischemia remains to be determined. We investigated the effects of the metabotropic glutamate receptor 1 (mGluR1) antagonist LY367385 on brain injury after transient (90 min) middle cerebral artery occlusion i...
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| Veröffentlicht in: | Journal of neurochemistry 2008-06, Vol.105 (5), p.1625-1634 |
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| creator | Murotomi, Kazutoshi Takagi, Norio Takayanagi, Gen Ono, Megumi Takeo, Satoshi Tanonaka, Kouichi |
| description | The contribution of metabotropic glutamate receptors to brain injury after in vivo cerebral ischemia remains to be determined. We investigated the effects of the metabotropic glutamate receptor 1 (mGluR1) antagonist LY367385 on brain injury after transient (90 min) middle cerebral artery occlusion in the rat and sought to explore their mechanisms. The intravenous administration of LY367385 (10 mg/kg) reduced the infarct volume at 24 h after the start of reperfusion. As the Gq-coupled mGluR1 receptor is known to activate the PKC/Src family kinase cascade, we focused on changes in the activation and amount of these kinases. Transient focal ischemia increased the amount of activated tyrosine kinase Src and PKC in the post-synaptic density (PSD) at 4 h of reperfusion. The administration of LY367385 attenuated the increases in the amounts of PSD-associated PKCγ and Src after transient focal ischemia. We further investigated phosphorylation of the NMDA receptor, which is a major target of Src family kinases to modulate the function of the receptor. Transient focal ischemia increased the tyrosine phosphorylation of NMDA receptor subunits NR2A and NR2B. Tyrosine phosphorylation of NR2A, but not that of NR2B, in the PSD at 4 h of reperfusion was inhibited by LY367385. These results suggest that the mGluR1 after transient focal ischemia is involved in the activation of Src, which may be linked to the modification of properties of the NMDA receptor and the development of cerebral infarction. |
| doi_str_mv | 10.1111/j.1471-4159.2008.05260.x |
| format | Article |
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We investigated the effects of the metabotropic glutamate receptor 1 (mGluR1) antagonist LY367385 on brain injury after transient (90 min) middle cerebral artery occlusion in the rat and sought to explore their mechanisms. The intravenous administration of LY367385 (10 mg/kg) reduced the infarct volume at 24 h after the start of reperfusion. As the Gq-coupled mGluR1 receptor is known to activate the PKC/Src family kinase cascade, we focused on changes in the activation and amount of these kinases. Transient focal ischemia increased the amount of activated tyrosine kinase Src and PKC in the post-synaptic density (PSD) at 4 h of reperfusion. The administration of LY367385 attenuated the increases in the amounts of PSD-associated PKCγ and Src after transient focal ischemia. We further investigated phosphorylation of the NMDA receptor, which is a major target of Src family kinases to modulate the function of the receptor. Transient focal ischemia increased the tyrosine phosphorylation of NMDA receptor subunits NR2A and NR2B. Tyrosine phosphorylation of NR2A, but not that of NR2B, in the PSD at 4 h of reperfusion was inhibited by LY367385. These results suggest that the mGluR1 after transient focal ischemia is involved in the activation of Src, which may be linked to the modification of properties of the NMDA receptor and the development of cerebral infarction.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/j.1471-4159.2008.05260.x</identifier><identifier>PMID: 18248625</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Oxford, UK : Blackwell Publishing Ltd</publisher><subject>Animals ; Benzoates - pharmacology ; Biochemistry ; Biological and medical sciences ; Brain damage ; Central nervous system ; Central neurotransmission. Neuromudulation. Pathways and receptors ; Cerebral Infarction - etiology ; Cerebral Infarction - metabolism ; Cerebral Infarction - prevention & control ; Excitatory Amino Acid Antagonists - pharmacology ; Excitatory Amino Acid Antagonists - therapeutic use ; Fundamental and applied biological sciences. Psychology ; Glycine - analogs & derivatives ; Glycine - pharmacology ; ischemia ; Ischemic Attack, Transient - complications ; Ischemic Attack, Transient - metabolism ; Ischemic Attack, Transient - prevention & control ; Kinases ; Male ; Medical sciences ; metabotropic glutamate receptor ; Neurology ; NMDA receptor ; Phosphorylation - drug effects ; post-synaptic density ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate - antagonists & inhibitors ; Receptors, Metabotropic Glutamate - metabolism ; Receptors, N-Methyl-D-Aspartate - metabolism ; Rodents ; Tyrosine - metabolism ; tyrosine phosphorylation ; Vascular diseases and vascular malformations of the nervous system ; Vertebrates: nervous system and sense organs</subject><ispartof>Journal of neurochemistry, 2008-06, Vol.105 (5), p.1625-1634</ispartof><rights>2008 The Authors. Journal Compilation © 2008 International Society for Neurochemistry</rights><rights>2008 INIST-CNRS</rights><rights>Journal compilation © 2008 International Society for Neurochemistry</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5950-fbd2feb972329aa45ef81253f3b6a31a1f348b2352c4f5e05e9a2464e8d64a003</citedby><cites>FETCH-LOGICAL-c5950-fbd2feb972329aa45ef81253f3b6a31a1f348b2352c4f5e05e9a2464e8d64a003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1471-4159.2008.05260.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1471-4159.2008.05260.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20359416$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18248625$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Murotomi, Kazutoshi</creatorcontrib><creatorcontrib>Takagi, Norio</creatorcontrib><creatorcontrib>Takayanagi, Gen</creatorcontrib><creatorcontrib>Ono, Megumi</creatorcontrib><creatorcontrib>Takeo, Satoshi</creatorcontrib><creatorcontrib>Tanonaka, Kouichi</creatorcontrib><title>mGluR1 antagonist decreases tyrosine phosphorylation of NMDA receptor and attenuates infarct size after transient focal cerebral ischemia</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>The contribution of metabotropic glutamate receptors to brain injury after in vivo cerebral ischemia remains to be determined. We investigated the effects of the metabotropic glutamate receptor 1 (mGluR1) antagonist LY367385 on brain injury after transient (90 min) middle cerebral artery occlusion in the rat and sought to explore their mechanisms. The intravenous administration of LY367385 (10 mg/kg) reduced the infarct volume at 24 h after the start of reperfusion. As the Gq-coupled mGluR1 receptor is known to activate the PKC/Src family kinase cascade, we focused on changes in the activation and amount of these kinases. Transient focal ischemia increased the amount of activated tyrosine kinase Src and PKC in the post-synaptic density (PSD) at 4 h of reperfusion. The administration of LY367385 attenuated the increases in the amounts of PSD-associated PKCγ and Src after transient focal ischemia. We further investigated phosphorylation of the NMDA receptor, which is a major target of Src family kinases to modulate the function of the receptor. Transient focal ischemia increased the tyrosine phosphorylation of NMDA receptor subunits NR2A and NR2B. Tyrosine phosphorylation of NR2A, but not that of NR2B, in the PSD at 4 h of reperfusion was inhibited by LY367385. These results suggest that the mGluR1 after transient focal ischemia is involved in the activation of Src, which may be linked to the modification of properties of the NMDA receptor and the development of cerebral infarction.</description><subject>Animals</subject><subject>Benzoates - pharmacology</subject><subject>Biochemistry</subject><subject>Biological and medical sciences</subject><subject>Brain damage</subject><subject>Central nervous system</subject><subject>Central neurotransmission. Neuromudulation. Pathways and receptors</subject><subject>Cerebral Infarction - etiology</subject><subject>Cerebral Infarction - metabolism</subject><subject>Cerebral Infarction - prevention & control</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>Excitatory Amino Acid Antagonists - therapeutic use</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glycine - analogs & derivatives</subject><subject>Glycine - pharmacology</subject><subject>ischemia</subject><subject>Ischemic Attack, Transient - complications</subject><subject>Ischemic Attack, Transient - metabolism</subject><subject>Ischemic Attack, Transient - prevention & control</subject><subject>Kinases</subject><subject>Male</subject><subject>Medical sciences</subject><subject>metabotropic glutamate receptor</subject><subject>Neurology</subject><subject>NMDA receptor</subject><subject>Phosphorylation - drug effects</subject><subject>post-synaptic density</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Metabotropic Glutamate - antagonists & inhibitors</subject><subject>Receptors, Metabotropic Glutamate - metabolism</subject><subject>Receptors, N-Methyl-D-Aspartate - metabolism</subject><subject>Rodents</subject><subject>Tyrosine - metabolism</subject><subject>tyrosine phosphorylation</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkd1uEzEQhVcIRNPCK4CFRO8S_Ls_F1xUAQqoFAnotTW7GbeONuvU9oqGN-CtmSVRkbgBS5ZH8nfG43OKggm-ELRerRdCV2KuhWkWkvN6wY0s-eLuQTG7v3hYzDiXcq64lkfFcUprzkWpS_G4OBK11HUpzaz4uTnvxy-CwZDhOgw-ZbbCLiIkTCzvYkh-QLa9CYl23PWQfRhYcOzy05szFrHDbQ6R5CsGOeMwQiahHxzELrPkfyADlzGyHGFIHofMXOigZx1GbCMVPnU3uPHwpHjkoE_49HCeFFfv3n5bvp9ffD7_sDy7mHemMXzu2pV02DaVVLIB0AZdLaRRTrUlKAHCKV23UhnZaWeQG2xA6lJjvSo1cK5OitN9320MtyOmbDc0AvY9DBjGZCteqVo05T9ByaltYyoCX_wFrsMYB_oEMaUhxkiC6j3UkacporPb6DcQd1ZwO4Vq13bKzk7Z2SlU-ztUe0fSZ4f-Y7vB1R_hIUUCXh4ASOStI6s7n-45yZVptJh-9HrPffc97v57APvxcjlVpH--1zsIFq4jvXH1VXKhCCYjqkb9Aga1x8A</recordid><startdate>200806</startdate><enddate>200806</enddate><creator>Murotomi, Kazutoshi</creator><creator>Takagi, Norio</creator><creator>Takayanagi, Gen</creator><creator>Ono, Megumi</creator><creator>Takeo, Satoshi</creator><creator>Tanonaka, Kouichi</creator><general>Oxford, UK : Blackwell Publishing Ltd</general><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>FBQ</scope><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>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>200806</creationdate><title>mGluR1 antagonist decreases tyrosine phosphorylation of NMDA receptor and attenuates infarct size after transient focal cerebral ischemia</title><author>Murotomi, Kazutoshi ; Takagi, Norio ; Takayanagi, Gen ; Ono, Megumi ; Takeo, Satoshi ; Tanonaka, Kouichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5950-fbd2feb972329aa45ef81253f3b6a31a1f348b2352c4f5e05e9a2464e8d64a003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Benzoates - pharmacology</topic><topic>Biochemistry</topic><topic>Biological and medical sciences</topic><topic>Brain damage</topic><topic>Central nervous system</topic><topic>Central neurotransmission. Neuromudulation. Pathways and receptors</topic><topic>Cerebral Infarction - etiology</topic><topic>Cerebral Infarction - metabolism</topic><topic>Cerebral Infarction - prevention & control</topic><topic>Excitatory Amino Acid Antagonists - pharmacology</topic><topic>Excitatory Amino Acid Antagonists - therapeutic use</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glycine - analogs & derivatives</topic><topic>Glycine - pharmacology</topic><topic>ischemia</topic><topic>Ischemic Attack, Transient - complications</topic><topic>Ischemic Attack, Transient - metabolism</topic><topic>Ischemic Attack, Transient - prevention & control</topic><topic>Kinases</topic><topic>Male</topic><topic>Medical sciences</topic><topic>metabotropic glutamate receptor</topic><topic>Neurology</topic><topic>NMDA receptor</topic><topic>Phosphorylation - drug effects</topic><topic>post-synaptic density</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Metabotropic Glutamate - antagonists & inhibitors</topic><topic>Receptors, Metabotropic Glutamate - metabolism</topic><topic>Receptors, N-Methyl-D-Aspartate - metabolism</topic><topic>Rodents</topic><topic>Tyrosine - metabolism</topic><topic>tyrosine phosphorylation</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Murotomi, Kazutoshi</creatorcontrib><creatorcontrib>Takagi, Norio</creatorcontrib><creatorcontrib>Takayanagi, Gen</creatorcontrib><creatorcontrib>Ono, Megumi</creatorcontrib><creatorcontrib>Takeo, Satoshi</creatorcontrib><creatorcontrib>Tanonaka, Kouichi</creatorcontrib><collection>AGRIS</collection><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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Murotomi, Kazutoshi</au><au>Takagi, Norio</au><au>Takayanagi, Gen</au><au>Ono, Megumi</au><au>Takeo, Satoshi</au><au>Tanonaka, Kouichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>mGluR1 antagonist decreases tyrosine phosphorylation of NMDA receptor and attenuates infarct size after transient focal cerebral ischemia</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2008-06</date><risdate>2008</risdate><volume>105</volume><issue>5</issue><spage>1625</spage><epage>1634</epage><pages>1625-1634</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>The contribution of metabotropic glutamate receptors to brain injury after in vivo cerebral ischemia remains to be determined. We investigated the effects of the metabotropic glutamate receptor 1 (mGluR1) antagonist LY367385 on brain injury after transient (90 min) middle cerebral artery occlusion in the rat and sought to explore their mechanisms. The intravenous administration of LY367385 (10 mg/kg) reduced the infarct volume at 24 h after the start of reperfusion. As the Gq-coupled mGluR1 receptor is known to activate the PKC/Src family kinase cascade, we focused on changes in the activation and amount of these kinases. Transient focal ischemia increased the amount of activated tyrosine kinase Src and PKC in the post-synaptic density (PSD) at 4 h of reperfusion. The administration of LY367385 attenuated the increases in the amounts of PSD-associated PKCγ and Src after transient focal ischemia. We further investigated phosphorylation of the NMDA receptor, which is a major target of Src family kinases to modulate the function of the receptor. Transient focal ischemia increased the tyrosine phosphorylation of NMDA receptor subunits NR2A and NR2B. Tyrosine phosphorylation of NR2A, but not that of NR2B, in the PSD at 4 h of reperfusion was inhibited by LY367385. These results suggest that the mGluR1 after transient focal ischemia is involved in the activation of Src, which may be linked to the modification of properties of the NMDA receptor and the development of cerebral infarction.</abstract><cop>Oxford, UK</cop><pub>Oxford, UK : Blackwell Publishing Ltd</pub><pmid>18248625</pmid><doi>10.1111/j.1471-4159.2008.05260.x</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Benzoates - pharmacology Biochemistry Biological and medical sciences Brain damage Central nervous system Central neurotransmission. Neuromudulation. Pathways and receptors Cerebral Infarction - etiology Cerebral Infarction - metabolism Cerebral Infarction - prevention & control Excitatory Amino Acid Antagonists - pharmacology Excitatory Amino Acid Antagonists - therapeutic use Fundamental and applied biological sciences. Psychology Glycine - analogs & derivatives Glycine - pharmacology ischemia Ischemic Attack, Transient - complications Ischemic Attack, Transient - metabolism Ischemic Attack, Transient - prevention & control Kinases Male Medical sciences metabotropic glutamate receptor Neurology NMDA receptor Phosphorylation - drug effects post-synaptic density Rats Rats, Sprague-Dawley Receptors, Metabotropic Glutamate - antagonists & inhibitors Receptors, Metabotropic Glutamate - metabolism Receptors, N-Methyl-D-Aspartate - metabolism Rodents Tyrosine - metabolism tyrosine phosphorylation Vascular diseases and vascular malformations of the nervous system Vertebrates: nervous system and sense organs |
| title | mGluR1 antagonist decreases tyrosine phosphorylation of NMDA receptor and attenuates infarct size after transient focal cerebral ischemia |
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