Impaired GABAergic transmission and altered hippocampal synaptic plasticity in collybistin‐deficient mice
Identifieur interne : 001055 ( Main/Corpus ); précédent : 001054; suivant : 001056Impaired GABAergic transmission and altered hippocampal synaptic plasticity in collybistin‐deficient mice
Auteurs : Theofilos Papadopoulos ; Martin Korte ; Volker Eulenburg ; Hisahiko Kubota ; Marina Retiounskaia ; Robert J. Harvey ; Kirsten Harvey ; Gregory A. O'Sullivan ; Bodo Laube ; Swen Hülsmann ; Jörg R P. Geiger ; Heinrich BetzSource :
- The EMBO Journal [ 0261-4189 ] ; 2007-09-05.
Abstract
Collybistin (Cb) is a brain‐specific guanine nucleotide exchange factor that has been implicated in plasma membrane targeting of the postsynaptic scaffolding protein gephyrin found at glycinergic and GABAergic synapses. Here we show that Cb‐deficient mice display a region‐specific loss of postsynaptic gephyrin and GABAA receptor clusters in the hippocampus and the basolateral amygdala. Cb deficiency is accompanied by significant changes in hippocampal synaptic plasticity, due to reduced dendritic GABAergic inhibition. Long‐term potentiation is enhanced, and long‐term depression reduced, in Cb‐deficient hippocampal slices. Consistent with the anatomical and electrophysiological findings, the animals show increased levels of anxiety and impaired spatial learning. Together, our data indicate that Cb is essential for gephyrin‐dependent clustering of a specific set of GABAA receptors, but not required for glycine receptor postsynaptic localization.
Url:
DOI: 10.1038/sj.emboj.7601819
Links to Exploration step
ISTEX:FA4AFA7F31539C796653DCCAAC5CDC1EDE16E7B8Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Impaired GABAergic transmission and altered hippocampal synaptic plasticity in collybistin‐deficient mice</title><author><name sortKey="Papadopoulos, Theofilos" sort="Papadopoulos, Theofilos" uniqKey="Papadopoulos T" first="Theofilos" last="Papadopoulos">Theofilos Papadopoulos</name><affiliation><mods:affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Korte, Martin" sort="Korte, Martin" uniqKey="Korte M" first="Martin" last="Korte">Martin Korte</name><affiliation><mods:affiliation>Zoological Institute, Technical University Braunschweig, Braunschweig, Germany</mods:affiliation></affiliation></author><author><name sortKey="Eulenburg, Volker" sort="Eulenburg, Volker" uniqKey="Eulenburg V" first="Volker" last="Eulenburg">Volker Eulenburg</name><affiliation><mods:affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Kubota, Hisahiko" sort="Kubota, Hisahiko" uniqKey="Kubota H" first="Hisahiko" last="Kubota">Hisahiko Kubota</name><affiliation><mods:affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Independent Hertie Research Group, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Retiounskaia, Marina" sort="Retiounskaia, Marina" uniqKey="Retiounskaia M" first="Marina" last="Retiounskaia">Marina Retiounskaia</name><affiliation><mods:affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Harvey, Robert J" sort="Harvey, Robert J" uniqKey="Harvey R" first="Robert J" last="Harvey">Robert J. Harvey</name><affiliation><mods:affiliation>Department of Pharmacology, The School of Pharmacy, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Harvey, Kirsten" sort="Harvey, Kirsten" uniqKey="Harvey K" first="Kirsten" last="Harvey">Kirsten Harvey</name><affiliation><mods:affiliation>Department of Pharmacology, The School of Pharmacy, London, UK</mods:affiliation></affiliation></author><author><name sortKey="O Sullivan, Gregory A" sort="O Sullivan, Gregory A" uniqKey="O Sullivan G" first="Gregory A" last="O'Sullivan">Gregory A. O'Sullivan</name><affiliation><mods:affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Laube, Bodo" sort="Laube, Bodo" uniqKey="Laube B" first="Bodo" last="Laube">Bodo Laube</name><affiliation><mods:affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hulsmann, Swen" sort="Hulsmann, Swen" uniqKey="Hulsmann S" first="Swen" last="Hülsmann">Swen Hülsmann</name><affiliation><mods:affiliation>Department of Neuro‐ and Sensory Physiology, University of Göttingen, Göttingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Geiger, Jorg R P" sort="Geiger, Jorg R P" uniqKey="Geiger J" first="Jörg R P" last="Geiger">Jörg R P. Geiger</name><affiliation><mods:affiliation>Independent Hertie Research Group, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Betz, Heinrich" sort="Betz, Heinrich" uniqKey="Betz H" first="Heinrich" last="Betz">Heinrich Betz</name><affiliation><mods:affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:FA4AFA7F31539C796653DCCAAC5CDC1EDE16E7B8</idno><date when="2007" year="2007">2007</date><idno type="doi">10.1038/sj.emboj.7601819</idno><idno type="url">https://api.istex.fr/document/FA4AFA7F31539C796653DCCAAC5CDC1EDE16E7B8/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001055</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Impaired GABAergic transmission and altered hippocampal synaptic plasticity in collybistin‐deficient mice</title><author><name sortKey="Papadopoulos, Theofilos" sort="Papadopoulos, Theofilos" uniqKey="Papadopoulos T" first="Theofilos" last="Papadopoulos">Theofilos Papadopoulos</name><affiliation><mods:affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Korte, Martin" sort="Korte, Martin" uniqKey="Korte M" first="Martin" last="Korte">Martin Korte</name><affiliation><mods:affiliation>Zoological Institute, Technical University Braunschweig, Braunschweig, Germany</mods:affiliation></affiliation></author><author><name sortKey="Eulenburg, Volker" sort="Eulenburg, Volker" uniqKey="Eulenburg V" first="Volker" last="Eulenburg">Volker Eulenburg</name><affiliation><mods:affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Kubota, Hisahiko" sort="Kubota, Hisahiko" uniqKey="Kubota H" first="Hisahiko" last="Kubota">Hisahiko Kubota</name><affiliation><mods:affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Independent Hertie Research Group, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Retiounskaia, Marina" sort="Retiounskaia, Marina" uniqKey="Retiounskaia M" first="Marina" last="Retiounskaia">Marina Retiounskaia</name><affiliation><mods:affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Harvey, Robert J" sort="Harvey, Robert J" uniqKey="Harvey R" first="Robert J" last="Harvey">Robert J. Harvey</name><affiliation><mods:affiliation>Department of Pharmacology, The School of Pharmacy, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Harvey, Kirsten" sort="Harvey, Kirsten" uniqKey="Harvey K" first="Kirsten" last="Harvey">Kirsten Harvey</name><affiliation><mods:affiliation>Department of Pharmacology, The School of Pharmacy, London, UK</mods:affiliation></affiliation></author><author><name sortKey="O Sullivan, Gregory A" sort="O Sullivan, Gregory A" uniqKey="O Sullivan G" first="Gregory A" last="O'Sullivan">Gregory A. O'Sullivan</name><affiliation><mods:affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Laube, Bodo" sort="Laube, Bodo" uniqKey="Laube B" first="Bodo" last="Laube">Bodo Laube</name><affiliation><mods:affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Hulsmann, Swen" sort="Hulsmann, Swen" uniqKey="Hulsmann S" first="Swen" last="Hülsmann">Swen Hülsmann</name><affiliation><mods:affiliation>Department of Neuro‐ and Sensory Physiology, University of Göttingen, Göttingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Geiger, Jorg R P" sort="Geiger, Jorg R P" uniqKey="Geiger J" first="Jörg R P" last="Geiger">Jörg R P. Geiger</name><affiliation><mods:affiliation>Independent Hertie Research Group, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author><author><name sortKey="Betz, Heinrich" sort="Betz, Heinrich" uniqKey="Betz H" first="Heinrich" last="Betz">Heinrich Betz</name><affiliation><mods:affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">The EMBO Journal</title><idno type="ISSN">0261-4189</idno><idno type="eISSN">1460-2075</idno><imprint><publisher>John Wiley & Sons, Ltd</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2007-09-05">2007-09-05</date><biblScope unit="volume">26</biblScope><biblScope unit="issue">17</biblScope><biblScope unit="page" from="3888">3888</biblScope><biblScope unit="page" to="3899">3899</biblScope></imprint><idno type="ISSN">0261-4189</idno></series><idno type="istex">FA4AFA7F31539C796653DCCAAC5CDC1EDE16E7B8</idno><idno type="DOI">10.1038/sj.emboj.7601819</idno><idno type="ArticleID">EMBJ7601819</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0261-4189</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Collybistin (Cb) is a brain‐specific guanine nucleotide exchange factor that has been implicated in plasma membrane targeting of the postsynaptic scaffolding protein gephyrin found at glycinergic and GABAergic synapses. Here we show that Cb‐deficient mice display a region‐specific loss of postsynaptic gephyrin and GABAA receptor clusters in the hippocampus and the basolateral amygdala. Cb deficiency is accompanied by significant changes in hippocampal synaptic plasticity, due to reduced dendritic GABAergic inhibition. Long‐term potentiation is enhanced, and long‐term depression reduced, in Cb‐deficient hippocampal slices. Consistent with the anatomical and electrophysiological findings, the animals show increased levels of anxiety and impaired spatial learning. Together, our data indicate that Cb is essential for gephyrin‐dependent clustering of a specific set of GABAA receptors, but not required for glycine receptor postsynaptic localization.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Theofilos Papadopoulos</name><affiliations><json:string>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</json:string></affiliations></json:item><json:item><name>Martin Korte</name><affiliations><json:string>Zoological Institute, Technical University Braunschweig, Braunschweig, Germany</json:string></affiliations></json:item><json:item><name>Volker Eulenburg</name><affiliations><json:string>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</json:string></affiliations></json:item><json:item><name>Hisahiko Kubota</name><affiliations><json:string>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</json:string><json:string>Independent Hertie Research Group, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</json:string></affiliations></json:item><json:item><name>Marina Retiounskaia</name><affiliations><json:string>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</json:string></affiliations></json:item><json:item><name>Robert J Harvey</name><affiliations><json:string>Department of Pharmacology, The School of Pharmacy, London, UK</json:string></affiliations></json:item><json:item><name>Kirsten Harvey</name><affiliations><json:string>Department of Pharmacology, The School of Pharmacy, London, UK</json:string></affiliations></json:item><json:item><name>Gregory A O'Sullivan</name><affiliations><json:string>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</json:string></affiliations></json:item><json:item><name>Bodo Laube</name><affiliations><json:string>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</json:string></affiliations></json:item><json:item><name>Swen Hülsmann</name><affiliations><json:string>Department of Neuro‐ and Sensory Physiology, University of Göttingen, Göttingen, Germany</json:string></affiliations></json:item><json:item><name>Jörg R P Geiger</name><affiliations><json:string>Independent Hertie Research Group, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</json:string></affiliations></json:item><json:item><name>Heinrich Betz</name><affiliations><json:string>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>GABAA receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>gephyrin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>glycine receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>GEF</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>long‐term potentiation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>spatial memory</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Collybistin (Cb) is a brain‐specific guanine nucleotide exchange factor that has been implicated in plasma membrane targeting of the postsynaptic scaffolding protein gephyrin found at glycinergic and GABAergic synapses. Here we show that Cb‐deficient mice display a region‐specific loss of postsynaptic gephyrin and GABAA receptor clusters in the hippocampus and the basolateral amygdala. Cb deficiency is accompanied by significant changes in hippocampal synaptic plasticity, due to reduced dendritic GABAergic inhibition. Long‐term potentiation is enhanced, and long‐term depression reduced, in Cb‐deficient hippocampal slices. Consistent with the anatomical and electrophysiological findings, the animals show increased levels of anxiety and impaired spatial learning. Together, our data indicate that Cb is essential for gephyrin‐dependent clustering of a specific set of GABAA receptors, but not required for glycine receptor postsynaptic localization.</abstract><qualityIndicators><score>6.512</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595 x 794 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>6</keywordCount><abstractCharCount>957</abstractCharCount><pdfWordCount>8214</pdfWordCount><pdfCharCount>50369</pdfCharCount><pdfPageCount>12</pdfPageCount><abstractWordCount>126</abstractWordCount></qualityIndicators><title>Impaired GABAergic transmission and altered hippocampal synaptic plasticity in collybistin‐deficient mice</title><genre><json:string>article</json:string></genre><host><volume>26</volume><pages><total>12</total><last>3899</last><first>3888</first></pages><issn><json:string>0261-4189</json:string></issn><issue>17</issue><subject><json:item><value>Neuroscience</value></json:item><json:item><value>Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-2075</json:string></eissn><title>The EMBO Journal</title><doi><json:string>10.1002/(ISSN)1460-2075</json:string></doi></host><publicationDate>2007</publicationDate><copyrightDate>2007</copyrightDate><doi><json:string>10.1038/sj.emboj.7601819</json:string></doi><id>FA4AFA7F31539C796653DCCAAC5CDC1EDE16E7B8</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/FA4AFA7F31539C796653DCCAAC5CDC1EDE16E7B8/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/FA4AFA7F31539C796653DCCAAC5CDC1EDE16E7B8/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/FA4AFA7F31539C796653DCCAAC5CDC1EDE16E7B8/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Impaired GABAergic transmission and altered hippocampal synaptic plasticity in collybistin‐deficient mice</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>John Wiley & Sons, Ltd</publisher><pubPlace>Chichester, UK</pubPlace><availability><p>WILEY</p></availability><date>2007</date></publicationStmt><notesStmt><note>Supplementary dataSupplementary Table ISupplementary Figure 1</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Impaired GABAergic transmission and altered hippocampal synaptic plasticity in collybistin‐deficient mice</title><author><persName><forename type="first">Theofilos</forename><surname>Papadopoulos</surname></persName><affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation></author><author><persName><forename type="first">Martin</forename><surname>Korte</surname></persName><affiliation>Zoological Institute, Technical University Braunschweig, Braunschweig, Germany</affiliation></author><author><persName><forename type="first">Volker</forename><surname>Eulenburg</surname></persName><affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation></author><author><persName><forename type="first">Hisahiko</forename><surname>Kubota</surname></persName><affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation><affiliation>Independent Hertie Research Group, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation></author><author><persName><forename type="first">Marina</forename><surname>Retiounskaia</surname></persName><affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation></author><author><persName><forename type="first">Robert J</forename><surname>Harvey</surname></persName><affiliation>Department of Pharmacology, The School of Pharmacy, London, UK</affiliation></author><author><persName><forename type="first">Kirsten</forename><surname>Harvey</surname></persName><affiliation>Department of Pharmacology, The School of Pharmacy, London, UK</affiliation></author><author><persName><forename type="first">Gregory A</forename><surname>O'Sullivan</surname></persName><affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation></author><author><persName><forename type="first">Bodo</forename><surname>Laube</surname></persName><affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation></author><author><persName><forename type="first">Swen</forename><surname>Hülsmann</surname></persName><affiliation>Department of Neuro‐ and Sensory Physiology, University of Göttingen, Göttingen, Germany</affiliation></author><author><persName><forename type="first">Jörg R P</forename><surname>Geiger</surname></persName><affiliation>Independent Hertie Research Group, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation></author><author><persName><forename type="first">Heinrich</forename><surname>Betz</surname></persName><affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation></author></analytic><monogr><title level="j">The EMBO Journal</title><idno type="pISSN">0261-4189</idno><idno type="eISSN">1460-2075</idno><idno type="DOI">10.1002/(ISSN)1460-2075</idno><imprint><publisher>John Wiley & Sons, Ltd</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2007-09-05"></date><biblScope unit="volume">26</biblScope><biblScope unit="issue">17</biblScope><biblScope unit="page" from="3888">3888</biblScope><biblScope unit="page" to="3899">3899</biblScope></imprint></monogr><idno type="istex">FA4AFA7F31539C796653DCCAAC5CDC1EDE16E7B8</idno><idno type="DOI">10.1038/sj.emboj.7601819</idno><idno type="ArticleID">EMBJ7601819</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2007</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Collybistin (Cb) is a brain‐specific guanine nucleotide exchange factor that has been implicated in plasma membrane targeting of the postsynaptic scaffolding protein gephyrin found at glycinergic and GABAergic synapses. Here we show that Cb‐deficient mice display a region‐specific loss of postsynaptic gephyrin and GABAA receptor clusters in the hippocampus and the basolateral amygdala. Cb deficiency is accompanied by significant changes in hippocampal synaptic plasticity, due to reduced dendritic GABAergic inhibition. Long‐term potentiation is enhanced, and long‐term depression reduced, in Cb‐deficient hippocampal slices. Consistent with the anatomical and electrophysiological findings, the animals show increased levels of anxiety and impaired spatial learning. Together, our data indicate that Cb is essential for gephyrin‐dependent clustering of a specific set of GABAA receptors, but not required for glycine receptor postsynaptic localization.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>GABAA receptor</term></item><item><term>gephyrin</term></item><item><term>glycine receptor</term></item><item><term>GEF</term></item><item><term>long‐term potentiation</term></item><item><term>spatial memory</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Index Terms</head><item><term>Neuroscience</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-03-23">Received</change><change when="2007-07-19">Registration</change><change when="2007-09-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/FA4AFA7F31539C796653DCCAAC5CDC1EDE16E7B8/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component type="serialArticle" version="2.0" xml:lang="en" xml:id="embj7601819"><header><publicationMeta level="product"><publisherInfo><publisherName>John Wiley & Sons, Ltd</publisherName><publisherLoc>Chichester, UK</publisherLoc></publisherInfo><doi>10.1002/(ISSN)1460-2075</doi><issn type="print">0261-4189</issn><issn type="electronic">1460-2075</issn><idGroup><id type="product" value="EMBJ"></id></idGroup><titleGroup><title type="main" sort="THE EMBO JOURNAL">The EMBO Journal</title></titleGroup></publicationMeta><publicationMeta level="part" position="170"><doi>10.1002/emboj.v26.17</doi><copyright ownership="publisher">Copyright © 2013 Wiley Periodicals, Inc</copyright><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue">17</numbering></numberingGroup><coverDate startDate="2007-09-05">September 5, 2007</coverDate></publicationMeta><publicationMeta level="unit" position="20" type="article" status="forIssue"><doi>10.1038/sj.emboj.7601819</doi><idGroup><id type="unit" value="EMBJ7601819"></id></idGroup><countGroup><count type="pageTotal" number="12"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">Article</title></titleGroup><copyright ownership="thirdParty">Copyright © 2007 European Molecular Biology Organization</copyright><eventGroup><event type="manuscriptReceived" date="2007-03-23"></event><event type="manuscriptAccepted" date="2007-07-19"></event><event type="publishedOnlineEarlyUnpaginated" date="2007-08-09"></event><event type="publishedOnlineFinalForm" date="2007-09-05"></event><event type="xmlConverted" agent="SPi Global Converter_TO_WileyML3Gv2.0 version:1.0; WileyML 3G Packaging Tool v1.0" date="2013-10-17"></event><event type="xmlCorrected" agent="Wiley-VCH" date="2013-11-19"></event><event type="firstOnline" date="2007-08-09"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-04"></event></eventGroup><numberingGroup><numbering type="pageFirst">3888</numbering><numbering type="pageLast">3899</numbering></numberingGroup><correspondenceTo>Corresponding author. Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Deutschordenstrassee 46, 60528 Frankfurt am Main, Germany. Tel.: +49 69 96769 220; Fax: +49 69 96769 441; E-mail: <email>neurochemie@mpih-frankfurt.mpg.de</email></correspondenceTo><subjectInfo><subject href="http://psi.embo.org/14602075/subject/13">Neuroscience</subject></subjectInfo><linkGroup><link type="toTypesetVersion" href="file:EMBJ.EMBJ7601819.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Impaired GABAergic transmission and altered hippocampal synaptic plasticity in collybistin‐deficient mice</title><title type="short">Role of collybistin in GABA<sub>A</sub>R clustering</title></titleGroup><creators><creator creatorRole="author" xml:id="embj7601819-cr-0001" affiliationRef="#embj7601819-aff-0001"><personName><givenNames>Theofilos</givenNames><familyName>Papadopoulos</familyName></personName></creator><creator creatorRole="author" xml:id="embj7601819-cr-0002" affiliationRef="#embj7601819-aff-0002"><personName><givenNames>Martin</givenNames><familyName>Korte</familyName></personName></creator><creator creatorRole="author" xml:id="embj7601819-cr-0003" affiliationRef="#embj7601819-aff-0001"><personName><givenNames>Volker</givenNames><familyName>Eulenburg</familyName></personName></creator><creator creatorRole="author" xml:id="embj7601819-cr-0004" affiliationRef="#embj7601819-aff-0001 #embj7601819-aff-0003"><personName><givenNames>Hisahiko</givenNames><familyName>Kubota</familyName></personName></creator><creator creatorRole="author" xml:id="embj7601819-cr-0005" affiliationRef="#embj7601819-aff-0001"><personName><givenNames>Marina</givenNames><familyName>Retiounskaia</familyName></personName></creator><creator creatorRole="author" xml:id="embj7601819-cr-0006" affiliationRef="#embj7601819-aff-0004"><personName><givenNames>Robert J</givenNames><familyName>Harvey</familyName></personName></creator><creator creatorRole="author" xml:id="embj7601819-cr-0007" affiliationRef="#embj7601819-aff-0004"><personName><givenNames>Kirsten</givenNames><familyName>Harvey</familyName></personName></creator><creator creatorRole="author" xml:id="embj7601819-cr-0008" affiliationRef="#embj7601819-aff-0001"><personName><givenNames>Gregory A</givenNames><familyName>O'Sullivan</familyName></personName></creator><creator creatorRole="author" xml:id="embj7601819-cr-0009" affiliationRef="#embj7601819-aff-0001"><personName><givenNames>Bodo</givenNames><familyName>Laube</familyName></personName></creator><creator creatorRole="author" xml:id="embj7601819-cr-0010" affiliationRef="#embj7601819-aff-0005"><personName><givenNames>Swen</givenNames><familyName>Hülsmann</familyName></personName></creator><creator creatorRole="author" xml:id="embj7601819-cr-0011" affiliationRef="#embj7601819-aff-0003"><personName><givenNames>Jörg R P</givenNames><familyName>Geiger</familyName></personName></creator><creator creatorRole="author" xml:id="embj7601819-cr-0012" affiliationRef="#embj7601819-aff-0001" corresponding="yes"><personName><givenNames>Heinrich</givenNames><familyName>Betz</familyName></personName></creator></creators><affiliationGroup><affiliation countryCode="DE" type="organization" xml:id="embj7601819-aff-0001"><orgName>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research</orgName><address><city>Frankfurt</city><country>Germany</country></address></affiliation><affiliation countryCode="DE" type="organization" xml:id="embj7601819-aff-0002"><orgName>Zoological Institute, Technical University Braunschweig</orgName><address><city>Braunschweig</city><country>Germany</country></address></affiliation><affiliation countryCode="DE" type="organization" xml:id="embj7601819-aff-0003"><orgName>Independent Hertie Research Group, Max‐Planck‐Institute for Brain Research</orgName><address><city>Frankfurt</city><country>Germany</country></address></affiliation><affiliation countryCode="" type="organization" xml:id="embj7601819-aff-0004"><orgName>Department of Pharmacology, The School of Pharmacy</orgName><address><city>London</city><country>UK</country></address></affiliation><affiliation countryCode="DE" type="organization" xml:id="embj7601819-aff-0005"><orgName>Department of Neuro‐ and Sensory Physiology, University of Göttingen</orgName><address><city>Göttingen</city><country>Germany</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="embj7601819-kwd-0001">GABA<sub>A</sub> receptor</keyword><keyword xml:id="embj7601819-kwd-0002">gephyrin</keyword><keyword xml:id="embj7601819-kwd-0003">glycine receptor</keyword><keyword xml:id="embj7601819-kwd-0004">GEF</keyword><keyword xml:id="embj7601819-kwd-0005">long‐term potentiation</keyword><keyword xml:id="embj7601819-kwd-0006">spatial memory</keyword></keywordGroup><supportingInformation><supportingInfoItem xml:id="embj7601819-sup-0001"><mediaResource alt="supplementary data" mimeType="application/doc" href="urn-x:wiley:02614189:media:embj7601819:embj7601819-sup-0001"></mediaResource><caption><p>Supplementary data</p></caption></supportingInfoItem><supportingInfoItem xml:id="embj7601819-sup-0002"><mediaResource alt="supplementary data" mimeType="application/jpg" href="urn-x:wiley:02614189:media:embj7601819:embj7601819-sup-0002"></mediaResource><caption><p>Supplementary Table I</p></caption></supportingInfoItem><supportingInfoItem xml:id="embj7601819-sup-0003"><mediaResource alt="supplementary data" mimeType="application/jpg" href="urn-x:wiley:02614189:media:embj7601819:embj7601819-sup-0003"></mediaResource><caption><p>Supplementary Figure 1</p></caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main"><p>Collybistin (Cb) is a brain‐specific guanine nucleotide exchange factor that has been implicated in plasma membrane targeting of the postsynaptic scaffolding protein gephyrin found at glycinergic and GABAergic synapses. Here we show that Cb‐deficient mice display a region‐specific loss of postsynaptic gephyrin and GABA<sub>A</sub> receptor clusters in the hippocampus and the basolateral amygdala. Cb deficiency is accompanied by significant changes in hippocampal synaptic plasticity, due to reduced dendritic GABAergic inhibition. Long‐term potentiation is enhanced, and long‐term depression reduced, in Cb‐deficient hippocampal slices. Consistent with the anatomical and electrophysiological findings, the animals show increased levels of anxiety and impaired spatial learning. Together, our data indicate that Cb is essential for gephyrin‐dependent clustering of a specific set of GABA<sub>A</sub> receptors, but not required for glycine receptor postsynaptic localization.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Impaired GABAergic transmission and altered hippocampal synaptic plasticity in collybistin‐deficient mice</title></titleInfo><titleInfo type="abbreviated"><title>Role of collybistin in GABAAR clustering</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Impaired GABAergic transmission and altered hippocampal synaptic plasticity in collybistin‐deficient mice</title></titleInfo><name type="personal"><namePart type="given">Theofilos</namePart><namePart type="family">Papadopoulos</namePart><affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Martin</namePart><namePart type="family">Korte</namePart><affiliation>Zoological Institute, Technical University Braunschweig, Braunschweig, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Volker</namePart><namePart type="family">Eulenburg</namePart><affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hisahiko</namePart><namePart type="family">Kubota</namePart><affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation><affiliation>Independent Hertie Research Group, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marina</namePart><namePart type="family">Retiounskaia</namePart><affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert J</namePart><namePart type="family">Harvey</namePart><affiliation>Department of Pharmacology, The School of Pharmacy, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kirsten</namePart><namePart type="family">Harvey</namePart><affiliation>Department of Pharmacology, The School of Pharmacy, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gregory A</namePart><namePart type="family">O'Sullivan</namePart><affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bodo</namePart><namePart type="family">Laube</namePart><affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Swen</namePart><namePart type="family">Hülsmann</namePart><affiliation>Department of Neuro‐ and Sensory Physiology, University of Göttingen, Göttingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jörg R P</namePart><namePart type="family">Geiger</namePart><affiliation>Independent Hertie Research Group, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Heinrich</namePart><namePart type="family">Betz</namePart><affiliation>Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Frankfurt, Germany</affiliation><description>Correspondence: Corresponding author. Department of Neurochemistry, Max‐Planck‐Institute for Brain Research, Deutschordenstrassee 46, 60528 Frankfurt am Main, Germany. Tel.: +49 69 96769 220; Fax: +49 69 96769 441; E-mail: </description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>John Wiley & Sons, Ltd</publisher><place><placeTerm type="text">Chichester, UK</placeTerm></place><dateIssued encoding="w3cdtf">2007-09-05</dateIssued><dateCaptured encoding="w3cdtf">2007-03-23</dateCaptured><dateValid encoding="w3cdtf">2007-07-19</dateValid><copyrightDate encoding="w3cdtf">2007</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Collybistin (Cb) is a brain‐specific guanine nucleotide exchange factor that has been implicated in plasma membrane targeting of the postsynaptic scaffolding protein gephyrin found at glycinergic and GABAergic synapses. Here we show that Cb‐deficient mice display a region‐specific loss of postsynaptic gephyrin and GABAA receptor clusters in the hippocampus and the basolateral amygdala. Cb deficiency is accompanied by significant changes in hippocampal synaptic plasticity, due to reduced dendritic GABAergic inhibition. Long‐term potentiation is enhanced, and long‐term depression reduced, in Cb‐deficient hippocampal slices. Consistent with the anatomical and electrophysiological findings, the animals show increased levels of anxiety and impaired spatial learning. Together, our data indicate that Cb is essential for gephyrin‐dependent clustering of a specific set of GABAA receptors, but not required for glycine receptor postsynaptic localization.</abstract><note type="additional physical form">Supplementary dataSupplementary Table ISupplementary Figure 1</note><subject><genre>Keywords</genre><topic>GABAA receptor</topic><topic>gephyrin</topic><topic>glycine receptor</topic><topic>GEF</topic><topic>long‐term potentiation</topic><topic>spatial memory</topic></subject><relatedItem type="host"><titleInfo><title>The EMBO Journal</title></titleInfo><genre type="Journal">journal</genre><subject><genre>Index Terms</genre><topic authorityURI="http://psi.embo.org/14602075/subject/13">Neuroscience</topic></subject><subject><genre>article category</genre><topic>Article</topic></subject><identifier type="ISSN">0261-4189</identifier><identifier type="eISSN">1460-2075</identifier><identifier type="DOI">10.1002/(ISSN)1460-2075</identifier><identifier type="PublisherID">EMBJ</identifier><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>17</number></detail><extent unit="pages"><start>3888</start><end>3899</end><total>12</total></extent></part></relatedItem><identifier type="istex">FA4AFA7F31539C796653DCCAAC5CDC1EDE16E7B8</identifier><identifier type="DOI">10.1038/sj.emboj.7601819</identifier><identifier type="ArticleID">EMBJ7601819</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2013 Wiley Periodicals, IncCopyright © 2007 European Molecular Biology Organization</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>John Wiley & Sons, Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Musique/explor/SchutzV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001055 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 001055 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Musique
|area= SchutzV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= ISTEX:FA4AFA7F31539C796653DCCAAC5CDC1EDE16E7B8
|texte= Impaired GABAergic transmission and altered hippocampal synaptic plasticity in collybistin‐deficient mice
}}
| This area was generated with Dilib version V0.6.38. |  |