S100B and neurofibromin immunostaining and X‐inactivation patterns of laser‐microdissected cells indicate a multicellular origin of some NF1‐associated neurofibromas
Identifieur interne : 001409 ( Istex/Corpus ); précédent : 001408; suivant : 001410S100B and neurofibromin immunostaining and X‐inactivation patterns of laser‐microdissected cells indicate a multicellular origin of some NF1‐associated neurofibromas
Auteurs : Tracy Tucker ; Vincent M. Riccardi ; Carolyn Brown ; John Fee ; Margaret Sutcliffe ; Juergen Vielkind ; Janine Wechsler ; Pierre Wolkenstein ; Jan M. FriedmanSource :
- Journal of Neuroscience Research [ 0360-4012 ] ; 2011-09.
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- KwdEn :
Abstract
Neurofibromatosis 1 (NF1) is an autosomal dominant disease that predisposes individuals to developing benign neurofibromas. Some features and consequences of NF1 appear to result from partial deficiency of neurofibromin (Nfn), the NF1 gene protein product, as a result of haploinsufficiency for the NF1 gene. Other features and consequences of NF1 appear to involve total deficiency of Nfn, which arises as a result of either loss of function of the second NF1 allele or excess degradation of Nfn produced by the second allele in a particular clone of cells. We used immunofluorescence to assess the presence of Nfn in putative Schwann cells (S100B+) and non‐Schwann cells (S100B−) in 36 NF1‐derived benign neurofibromas classified histologically as diffuse or encapsulated. The S100B+/Nfn− cell population made up only 18% ± 10% (mean ± standard deviation) of the neurofibroma cells in both the diffuse and encapsulated neurofibromas. The proportion of S100B+/Nfn+ cells was significantly higher and the proportion of S100B−/Nfn− cells was significantly lower in diffuse neurofibromas than in encapsulated neurofibromas. We isolated S100B+/Nfn+, S100B+/Nfn−, and S100B−/Nfn+ cells by laser microdissection and, using X‐chromosome inactivation profiles, assessed clonality for each cell type. We showed that, although some neurofibromas include a subpopulation of S100B+/Nfn− cells consistent with clonal expansion of a Schwann cell progenitor that has lost function of both NF1 alleles, other neurofibromas do not show evidence of monoclonal proliferation of Schwann cells. Our findings suggest that, although clonal loss of neurofibromin function is probably involved in the development of some NF1‐associated neurofibromas, other pathogenic processes also occur. © 2011 Wiley‐Liss, Inc.
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DOI: 10.1002/jnr.22654
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Some features and consequences of NF1 appear to result from partial deficiency of neurofibromin (Nfn), the NF1 gene protein product, as a result of haploinsufficiency for the NF1 gene. Other features and consequences of NF1 appear to involve total deficiency of Nfn, which arises as a result of either loss of function of the second NF1 allele or excess degradation of Nfn produced by the second allele in a particular clone of cells. We used immunofluorescence to assess the presence of Nfn in putative Schwann cells (S100B+) and non‐Schwann cells (S100B−) in 36 NF1‐derived benign neurofibromas classified histologically as diffuse or encapsulated. The S100B+/Nfn− cell population made up only 18% ± 10% (mean ± standard deviation) of the neurofibroma cells in both the diffuse and encapsulated neurofibromas. The proportion of S100B+/Nfn+ cells was significantly higher and the proportion of S100B−/Nfn− cells was significantly lower in diffuse neurofibromas than in encapsulated neurofibromas. We isolated S100B+/Nfn+, S100B+/Nfn−, and S100B−/Nfn+ cells by laser microdissection and, using X‐chromosome inactivation profiles, assessed clonality for each cell type. We showed that, although some neurofibromas include a subpopulation of S100B+/Nfn− cells consistent with clonal expansion of a Schwann cell progenitor that has lost function of both NF1 alleles, other neurofibromas do not show evidence of monoclonal proliferation of Schwann cells. Our findings suggest that, although clonal loss of neurofibromin function is probably involved in the development of some NF1‐associated neurofibromas, other pathogenic processes also occur. © 2011 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Tracy Tucker</name><affiliations><json:string>Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada</json:string><json:string>Children's and Women's Hospital, Box 153, 4500 Oak Street, Room J106, Vancouver, British Columbia, Canada V6H 3N1</json:string></affiliations></json:item><json:item><name>Vincent M. Riccardi</name><affiliations><json:string>The Neurofibromatosis Institute, La Crescenta, California</json:string></affiliations></json:item><json:item><name>Carolyn Brown</name><affiliations><json:string>Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>John Fee</name><affiliations><json:string>Cancer Endocrinology, BC Cancer Research Centre, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>Margaret Sutcliffe</name><affiliations><json:string>Cancer Endocrinology, BC Cancer Research Centre, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>Juergen Vielkind</name><affiliations><json:string>Cancer Endocrinology, BC Cancer Research Centre, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>Janine Wechsler</name><affiliations><json:string>Department of Pathology, Henri‐Mondor Hospital, Créteil, France</json:string></affiliations></json:item><json:item><name>Pierre Wolkenstein</name><affiliations><json:string>Department of Dermatology, Henri‐Mondor Hospital, Créteil, France</json:string></affiliations></json:item><json:item><name>Jan M. 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Some features and consequences of NF1 appear to result from partial deficiency of neurofibromin (Nfn), the NF1 gene protein product, as a result of haploinsufficiency for the NF1 gene. Other features and consequences of NF1 appear to involve total deficiency of Nfn, which arises as a result of either loss of function of the second NF1 allele or excess degradation of Nfn produced by the second allele in a particular clone of cells. We used immunofluorescence to assess the presence of Nfn in putative Schwann cells (S100B+) and non‐Schwann cells (S100B−) in 36 NF1‐derived benign neurofibromas classified histologically as diffuse or encapsulated. The S100B+/Nfn− cell population made up only 18% ± 10% (mean ± standard deviation) of the neurofibroma cells in both the diffuse and encapsulated neurofibromas. The proportion of S100B+/Nfn+ cells was significantly higher and the proportion of S100B−/Nfn− cells was significantly lower in diffuse neurofibromas than in encapsulated neurofibromas. We isolated S100B+/Nfn+, S100B+/Nfn−, and S100B−/Nfn+ cells by laser microdissection and, using X‐chromosome inactivation profiles, assessed clonality for each cell type. We showed that, although some neurofibromas include a subpopulation of S100B+/Nfn− cells consistent with clonal expansion of a Schwann cell progenitor that has lost function of both NF1 alleles, other neurofibromas do not show evidence of monoclonal proliferation of Schwann cells. 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Canada</affiliation></author><author xml:id="author-6"><persName><forename type="first">Juergen</forename><surname>Vielkind</surname></persName><affiliation>Cancer Endocrinology, BC Cancer Research Centre, Vancouver, British Columbia, Canada</affiliation></author><author xml:id="author-7"><persName><forename type="first">Janine</forename><surname>Wechsler</surname></persName><affiliation>Department of Pathology, Henri‐Mondor Hospital, Créteil, France</affiliation></author><author xml:id="author-8"><persName><forename type="first">Pierre</forename><surname>Wolkenstein</surname></persName><affiliation>Department of Dermatology, Henri‐Mondor Hospital, Créteil, France</affiliation></author><author xml:id="author-9"><persName><forename type="first">Jan M.</forename><surname>Friedman</surname></persName><affiliation>Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada</affiliation></author></analytic><monogr><title level="j">Journal of 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Neurosci. Res.</title><idno type="pISSN">0360-4012</idno><idno type="eISSN">1097-4547</idno><idno type="DOI">10.1002/(ISSN)1097-4547</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-09"></date><biblScope unit="volume">89</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1451">1451</biblScope><biblScope unit="page" to="1460">1460</biblScope></imprint></monogr><idno type="istex">A646F27D79A74DF6EA5CAE535C9B2341C9089EF5</idno><idno type="DOI">10.1002/jnr.22654</idno><idno type="ArticleID">JNR22654</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Neurofibromatosis 1 (NF1) is an autosomal dominant disease that predisposes individuals to developing benign neurofibromas. Some features and consequences of NF1 appear to result from partial deficiency of neurofibromin (Nfn), the NF1 gene protein product, as a result of haploinsufficiency for the NF1 gene. Other features and consequences of NF1 appear to involve total deficiency of Nfn, which arises as a result of either loss of function of the second NF1 allele or excess degradation of Nfn produced by the second allele in a particular clone of cells. We used immunofluorescence to assess the presence of Nfn in putative Schwann cells (S100B+) and non‐Schwann cells (S100B−) in 36 NF1‐derived benign neurofibromas classified histologically as diffuse or encapsulated. The S100B+/Nfn− cell population made up only 18% ± 10% (mean ± standard deviation) of the neurofibroma cells in both the diffuse and encapsulated neurofibromas. The proportion of S100B+/Nfn+ cells was significantly higher and the proportion of S100B−/Nfn− cells was significantly lower in diffuse neurofibromas than in encapsulated neurofibromas. We isolated S100B+/Nfn+, S100B+/Nfn−, and S100B−/Nfn+ cells by laser microdissection and, using X‐chromosome inactivation profiles, assessed clonality for each cell type. We showed that, although some neurofibromas include a subpopulation of S100B+/Nfn− cells consistent with clonal expansion of a Schwann cell progenitor that has lost function of both NF1 alleles, other neurofibromas do not show evidence of monoclonal proliferation of Schwann cells. 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Neurosci. Res.</title></titleGroup></publicationMeta><publicationMeta level="part" position="90"><doi origin="wiley" registered="yes">10.1002/jnr.v89.9</doi><numberingGroup><numbering type="journalVolume" number="89">89</numbering><numbering type="journalIssue">9</numbering></numberingGroup><coverDate startDate="2011-09">September 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="120" status="forIssue"><doi origin="wiley" registered="yes">10.1002/jnr.22654</doi><idGroup><id type="unit" value="JNR22654"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="publisher">Copyright © 2011 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2010-12-22"></event><event type="manuscriptRevised" date="2011-02-22"></event><event type="manuscriptAccepted" date="2011-03-03"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.5.2 mode:FullText" date="2011-07-25"></event><event type="publishedOnlineEarlyUnpaginated" date="2011-06-14"></event><event type="publishedOnlineFinalForm" date="2011-07-06"></event><event type="firstOnline" date="2011-06-14"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-31"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-30"></event></eventGroup><numberingGroup><numbering type="pageFirst">1451</numbering><numbering type="pageLast">1460</numbering></numberingGroup><correspondenceTo>Children's and Women's Hospital, Box 153, 4500 Oak Street, Room J106, Vancouver, British Columbia, Canada V6H 3N1</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JNR.JNR22654.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="46"></count><count type="wordTotal" number="6694"></count></countGroup><titleGroup><title type="main" xml:lang="en">S100B and neurofibromin immunostaining and X‐inactivation patterns of laser‐microdissected cells indicate a multicellular origin of some NF1‐associated neurofibromas</title><title type="short" xml:lang="en">S100B and Neurofibromin in Neurofibromas</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Tracy</givenNames><familyName>Tucker</familyName></personName><contactDetails><email>tbtucker@interchange.ubc.ca</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Vincent M.</givenNames><familyName>Riccardi</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Carolyn</givenNames><familyName>Brown</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>John</givenNames><familyName>Fee</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Margaret</givenNames><familyName>Sutcliffe</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Juergen</givenNames><familyName>Vielkind</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Janine</givenNames><familyName>Wechsler</familyName></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Pierre</givenNames><familyName>Wolkenstein</familyName></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jan M.</givenNames><familyName>Friedman</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CA" type="organization"><unparsedAffiliation>Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>The Neurofibromatosis Institute, La Crescenta, California</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="CA" type="organization"><unparsedAffiliation>Cancer Endocrinology, BC Cancer Research Centre, Vancouver, British Columbia, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="FR" type="organization"><unparsedAffiliation>Department of Pathology, Henri‐Mondor Hospital, Créteil, France</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="FR" type="organization"><unparsedAffiliation>Department of Dermatology, Henri‐Mondor Hospital, Créteil, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">neurofibroma</keyword><keyword xml:id="kwd2">clonality</keyword><keyword xml:id="kwd3">S100B</keyword><keyword xml:id="kwd4">neurofibromin</keyword><keyword xml:id="kwd5">benign</keyword></keywordGroup><fundingInfo><fundingAgency>University of British Columbia</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Genome Canada/Genome BC Cancer Genomics and Health Canada</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Neurofibromatosis 1 (NF1) is an autosomal dominant disease that predisposes individuals to developing benign neurofibromas. Some features and consequences of NF1 appear to result from partial deficiency of neurofibromin (Nfn), the <i>NF1</i> gene protein product, as a result of haploinsufficiency for the <i>NF1</i> gene. Other features and consequences of NF1 appear to involve total deficiency of Nfn, which arises as a result of either loss of function of the second <i>NF1</i> allele or excess degradation of Nfn produced by the second allele in a particular clone of cells. We used immunofluorescence to assess the presence of Nfn in putative Schwann cells (S100B<sup>+</sup>) and non‐Schwann cells (S100B<sup>−</sup>) in 36 NF1‐derived benign neurofibromas classified histologically as diffuse or encapsulated. The S100B<sup>+</sup>/Nfn<sup>−</sup> cell population made up only 18% ± 10% (mean ± standard deviation) of the neurofibroma cells in both the diffuse and encapsulated neurofibromas. The proportion of S100B<sup>+</sup>/Nfn<sup>+</sup> cells was significantly higher and the proportion of S100B<sup>−</sup>/Nfn<sup>−</sup> cells was significantly lower in diffuse neurofibromas than in encapsulated neurofibromas. We isolated S100B<sup>+</sup>/Nfn<sup>+</sup>, S100B<sup>+</sup>/Nfn<sup>−</sup>, and S100B<sup>−</sup>/Nfn<sup>+</sup> cells by laser microdissection and, using X‐chromosome inactivation profiles, assessed clonality for each cell type. We showed that, although some neurofibromas include a subpopulation of S100B<sup>+</sup>/Nfn<sup>−</sup> cells consistent with clonal expansion of a Schwann cell progenitor that has lost function of both <i>NF1</i> alleles, other neurofibromas do not show evidence of monoclonal proliferation of Schwann cells. Our findings suggest that, although clonal loss of neurofibromin function is probably involved in the development of some NF1‐associated neurofibromas, other pathogenic processes also occur. © 2011 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>S100B and neurofibromin immunostaining and X‐inactivation patterns of laser‐microdissected cells indicate a multicellular origin of some NF1‐associated neurofibromas</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>S100B and Neurofibromin in Neurofibromas</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>S100B and neurofibromin immunostaining and X‐inactivation patterns of laser‐microdissected cells indicate a multicellular origin of some NF1‐associated neurofibromas</title></titleInfo><name type="personal"><namePart type="given">Tracy</namePart><namePart type="family">Tucker</namePart><affiliation>Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada</affiliation><affiliation>Children's and Women's Hospital, Box 153, 4500 Oak Street, Room J106, Vancouver, British Columbia, Canada V6H 3N1</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Vincent M.</namePart><namePart type="family">Riccardi</namePart><affiliation>The Neurofibromatosis Institute, La Crescenta, California</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carolyn</namePart><namePart type="family">Brown</namePart><affiliation>Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John</namePart><namePart type="family">Fee</namePart><affiliation>Cancer Endocrinology, BC Cancer Research Centre, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Margaret</namePart><namePart type="family">Sutcliffe</namePart><affiliation>Cancer Endocrinology, BC Cancer Research Centre, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Juergen</namePart><namePart type="family">Vielkind</namePart><affiliation>Cancer Endocrinology, BC Cancer Research Centre, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Janine</namePart><namePart type="family">Wechsler</namePart><affiliation>Department of Pathology, Henri‐Mondor Hospital, Créteil, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pierre</namePart><namePart type="family">Wolkenstein</namePart><affiliation>Department of Dermatology, Henri‐Mondor Hospital, Créteil, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jan M.</namePart><namePart type="family">Friedman</namePart><affiliation>Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-09</dateIssued><dateCaptured encoding="w3cdtf">2010-12-22</dateCaptured><dateValid encoding="w3cdtf">2011-03-03</dateValid><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">3</extent><extent unit="tables">2</extent><extent unit="references">46</extent><extent unit="words">6694</extent></physicalDescription><abstract lang="en">Neurofibromatosis 1 (NF1) is an autosomal dominant disease that predisposes individuals to developing benign neurofibromas. Some features and consequences of NF1 appear to result from partial deficiency of neurofibromin (Nfn), the NF1 gene protein product, as a result of haploinsufficiency for the NF1 gene. Other features and consequences of NF1 appear to involve total deficiency of Nfn, which arises as a result of either loss of function of the second NF1 allele or excess degradation of Nfn produced by the second allele in a particular clone of cells. We used immunofluorescence to assess the presence of Nfn in putative Schwann cells (S100B+) and non‐Schwann cells (S100B−) in 36 NF1‐derived benign neurofibromas classified histologically as diffuse or encapsulated. The S100B+/Nfn− cell population made up only 18% ± 10% (mean ± standard deviation) of the neurofibroma cells in both the diffuse and encapsulated neurofibromas. The proportion of S100B+/Nfn+ cells was significantly higher and the proportion of S100B−/Nfn− cells was significantly lower in diffuse neurofibromas than in encapsulated neurofibromas. We isolated S100B+/Nfn+, S100B+/Nfn−, and S100B−/Nfn+ cells by laser microdissection and, using X‐chromosome inactivation profiles, assessed clonality for each cell type. We showed that, although some neurofibromas include a subpopulation of S100B+/Nfn− cells consistent with clonal expansion of a Schwann cell progenitor that has lost function of both NF1 alleles, other neurofibromas do not show evidence of monoclonal proliferation of Schwann cells. Our findings suggest that, although clonal loss of neurofibromin function is probably involved in the development of some NF1‐associated neurofibromas, other pathogenic processes also occur. © 2011 Wiley‐Liss, Inc.</abstract><note type="funding">University of British Columbia</note><note type="funding">Genome Canada/Genome BC Cancer Genomics and Health Canada</note><subject lang="en"><genre>keywords</genre><topic>neurofibroma</topic><topic>clonality</topic><topic>S100B</topic><topic>neurofibromin</topic><topic>benign</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Neuroscience Research</title></titleInfo><titleInfo type="abbreviated"><title>J. Neurosci. Res.</title></titleInfo><genre type="journal">journal</genre><subject><genre>article-category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0360-4012</identifier><identifier type="eISSN">1097-4547</identifier><identifier type="DOI">10.1002/(ISSN)1097-4547</identifier><identifier type="PublisherID">JNR</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>89</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>1451</start><end>1460</end><total>10</total></extent></part></relatedItem><identifier type="istex">A646F27D79A74DF6EA5CAE535C9B2341C9089EF5</identifier><identifier type="DOI">10.1002/jnr.22654</identifier><identifier type="ArticleID">JNR22654</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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