The second brain and Parkinson’s disease
Identifieur interne : 001B02 ( Main/Corpus ); précédent : 001B01; suivant : 001B03The second brain and Parkinson’s disease
Auteurs : Thibaud Lebouvier ; Tanguy Chaumette ; Sébastien Paillusson ; Charles Duyckaerts ; Stanislas Bruley Des Varannes ; Michel Neunlist ; Pascal DerkinderenSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2009-09.
English descriptors
Abstract
Parkinson’s disease is the second most common neurodegenerative disease after Alzheimer’s disease. It has been classically considered that the pathological hallmarks of Parkinson’s disease, namely Lewy bodies and Lewy neurites, affect primarily the substantia nigra. Nevertheless, it has become increasingly evident in recent years that Parkinson’s disease is a multicentric neurodegenerative process that affects several neuronal structures outside the substantia nigra, among which is the enteric nervous system. Remarkably, recent reports have shown that the lesions in the enteric nervous system occurred at a very early stage of the disease, even before the involvement of the central nervous system. This led to the postulate that the enteric nervous system could be critical in the pathophysiology of Parkinson’s disease, as it could represent a route of entry for a putative environmental factor to initiate the pathological process (Braak’s hypothesis). Besides their putative role in the spreading of the pathological process, it has also been suggested that the pathological alterations within the enteric nervous system could be involved in the gastrointestinal dysfunction frequently encountered by parkinsonian patients. The scope of the present article is to review the available studies on the enteric nervous system in Parkinson’s disease patients and in animal models of the disease. We further discuss the strategies that will help in our understanding of the roles of the enteric nervous system, both in the pathophysiology of the disease and in the pathophysiology of the gastrointestinal symptoms.
Url:
DOI: 10.1111/j.1460-9568.2009.06873.x
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ISTEX:17D86D30AE525BF1E4D0AB39CA069EF77CD38BCELe document en format XML
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It has been classically considered that the pathological hallmarks of Parkinson’s disease, namely Lewy bodies and Lewy neurites, affect primarily the substantia nigra. Nevertheless, it has become increasingly evident in recent years that Parkinson’s disease is a multicentric neurodegenerative process that affects several neuronal structures outside the substantia nigra, among which is the enteric nervous system. Remarkably, recent reports have shown that the lesions in the enteric nervous system occurred at a very early stage of the disease, even before the involvement of the central nervous system. This led to the postulate that the enteric nervous system could be critical in the pathophysiology of Parkinson’s disease, as it could represent a route of entry for a putative environmental factor to initiate the pathological process (Braak’s hypothesis). Besides their putative role in the spreading of the pathological process, it has also been suggested that the pathological alterations within the enteric nervous system could be involved in the gastrointestinal dysfunction frequently encountered by parkinsonian patients. The scope of the present article is to review the available studies on the enteric nervous system in Parkinson’s disease patients and in animal models of the disease. We further discuss the strategies that will help in our understanding of the roles of the enteric nervous system, both in the pathophysiology of the disease and in the pathophysiology of the gastrointestinal symptoms.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Thibaud Lebouvier</name><affiliations><json:string>Inserm, U913, CHU Nantes, 44093 Nantes, France</json:string><json:string>University of Nantes, Nantes, France</json:string><json:string>CHU Nantes, Institut des Maladies de l’Appareil Digestif, Nantes, France</json:string><json:string>CHU Nantes, Department of Neurology, Nantes, France</json:string><json:string>Inserm, CIC‐04, Nantes, France</json:string></affiliations></json:item><json:item><name>Tanguy Chaumette</name><affiliations><json:string>Inserm, U913, CHU Nantes, 44093 Nantes, France</json:string><json:string>University of Nantes, Nantes, France</json:string><json:string>CHU Nantes, Institut des Maladies de l’Appareil Digestif, Nantes, France</json:string></affiliations></json:item><json:item><name>Sébastien Paillusson</name><affiliations><json:string>Inserm, U913, CHU Nantes, 44093 Nantes, France</json:string><json:string>University of Nantes, Nantes, France</json:string><json:string>CHU Nantes, Institut des Maladies de l’Appareil Digestif, Nantes, France</json:string></affiliations></json:item><json:item><name>Charles Duyckaerts</name><affiliations><json:string>Laboratoire de Neuropathologie R. 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It has been classically considered that the pathological hallmarks of Parkinson’s disease, namely Lewy bodies and Lewy neurites, affect primarily the substantia nigra. Nevertheless, it has become increasingly evident in recent years that Parkinson’s disease is a multicentric neurodegenerative process that affects several neuronal structures outside the substantia nigra, among which is the enteric nervous system. Remarkably, recent reports have shown that the lesions in the enteric nervous system occurred at a very early stage of the disease, even before the involvement of the central nervous system. This led to the postulate that the enteric nervous system could be critical in the pathophysiology of Parkinson’s disease, as it could represent a route of entry for a putative environmental factor to initiate the pathological process (Braak’s hypothesis). Besides their putative role in the spreading of the pathological process, it has also been suggested that the pathological alterations within the enteric nervous system could be involved in the gastrointestinal dysfunction frequently encountered by parkinsonian patients. The scope of the present article is to review the available studies on the enteric nervous system in Parkinson’s disease patients and in animal models of the disease. We further discuss the strategies that will help in our understanding of the roles of the enteric nervous system, both in the pathophysiology of the disease and in the pathophysiology of the gastrointestinal symptoms.</abstract><qualityIndicators><score>7.844</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595.276 x 810.709 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1619</abstractCharCount><pdfWordCount>6884</pdfWordCount><pdfCharCount>43288</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>237</abstractWordCount></qualityIndicators><title>The second brain and Parkinson’s disease</title><genre><json:string>review-article</json:string></genre><host><volume>30</volume><publisherId><json:string>EJN</json:string></publisherId><pages><total>7</total><last>741</last><first>735</first></pages><issn><json:string>0953-816X</json:string></issn><issue>5</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-9568</json:string></eissn><title>European Journal of Neuroscience</title><doi><json:string>10.1111/(ISSN)1460-9568</json:string></doi></host><publicationDate>2009</publicationDate><copyrightDate>2009</copyrightDate><doi><json:string>10.1111/j.1460-9568.2009.06873.x</json:string></doi><id>17D86D30AE525BF1E4D0AB39CA069EF77CD38BCE</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/17D86D30AE525BF1E4D0AB39CA069EF77CD38BCE/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/17D86D30AE525BF1E4D0AB39CA069EF77CD38BCE/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/17D86D30AE525BF1E4D0AB39CA069EF77CD38BCE/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">The second brain and Parkinson’s disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2009</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">The second brain and Parkinson’s disease</title><author><persName><forename type="first">Thibaud</forename><surname>Lebouvier</surname></persName><affiliation>Inserm, U913, CHU Nantes, 44093 Nantes, France</affiliation><affiliation>University of Nantes, Nantes, France</affiliation><affiliation>CHU Nantes, Institut des Maladies de l’Appareil Digestif, Nantes, France</affiliation><affiliation>CHU Nantes, Department of Neurology, Nantes, France</affiliation><affiliation>Inserm, CIC‐04, Nantes, France</affiliation></author><author><persName><forename type="first">Tanguy</forename><surname>Chaumette</surname></persName><affiliation>Inserm, U913, CHU Nantes, 44093 Nantes, France</affiliation><affiliation>University of Nantes, Nantes, France</affiliation><affiliation>CHU Nantes, Institut des Maladies de l’Appareil Digestif, Nantes, France</affiliation></author><author><persName><forename type="first">Sébastien</forename><surname>Paillusson</surname></persName><affiliation>Inserm, U913, CHU Nantes, 44093 Nantes, France</affiliation><affiliation>University of Nantes, Nantes, France</affiliation><affiliation>CHU Nantes, Institut des Maladies de l’Appareil Digestif, Nantes, France</affiliation></author><author><persName><forename type="first">Charles</forename><surname>Duyckaerts</surname></persName><affiliation>Laboratoire de Neuropathologie R. 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It has been classically considered that the pathological hallmarks of Parkinson’s disease, namely Lewy bodies and Lewy neurites, affect primarily the substantia nigra. Nevertheless, it has become increasingly evident in recent years that Parkinson’s disease is a multicentric neurodegenerative process that affects several neuronal structures outside the substantia nigra, among which is the enteric nervous system. Remarkably, recent reports have shown that the lesions in the enteric nervous system occurred at a very early stage of the disease, even before the involvement of the central nervous system. This led to the postulate that the enteric nervous system could be critical in the pathophysiology of Parkinson’s disease, as it could represent a route of entry for a putative environmental factor to initiate the pathological process (Braak’s hypothesis). Besides their putative role in the spreading of the pathological process, it has also been suggested that the pathological alterations within the enteric nervous system could be involved in the gastrointestinal dysfunction frequently encountered by parkinsonian patients. The scope of the present article is to review the available studies on the enteric nervous system in Parkinson’s disease patients and in animal models of the disease. We further discuss the strategies that will help in our understanding of the roles of the enteric nervous system, both in the pathophysiology of the disease and in the pathophysiology of the gastrointestinal symptoms.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>α‐synuclein</term></item><item><term>enteric nervous system</term></item><item><term>Lewy bodies</term></item><item><term>Parkinson’s disease</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2009-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/17D86D30AE525BF1E4D0AB39CA069EF77CD38BCE/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 version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1460-9568</doi><issn type="print">0953-816X</issn><issn type="electronic">1460-9568</issn><idGroup><id type="product" value="EJN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROSCIENCE">European Journal of Neuroscience</title></titleGroup></publicationMeta><publicationMeta level="part" position="09005"><doi origin="wiley">10.1111/ejn.2009.30.issue-5</doi><numberingGroup><numbering type="journalVolume" number="30">30</numbering><numbering type="journalIssue" number="5">5</numbering></numberingGroup><coverDate startDate="2009-09">September 2009</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="1" status="forIssue"><doi origin="wiley">10.1111/j.1460-9568.2009.06873.x</doi><idGroup><id type="unit" value="EJN6873"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="tocHeading1"> </title><title type="tocHeading2">REVIEW ARTICLE</title></titleGroup><copyright>© The Authors (2009). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd</copyright><eventGroup><event type="firstOnline" date="2009-08-27"></event><event type="publishedOnlineFinalForm" date="2009-08-28"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-02"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-12"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="735">735</numbering><numbering type="pageLast" number="741">741</numbering></numberingGroup><correspondenceTo>Dr P. Derkinderen, <sup>1</sup>Inserm, U913, as above.
E‐mail: <email>derkinderenp@yahoo.fr</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EJN.EJN6873.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 10 May 2009, revised 5 June 2009, accepted 29 June 2009</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="0"></count></countGroup><titleGroup><title type="main">The second brain and Parkinson’s disease</title><title type="shortAuthors">T. Lebouvier <i>et al.</i></title><title type="short">The second brain and Parkinson’s disease</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2 #a3 #a4 #a5"><personName><givenNames>Thibaud</givenNames><familyName>Lebouvier</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1 #a2 #a3"><personName><givenNames>Tanguy</givenNames><familyName>Chaumette</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1 #a2 #a3"><personName><givenNames>Sébastien</givenNames><familyName>Paillusson</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a6"><personName><givenNames>Charles</givenNames><familyName>Duyckaerts</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1 #a2 #a3 #a5"><personName><givenNames>Stanislas</givenNames><familyName>Bruley des Varannes</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1 #a2 #a3 #a4"><personName><givenNames>Michel</givenNames><familyName>Neunlist</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1 #a2 #a3 #a4 #a5"><personName><givenNames>Pascal</givenNames><familyName>Derkinderen</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="FR"><unparsedAffiliation>Inserm, U913, CHU Nantes, 44093 Nantes, France</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="FR"><unparsedAffiliation>University of Nantes, Nantes, France</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="FR"><unparsedAffiliation>CHU Nantes, Institut des Maladies de l’Appareil Digestif, Nantes, France</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="FR"><unparsedAffiliation>CHU Nantes, Department of Neurology, Nantes, France</unparsedAffiliation></affiliation><affiliation xml:id="a5" countryCode="FR"><unparsedAffiliation>Inserm, CIC‐04, Nantes, France</unparsedAffiliation></affiliation><affiliation xml:id="a6" countryCode="FR"><unparsedAffiliation>Laboratoire de Neuropathologie R. Escourolle, Hôpital de la Salpêtrière, Paris, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">α‐synuclein</keyword><keyword xml:id="k2">enteric nervous system</keyword><keyword xml:id="k3">Lewy bodies</keyword><keyword xml:id="k4">Parkinson’s disease</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Parkinson’s disease is the second most common neurodegenerative disease after Alzheimer’s disease. It has been classically considered that the pathological hallmarks of Parkinson’s disease, namely Lewy bodies and Lewy neurites, affect primarily the substantia nigra. Nevertheless, it has become increasingly evident in recent years that Parkinson’s disease is a multicentric neurodegenerative process that affects several neuronal structures outside the substantia nigra, among which is the enteric nervous system. Remarkably, recent reports have shown that the lesions in the enteric nervous system occurred at a very early stage of the disease, even before the involvement of the central nervous system. This led to the postulate that the enteric nervous system could be critical in the pathophysiology of Parkinson’s disease, as it could represent a route of entry for a putative environmental factor to initiate the pathological process (Braak’s hypothesis). Besides their putative role in the spreading of the pathological process, it has also been suggested that the pathological alterations within the enteric nervous system could be involved in the gastrointestinal dysfunction frequently encountered by parkinsonian patients. The scope of the present article is to review the available studies on the enteric nervous system in Parkinson’s disease patients and in animal models of the disease. We further discuss the strategies that will help in our understanding of the roles of the enteric nervous system, both in the pathophysiology of the disease and in the pathophysiology of the gastrointestinal symptoms.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The second brain and Parkinson’s disease</title></titleInfo><titleInfo type="abbreviated"><title>The second brain and Parkinson’s disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The second brain and Parkinson’s disease</title></titleInfo><name type="personal"><namePart type="given">Thibaud</namePart><namePart type="family">Lebouvier</namePart><affiliation>Inserm, U913, CHU Nantes, 44093 Nantes, France</affiliation><affiliation>University of Nantes, Nantes, France</affiliation><affiliation>CHU Nantes, Institut des Maladies de l’Appareil Digestif, Nantes, France</affiliation><affiliation>CHU Nantes, Department of Neurology, Nantes, France</affiliation><affiliation>Inserm, CIC‐04, Nantes, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tanguy</namePart><namePart type="family">Chaumette</namePart><affiliation>Inserm, U913, CHU Nantes, 44093 Nantes, France</affiliation><affiliation>University of Nantes, Nantes, France</affiliation><affiliation>CHU Nantes, Institut des Maladies de l’Appareil Digestif, Nantes, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sébastien</namePart><namePart type="family">Paillusson</namePart><affiliation>Inserm, U913, CHU Nantes, 44093 Nantes, France</affiliation><affiliation>University of Nantes, Nantes, France</affiliation><affiliation>CHU Nantes, Institut des Maladies de l’Appareil Digestif, Nantes, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Charles</namePart><namePart type="family">Duyckaerts</namePart><affiliation>Laboratoire de Neuropathologie R. Escourolle, Hôpital de la Salpêtrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stanislas</namePart><namePart type="family">Bruley des Varannes</namePart><affiliation>Inserm, U913, CHU Nantes, 44093 Nantes, France</affiliation><affiliation>University of Nantes, Nantes, France</affiliation><affiliation>CHU Nantes, Institut des Maladies de l’Appareil Digestif, Nantes, France</affiliation><affiliation>Inserm, CIC‐04, Nantes, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michel</namePart><namePart type="family">Neunlist</namePart><affiliation>Inserm, U913, CHU Nantes, 44093 Nantes, France</affiliation><affiliation>University of Nantes, Nantes, France</affiliation><affiliation>CHU Nantes, Institut des Maladies de l’Appareil Digestif, Nantes, France</affiliation><affiliation>CHU Nantes, Department of Neurology, Nantes, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pascal</namePart><namePart type="family">Derkinderen</namePart><affiliation>Inserm, U913, CHU Nantes, 44093 Nantes, France</affiliation><affiliation>University of Nantes, Nantes, France</affiliation><affiliation>CHU Nantes, Institut des Maladies de l’Appareil Digestif, Nantes, France</affiliation><affiliation>CHU Nantes, Department of Neurology, Nantes, France</affiliation><affiliation>Inserm, CIC‐04, Nantes, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2009-09</dateIssued><edition>Received 10 May 2009, revised 5 June 2009, accepted 29 June 2009</edition><copyrightDate encoding="w3cdtf">2009</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">1</extent></physicalDescription><abstract lang="en">Parkinson’s disease is the second most common neurodegenerative disease after Alzheimer’s disease. It has been classically considered that the pathological hallmarks of Parkinson’s disease, namely Lewy bodies and Lewy neurites, affect primarily the substantia nigra. Nevertheless, it has become increasingly evident in recent years that Parkinson’s disease is a multicentric neurodegenerative process that affects several neuronal structures outside the substantia nigra, among which is the enteric nervous system. Remarkably, recent reports have shown that the lesions in the enteric nervous system occurred at a very early stage of the disease, even before the involvement of the central nervous system. This led to the postulate that the enteric nervous system could be critical in the pathophysiology of Parkinson’s disease, as it could represent a route of entry for a putative environmental factor to initiate the pathological process (Braak’s hypothesis). Besides their putative role in the spreading of the pathological process, it has also been suggested that the pathological alterations within the enteric nervous system could be involved in the gastrointestinal dysfunction frequently encountered by parkinsonian patients. The scope of the present article is to review the available studies on the enteric nervous system in Parkinson’s disease patients and in animal models of the disease. We further discuss the strategies that will help in our understanding of the roles of the enteric nervous system, both in the pathophysiology of the disease and in the pathophysiology of the gastrointestinal symptoms.</abstract><subject lang="en"><genre>Keywords</genre><topic>α‐synuclein</topic><topic>enteric nervous system</topic><topic>Lewy bodies</topic><topic>Parkinson’s disease</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neuroscience</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0953-816X</identifier><identifier type="eISSN">1460-9568</identifier><identifier type="DOI">10.1111/(ISSN)1460-9568</identifier><identifier type="PublisherID">EJN</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>30</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>735</start><end>741</end><total>7</total></extent></part></relatedItem><identifier type="istex">17D86D30AE525BF1E4D0AB39CA069EF77CD38BCE</identifier><identifier type="DOI">10.1111/j.1460-9568.2009.06873.x</identifier><identifier type="ArticleID">EJN6873</identifier><accessCondition type="use and reproduction" contentType="copyright">© The Authors (2009). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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