A primate model of Huntington's disease: cross-species implantation of striatal precursor cells to the excitotoxically lesioned baboon caudate-putamen
Identifieur interne : 002182 ( Main/Corpus ); précédent : 002181; suivant : 002183A primate model of Huntington's disease: cross-species implantation of striatal precursor cells to the excitotoxically lesioned baboon caudate-putamen
Auteurs : O. Isacson ; D. Riche ; P. Hantraye ; V. Sofroniew ; M. MaziereSource :
- Experimental Brain Research [ 0014-4819 ] ; 1989-03-01.
Abstract
Summary: Ibotenic acid was injected unilaterally into the baboon caudate-putamen (CP) to achieve a neural degeneration model in the primate, with a neuropathology similar to Huntington's disease. Four to six weeks later injections of cell suspensions of striatal precursor cells, obtained by dissection of the fetal rat striatal region (13–15 days gestational age), were made into the excitotoxically lesioned CP of 3 baboons immunosuppressed by Cyclosporin A. Morphological analysis indicated that in one of the baboons, which had the largest lesion of the CP and the shortest survival time (6 weeks after implantation), there was a surviving striatal implant. The implanted neurons grew in high densities in cellular aggregates within the host gliotic CP. These neurons had a neuronal size phenotypical for rat striatum, i.e. on average about a 25% smaller neuronal cell diameter than a similar population in the baboon caudate-putamen. Glial-fibrillary-acid-protein immunoreactivity was present on large astrocytes within the striatal implant, with a distinct border towards the lesion-induced astrogliosis of the host. Neuronal markers for acetylcholinesterase and Leu-enkephalin were distributed in a typical patchy manner in the striatal implants along with fiber staining for tyrosine-hydroxylase-like immunoreactivity (TH) possibly derived from afferent host dopaminergic axons. Some of these fibers in the implants came from intrinsic TH-positive neuronal somata, probably of neocortical fetal origin and transiently expressing the enzyme. In conclusion, the results indicate that neuronal replacement can be achieved by crossspecies implantation of fetal striatal precursor cells to the previously neuron depleted primate CP under immunosuppression but that the survival and growth of such implants may be variable and subject to unfavourable trophic conditions.
Url:
DOI: 10.1007/BF00248544
Links to Exploration step
ISTEX:74ED9826924BDCC9E21366E8D866A5C691F31446Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">A primate model of Huntington's disease: cross-species implantation of striatal precursor cells to the excitotoxically lesioned baboon caudate-putamen</title><author><name sortKey="Isacson, O" sort="Isacson, O" uniqKey="Isacson O" first="O." last="Isacson">O. Isacson</name><affiliation><mods:affiliation>Department of Anatomy, University of Cambridge, Downing Street, CB2 3DY, Cambridge, UK</mods:affiliation></affiliation></author><author><name sortKey="Riche, D" sort="Riche, D" uniqKey="Riche D" first="D." last="Riche">D. Riche</name><affiliation><mods:affiliation>Equipe de Neuroanatomie Fonctionelle, C.N.R.S., F-91198, Gif-sur-Yvette, France</mods:affiliation></affiliation></author><author><name sortKey="Hantraye, P" sort="Hantraye, P" uniqKey="Hantraye P" first="P." last="Hantraye">P. Hantraye</name><affiliation><mods:affiliation>Département de Biologie, Service Hospitalier Frédéric Joliot, C.E.A., Institut de Recherche Fondamentale, F-91406, Orsay, France</mods:affiliation></affiliation></author><author><name sortKey="Sofroniew, V" sort="Sofroniew, V" uniqKey="Sofroniew V" first="V." last="Sofroniew">V. Sofroniew</name><affiliation><mods:affiliation>Department of Anatomy, University of Cambridge, Downing Street, CB2 3DY, Cambridge, UK</mods:affiliation></affiliation></author><author><name sortKey="Maziere, M" sort="Maziere, M" uniqKey="Maziere M" first="M." last="Maziere">M. Maziere</name><affiliation><mods:affiliation>Département de Biologie, Service Hospitalier Frédéric Joliot, C.E.A., Institut de Recherche Fondamentale, F-91406, Orsay, France</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:74ED9826924BDCC9E21366E8D866A5C691F31446</idno><date when="1989" year="1989">1989</date><idno type="doi">10.1007/BF00248544</idno><idno type="url">https://api.istex.fr/document/74ED9826924BDCC9E21366E8D866A5C691F31446/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002182</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">A primate model of Huntington's disease: cross-species implantation of striatal precursor cells to the excitotoxically lesioned baboon caudate-putamen</title><author><name sortKey="Isacson, O" sort="Isacson, O" uniqKey="Isacson O" first="O." last="Isacson">O. Isacson</name><affiliation><mods:affiliation>Department of Anatomy, University of Cambridge, Downing Street, CB2 3DY, Cambridge, UK</mods:affiliation></affiliation></author><author><name sortKey="Riche, D" sort="Riche, D" uniqKey="Riche D" first="D." last="Riche">D. Riche</name><affiliation><mods:affiliation>Equipe de Neuroanatomie Fonctionelle, C.N.R.S., F-91198, Gif-sur-Yvette, France</mods:affiliation></affiliation></author><author><name sortKey="Hantraye, P" sort="Hantraye, P" uniqKey="Hantraye P" first="P." last="Hantraye">P. Hantraye</name><affiliation><mods:affiliation>Département de Biologie, Service Hospitalier Frédéric Joliot, C.E.A., Institut de Recherche Fondamentale, F-91406, Orsay, France</mods:affiliation></affiliation></author><author><name sortKey="Sofroniew, V" sort="Sofroniew, V" uniqKey="Sofroniew V" first="V." last="Sofroniew">V. Sofroniew</name><affiliation><mods:affiliation>Department of Anatomy, University of Cambridge, Downing Street, CB2 3DY, Cambridge, UK</mods:affiliation></affiliation></author><author><name sortKey="Maziere, M" sort="Maziere, M" uniqKey="Maziere M" first="M." last="Maziere">M. Maziere</name><affiliation><mods:affiliation>Département de Biologie, Service Hospitalier Frédéric Joliot, C.E.A., Institut de Recherche Fondamentale, F-91406, Orsay, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Experimental Brain Research</title><title level="j" type="abbrev">Exp Brain Res</title><idno type="ISSN">0014-4819</idno><idno type="eISSN">1432-1106</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1989-03-01">1989-03-01</date><biblScope unit="volume">75</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="213">213</biblScope><biblScope unit="page" to="220">220</biblScope></imprint><idno type="ISSN">0014-4819</idno></series><idno type="istex">74ED9826924BDCC9E21366E8D866A5C691F31446</idno><idno type="DOI">10.1007/BF00248544</idno><idno type="ArticleID">Art21</idno><idno type="ArticleID">BF00248544</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0014-4819</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Ibotenic acid was injected unilaterally into the baboon caudate-putamen (CP) to achieve a neural degeneration model in the primate, with a neuropathology similar to Huntington's disease. Four to six weeks later injections of cell suspensions of striatal precursor cells, obtained by dissection of the fetal rat striatal region (13–15 days gestational age), were made into the excitotoxically lesioned CP of 3 baboons immunosuppressed by Cyclosporin A. Morphological analysis indicated that in one of the baboons, which had the largest lesion of the CP and the shortest survival time (6 weeks after implantation), there was a surviving striatal implant. The implanted neurons grew in high densities in cellular aggregates within the host gliotic CP. These neurons had a neuronal size phenotypical for rat striatum, i.e. on average about a 25% smaller neuronal cell diameter than a similar population in the baboon caudate-putamen. Glial-fibrillary-acid-protein immunoreactivity was present on large astrocytes within the striatal implant, with a distinct border towards the lesion-induced astrogliosis of the host. Neuronal markers for acetylcholinesterase and Leu-enkephalin were distributed in a typical patchy manner in the striatal implants along with fiber staining for tyrosine-hydroxylase-like immunoreactivity (TH) possibly derived from afferent host dopaminergic axons. Some of these fibers in the implants came from intrinsic TH-positive neuronal somata, probably of neocortical fetal origin and transiently expressing the enzyme. In conclusion, the results indicate that neuronal replacement can be achieved by crossspecies implantation of fetal striatal precursor cells to the previously neuron depleted primate CP under immunosuppression but that the survival and growth of such implants may be variable and subject to unfavourable trophic conditions.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>O. Isacson</name><affiliations><json:string>Department of Anatomy, University of Cambridge, Downing Street, CB2 3DY, Cambridge, UK</json:string></affiliations></json:item><json:item><name>D. Riche</name><affiliations><json:string>Equipe de Neuroanatomie Fonctionelle, C.N.R.S., F-91198, Gif-sur-Yvette, France</json:string></affiliations></json:item><json:item><name>P. Hantraye</name><affiliations><json:string>Département de Biologie, Service Hospitalier Frédéric Joliot, C.E.A., Institut de Recherche Fondamentale, F-91406, Orsay, France</json:string></affiliations></json:item><json:item><name>M. V. Sofroniew</name><affiliations><json:string>Department of Anatomy, University of Cambridge, Downing Street, CB2 3DY, Cambridge, UK</json:string></affiliations></json:item><json:item><name>M. Maziere</name><affiliations><json:string>Département de Biologie, Service Hospitalier Frédéric Joliot, C.E.A., Institut de Recherche Fondamentale, F-91406, Orsay, France</json:string></affiliations></json:item></author><articleId><json:string>Art21</json:string><json:string>BF00248544</json:string></articleId><language><json:string>eng</json:string></language><abstract>Summary: Ibotenic acid was injected unilaterally into the baboon caudate-putamen (CP) to achieve a neural degeneration model in the primate, with a neuropathology similar to Huntington's disease. Four to six weeks later injections of cell suspensions of striatal precursor cells, obtained by dissection of the fetal rat striatal region (13–15 days gestational age), were made into the excitotoxically lesioned CP of 3 baboons immunosuppressed by Cyclosporin A. Morphological analysis indicated that in one of the baboons, which had the largest lesion of the CP and the shortest survival time (6 weeks after implantation), there was a surviving striatal implant. The implanted neurons grew in high densities in cellular aggregates within the host gliotic CP. These neurons had a neuronal size phenotypical for rat striatum, i.e. on average about a 25% smaller neuronal cell diameter than a similar population in the baboon caudate-putamen. Glial-fibrillary-acid-protein immunoreactivity was present on large astrocytes within the striatal implant, with a distinct border towards the lesion-induced astrogliosis of the host. Neuronal markers for acetylcholinesterase and Leu-enkephalin were distributed in a typical patchy manner in the striatal implants along with fiber staining for tyrosine-hydroxylase-like immunoreactivity (TH) possibly derived from afferent host dopaminergic axons. Some of these fibers in the implants came from intrinsic TH-positive neuronal somata, probably of neocortical fetal origin and transiently expressing the enzyme. In conclusion, the results indicate that neuronal replacement can be achieved by crossspecies implantation of fetal striatal precursor cells to the previously neuron depleted primate CP under immunosuppression but that the survival and growth of such implants may be variable and subject to unfavourable trophic conditions.</abstract><qualityIndicators><score>7.654</score><pdfVersion>1.3</pdfVersion><pdfPageSize>590.28 x 785 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1872</abstractCharCount><pdfWordCount>4654</pdfWordCount><pdfCharCount>26356</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>265</abstractWordCount></qualityIndicators><title>A primate model of Huntington's disease: cross-species implantation of striatal precursor cells to the excitotoxically lesioned baboon caudate-putamen</title><genre><json:string>research-article</json:string></genre><host><volume>75</volume><pages><last>220</last><first>213</first></pages><issn><json:string>0014-4819</json:string></issn><issue>1</issue><subject><json:item><value>Neurosciences</value></json:item><json:item><value>Neurology</value></json:item></subject><journalId><json:string>221</json:string></journalId><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1432-1106</json:string></eissn><title>Experimental Brain Research</title><publicationDate>1989</publicationDate><copyrightDate>1989</copyrightDate></host><publicationDate>1989</publicationDate><copyrightDate>1989</copyrightDate><doi><json:string>10.1007/BF00248544</json:string></doi><id>74ED9826924BDCC9E21366E8D866A5C691F31446</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/74ED9826924BDCC9E21366E8D866A5C691F31446/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/74ED9826924BDCC9E21366E8D866A5C691F31446/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/74ED9826924BDCC9E21366E8D866A5C691F31446/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">A primate model of Huntington's disease: cross-species implantation of striatal precursor cells to the excitotoxically lesioned baboon caudate-putamen</title><respStmt xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><availability><p>SPRINGER</p></availability><date>1988-06-20</date></publicationStmt><notesStmt><note>Research Note</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">A primate model of Huntington's disease: cross-species implantation of striatal precursor cells to the excitotoxically lesioned baboon caudate-putamen</title><author corresp="yes"><persName><forename type="first">O.</forename><surname>Isacson</surname></persName><affiliation>Department of Anatomy, University of Cambridge, Downing Street, CB2 3DY, Cambridge, UK</affiliation></author><author><persName><forename type="first">D.</forename><surname>Riche</surname></persName><affiliation>Equipe de Neuroanatomie Fonctionelle, C.N.R.S., F-91198, Gif-sur-Yvette, France</affiliation></author><author><persName><forename type="first">P.</forename><surname>Hantraye</surname></persName><affiliation>Département de Biologie, Service Hospitalier Frédéric Joliot, C.E.A., Institut de Recherche Fondamentale, F-91406, Orsay, France</affiliation></author><author><persName><forename type="first">M.</forename><surname>Sofroniew</surname></persName><affiliation>Department of Anatomy, University of Cambridge, Downing Street, CB2 3DY, Cambridge, UK</affiliation></author><author><persName><forename type="first">M.</forename><surname>Maziere</surname></persName><affiliation>Département de Biologie, Service Hospitalier Frédéric Joliot, C.E.A., Institut de Recherche Fondamentale, F-91406, Orsay, France</affiliation></author></analytic><monogr><title level="j">Experimental Brain Research</title><title level="j" type="abbrev">Exp Brain Res</title><idno type="JournalID">221</idno><idno type="pISSN">0014-4819</idno><idno type="eISSN">1432-1106</idno><idno type="IssueArticleCount">21</idno><idno type="VolumeIssueCount">3</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1989-03-01"></date><biblScope unit="volume">75</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="213">213</biblScope><biblScope unit="page" to="220">220</biblScope></imprint></monogr><idno type="istex">74ED9826924BDCC9E21366E8D866A5C691F31446</idno><idno type="DOI">10.1007/BF00248544</idno><idno type="ArticleID">Art21</idno><idno type="ArticleID">BF00248544</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1988-06-20</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Summary: Ibotenic acid was injected unilaterally into the baboon caudate-putamen (CP) to achieve a neural degeneration model in the primate, with a neuropathology similar to Huntington's disease. Four to six weeks later injections of cell suspensions of striatal precursor cells, obtained by dissection of the fetal rat striatal region (13–15 days gestational age), were made into the excitotoxically lesioned CP of 3 baboons immunosuppressed by Cyclosporin A. Morphological analysis indicated that in one of the baboons, which had the largest lesion of the CP and the shortest survival time (6 weeks after implantation), there was a surviving striatal implant. The implanted neurons grew in high densities in cellular aggregates within the host gliotic CP. These neurons had a neuronal size phenotypical for rat striatum, i.e. on average about a 25% smaller neuronal cell diameter than a similar population in the baboon caudate-putamen. Glial-fibrillary-acid-protein immunoreactivity was present on large astrocytes within the striatal implant, with a distinct border towards the lesion-induced astrogliosis of the host. Neuronal markers for acetylcholinesterase and Leu-enkephalin were distributed in a typical patchy manner in the striatal implants along with fiber staining for tyrosine-hydroxylase-like immunoreactivity (TH) possibly derived from afferent host dopaminergic axons. Some of these fibers in the implants came from intrinsic TH-positive neuronal somata, probably of neocortical fetal origin and transiently expressing the enzyme. In conclusion, the results indicate that neuronal replacement can be achieved by crossspecies implantation of fetal striatal precursor cells to the previously neuron depleted primate CP under immunosuppression but that the survival and growth of such implants may be variable and subject to unfavourable trophic conditions.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Biomedicine</head><item><term>Neurosciences</term></item><item><term>Neurology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1988-06-20">Created</change><change when="1989-03-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-1">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/74ED9826924BDCC9E21366E8D866A5C691F31446/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Springer, Publisher found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer-Verlag</PublisherName><PublisherLocation>Berlin/Heidelberg</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>221</JournalID><JournalPrintISSN>0014-4819</JournalPrintISSN><JournalElectronicISSN>1432-1106</JournalElectronicISSN><JournalTitle>Experimental Brain Research</JournalTitle><JournalAbbreviatedTitle>Exp Brain Res</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Biomedicine</JournalSubject><JournalSubject Type="Secondary">Neurosciences</JournalSubject><JournalSubject Type="Secondary">Neurology</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>75</VolumeIDStart><VolumeIDEnd>75</VolumeIDEnd><VolumeIssueCount>3</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>1</IssueIDStart><IssueIDEnd>1</IssueIDEnd><IssueArticleCount>21</IssueArticleCount><IssueHistory><CoverDate><Year>1989</Year><Month>3</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1989</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art21"><ArticleInfo Language="En" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF00248544</ArticleID><ArticleDOI>10.1007/BF00248544</ArticleDOI><ArticleSequenceNumber>21</ArticleSequenceNumber><ArticleTitle Language="En">A primate model of Huntington's disease: cross-species implantation of striatal precursor cells to the excitotoxically lesioned baboon caudate-putamen</ArticleTitle><ArticleCategory>Research Note</ArticleCategory><ArticleFirstPage>213</ArticleFirstPage><ArticleLastPage>220</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2004</Year><Month>8</Month><Day>3</Day></RegistrationDate><Received><Year>1988</Year><Month>6</Month><Day>20</Day></Received><Accepted><Year>1988</Year><Month>10</Month><Day>31</Day></Accepted></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1989</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>221</JournalID><VolumeIDStart>75</VolumeIDStart><VolumeIDEnd>75</VolumeIDEnd><IssueIDStart>1</IssueIDStart><IssueIDEnd>1</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" CorrespondingAffiliationID="Aff2"><AuthorName DisplayOrder="Western"><GivenName>O.</GivenName><FamilyName>Isacson</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff3"><AuthorName DisplayOrder="Western"><GivenName>D.</GivenName><FamilyName>Riche</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff4"><AuthorName DisplayOrder="Western"><GivenName>P.</GivenName><FamilyName>Hantraye</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>M.</GivenName><GivenName>V.</GivenName><FamilyName>Sofroniew</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff4"><AuthorName DisplayOrder="Western"><GivenName>M.</GivenName><FamilyName>Maziere</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Department of Anatomy</OrgDivision><OrgName>University of Cambridge</OrgName><OrgAddress><Street>Downing Street</Street><Postcode>CB2 3DY</Postcode><City>Cambridge</City><Country>UK</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgName>Equipe de Neuroanatomie Fonctionelle, C.N.R.S.</OrgName><OrgAddress><Postcode>F-91198</Postcode><City>Gif-sur-Yvette</City><Country>France</Country></OrgAddress></Affiliation><Affiliation ID="Aff4"><OrgDivision>Département de Biologie</OrgDivision><OrgName>Service Hospitalier Frédéric Joliot, C.E.A., Institut de Recherche Fondamentale</OrgName><OrgAddress><Postcode>F-91406</Postcode><City>Orsay</City><Country>France</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgName>McLean Hospital</OrgName><OrgAddress><Postcode>02178</Postcode><City>Belmont</City><State>MA</State><Country>USA</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Ibotenic acid was injected unilaterally into the baboon caudate-putamen (CP) to achieve a neural degeneration model in the primate, with a neuropathology similar to Huntington's disease. Four to six weeks later injections of cell suspensions of striatal precursor cells, obtained by dissection of the fetal rat striatal region (13–15 days gestational age), were made into the excitotoxically lesioned CP of 3 baboons immunosuppressed by Cyclosporin A. Morphological analysis indicated that in one of the baboons, which had the largest lesion of the CP and the shortest survival time (6 weeks after implantation), there was a surviving striatal implant. The implanted neurons grew in high densities in cellular aggregates within the host gliotic CP. These neurons had a neuronal size phenotypical for rat striatum, i.e. on average about a 25% smaller neuronal cell diameter than a similar population in the baboon caudate-putamen. Glial-fibrillary-acid-protein immunoreactivity was present on large astrocytes within the striatal implant, with a distinct border towards the lesion-induced astrogliosis of the host. Neuronal markers for acetylcholinesterase and Leu-enkephalin were distributed in a typical patchy manner in the striatal implants along with fiber staining for tyrosine-hydroxylase-like immunoreactivity (TH) possibly derived from afferent host dopaminergic axons. Some of these fibers in the implants came from intrinsic TH-positive neuronal somata, probably of neocortical fetal origin and transiently expressing the enzyme. In conclusion, the results indicate that neuronal replacement can be achieved by crossspecies implantation of fetal striatal precursor cells to the previously neuron depleted primate CP under immunosuppression but that the survival and growth of such implants may be variable and subject to unfavourable trophic conditions.</Para></Abstract><KeywordGroup Language="En"><Heading>Key words</Heading><Keyword>Huntington's disease</Keyword><Keyword>Excitotoxins</Keyword><Keyword>Primates</Keyword><Keyword>Caudate-putamen</Keyword><Keyword>Neuronal transplantation</Keyword><Keyword>Cross-species</Keyword><Keyword>Fetal striatum</Keyword><Keyword>Morphology</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>A primate model of Huntington's disease: cross-species implantation of striatal precursor cells to the excitotoxically lesioned baboon caudate-putamen</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>A primate model of Huntington's disease: cross-species implantation of striatal precursor cells to the excitotoxically lesioned baboon caudate-putamen</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">O.</namePart><namePart type="family">Isacson</namePart><affiliation>Department of Anatomy, University of Cambridge, Downing Street, CB2 3DY, Cambridge, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Riche</namePart><affiliation>Equipe de Neuroanatomie Fonctionelle, C.N.R.S., F-91198, Gif-sur-Yvette, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Hantraye</namePart><affiliation>Département de Biologie, Service Hospitalier Frédéric Joliot, C.E.A., Institut de Recherche Fondamentale, F-91406, Orsay, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="given">V.</namePart><namePart type="family">Sofroniew</namePart><affiliation>Department of Anatomy, University of Cambridge, Downing Street, CB2 3DY, Cambridge, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Maziere</namePart><affiliation>Département de Biologie, Service Hospitalier Frédéric Joliot, C.E.A., Institut de Recherche Fondamentale, F-91406, Orsay, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Berlin/Heidelberg</placeTerm></place><dateCreated encoding="w3cdtf">1988-06-20</dateCreated><dateIssued encoding="w3cdtf">1989-03-01</dateIssued><copyrightDate encoding="w3cdtf">1989</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 lang="en">Summary: Ibotenic acid was injected unilaterally into the baboon caudate-putamen (CP) to achieve a neural degeneration model in the primate, with a neuropathology similar to Huntington's disease. Four to six weeks later injections of cell suspensions of striatal precursor cells, obtained by dissection of the fetal rat striatal region (13–15 days gestational age), were made into the excitotoxically lesioned CP of 3 baboons immunosuppressed by Cyclosporin A. Morphological analysis indicated that in one of the baboons, which had the largest lesion of the CP and the shortest survival time (6 weeks after implantation), there was a surviving striatal implant. The implanted neurons grew in high densities in cellular aggregates within the host gliotic CP. These neurons had a neuronal size phenotypical for rat striatum, i.e. on average about a 25% smaller neuronal cell diameter than a similar population in the baboon caudate-putamen. Glial-fibrillary-acid-protein immunoreactivity was present on large astrocytes within the striatal implant, with a distinct border towards the lesion-induced astrogliosis of the host. Neuronal markers for acetylcholinesterase and Leu-enkephalin were distributed in a typical patchy manner in the striatal implants along with fiber staining for tyrosine-hydroxylase-like immunoreactivity (TH) possibly derived from afferent host dopaminergic axons. Some of these fibers in the implants came from intrinsic TH-positive neuronal somata, probably of neocortical fetal origin and transiently expressing the enzyme. In conclusion, the results indicate that neuronal replacement can be achieved by crossspecies implantation of fetal striatal precursor cells to the previously neuron depleted primate CP under immunosuppression but that the survival and growth of such implants may be variable and subject to unfavourable trophic conditions.</abstract><note>Research Note</note><relatedItem type="host"><titleInfo><title>Experimental Brain Research</title></titleInfo><titleInfo type="abbreviated"><title>Exp Brain Res</title></titleInfo><genre type="Journal" displayLabel="Archive Journal"></genre><originInfo><dateIssued encoding="w3cdtf">1989-03-01</dateIssued><copyrightDate encoding="w3cdtf">1989</copyrightDate></originInfo><subject><genre>Biomedicine</genre><topic>Neurosciences</topic><topic>Neurology</topic></subject><identifier type="ISSN">0014-4819</identifier><identifier type="eISSN">1432-1106</identifier><identifier type="JournalID">221</identifier><identifier type="IssueArticleCount">21</identifier><identifier type="VolumeIssueCount">3</identifier><part><date>1989</date><detail type="volume"><number>75</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="pages"><start>213</start><end>220</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 1989</recordOrigin></recordInfo></relatedItem><identifier type="istex">74ED9826924BDCC9E21366E8D866A5C691F31446</identifier><identifier type="DOI">10.1007/BF00248544</identifier><identifier type="ArticleID">Art21</identifier><identifier type="ArticleID">BF00248544</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag</accessCondition><recordInfo><recordContentSource>SPRINGER</recordContentSource><recordOrigin>Springer-Verlag, 1989</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002182 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 002182 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= ISTEX:74ED9826924BDCC9E21366E8D866A5C691F31446
|texte= A primate model of Huntington's disease: cross-species implantation of striatal precursor cells to the excitotoxically lesioned baboon caudate-putamen
}}
| This area was generated with Dilib version V0.6.23. |  |