The relationship between axonal transport of protein and demyelination in the optic nerves of mice infected with Semliki Forest Virus
Identifieur interne : 000355 ( Istex/Corpus ); précédent : 000354; suivant : 000356The relationship between axonal transport of protein and demyelination in the optic nerves of mice infected with Semliki Forest Virus
Auteurs : E. M. Tansey ; Hisako IkedaSource :
- Brain Research [ 0006-8993 ] ; 1986.
English descriptors
- Teeft :
- Avirulent semliki forest virus, Axon, Axonal, Axonal transport, Axoplasmic flow, Bap, Cerebrospinal fluid, Colliculus, Control mice, Demyelinating, Demyelination, Fibre, Histogram, Inoculation, Intravitreal, Intravitreal injection, Intravitreal injections, Ipsilateral counts, Liquid scintillation, Mouse, Myelin, Myelin sheath, Open circles, Optic, Optic nerve, Optic nerve fibres, Optic nerve terminals, Optic nerves, Radioactivity, Retina, Retinal ganglion cells, Scintillation, Semliki, Semliki forest virus, Slow axonal transport, Superior colliculus, Webb.
Abstract
Abstract: Fast and slow axonal transport of protein have been studied in the optic nerves of mice infected with Semliki Forest Virus (SFV) that causes patchy demyelination throughout the CNS. Intravitreal injections of [3H]proline were given at regular intervals after virus inoculation, the labelled protein in the superior colliculi was then measured after survival periods of 18 h or 10 days, for fast and slow axonal transport studies, respectively. Fast transport studies showed an enhanced amount of protein arriving at the optic nerve terminals (superior colliculus) of the SFV-infected mice prior to the onset of demyelination. In contrast, the slow transport studies showed an enhanced amount of protein at the superior colliculus of the SFV-infected mice during the demyelination period. There was no concomitant increase in labelled protein in the retina at any time after the SFV infection. It is proposed that alteration in the transport of the protein constituents other than major myelin specific components may cause disruption of myelin maintenance in SFV infection.
Url:
DOI: 10.1016/0006-8993(86)91364-8
Links to Exploration step
ISTEX:ED968AD88C6101AC2657186E4503F8EFE8B80825Le document en format XML
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Tansey</name><affiliation><mods:affiliation>Vision Research Unit of the Sherrington School, The Rayne Institute, St. Thomas' Hospital, London, U.K.</mods:affiliation></affiliation></author><author><name sortKey="Ikeda, Hisako" sort="Ikeda, Hisako" uniqKey="Ikeda H" first="Hisako" last="Ikeda">Hisako Ikeda</name><affiliation><mods:affiliation>Vision Research Unit of the Sherrington School, The Rayne Institute, St. Thomas' Hospital, London, U.K.</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:ED968AD88C6101AC2657186E4503F8EFE8B80825</idno><date when="1986" year="1986">1986</date><idno type="doi">10.1016/0006-8993(86)91364-8</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-MNXGMCV3-7/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000355</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000355</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">The relationship between axonal transport of protein and demyelination in the optic nerves of mice infected with Semliki Forest Virus</title><author><name sortKey="Tansey, E M" sort="Tansey, E M" uniqKey="Tansey E" first="E. M." last="Tansey">E. M. Tansey</name><affiliation><mods:affiliation>Vision Research Unit of the Sherrington School, The Rayne Institute, St. Thomas' Hospital, London, U.K.</mods:affiliation></affiliation></author><author><name sortKey="Ikeda, Hisako" sort="Ikeda, Hisako" uniqKey="Ikeda H" first="Hisako" last="Ikeda">Hisako Ikeda</name><affiliation><mods:affiliation>Vision Research Unit of the Sherrington School, The Rayne Institute, St. Thomas' Hospital, London, U.K.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain Research</title><title level="j" type="abbrev">BRES</title><idno type="ISSN">0006-8993</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1986">1986</date><biblScope unit="volume">397</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="9">9</biblScope><biblScope unit="page" to="15">15</biblScope></imprint><idno type="ISSN">0006-8993</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8993</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Avirulent semliki forest virus</term><term>Axon</term><term>Axonal</term><term>Axonal transport</term><term>Axoplasmic flow</term><term>Bap</term><term>Cerebrospinal fluid</term><term>Colliculus</term><term>Control mice</term><term>Demyelinating</term><term>Demyelination</term><term>Fibre</term><term>Histogram</term><term>Inoculation</term><term>Intravitreal</term><term>Intravitreal injection</term><term>Intravitreal injections</term><term>Ipsilateral counts</term><term>Liquid scintillation</term><term>Mouse</term><term>Myelin</term><term>Myelin sheath</term><term>Open circles</term><term>Optic</term><term>Optic nerve</term><term>Optic nerve fibres</term><term>Optic nerve terminals</term><term>Optic nerves</term><term>Radioactivity</term><term>Retina</term><term>Retinal ganglion cells</term><term>Scintillation</term><term>Semliki</term><term>Semliki forest virus</term><term>Slow axonal transport</term><term>Superior colliculus</term><term>Webb</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Fast and slow axonal transport of protein have been studied in the optic nerves of mice infected with Semliki Forest Virus (SFV) that causes patchy demyelination throughout the CNS. Intravitreal injections of [3H]proline were given at regular intervals after virus inoculation, the labelled protein in the superior colliculi was then measured after survival periods of 18 h or 10 days, for fast and slow axonal transport studies, respectively. Fast transport studies showed an enhanced amount of protein arriving at the optic nerve terminals (superior colliculus) of the SFV-infected mice prior to the onset of demyelination. In contrast, the slow transport studies showed an enhanced amount of protein at the superior colliculus of the SFV-infected mice during the demyelination period. There was no concomitant increase in labelled protein in the retina at any time after the SFV infection. 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Tansey</name><affiliations><json:string>Vision Research Unit of the Sherrington School, The Rayne Institute, St. Thomas' Hospital, London, U.K.</json:string></affiliations></json:item><json:item><name>Hisako Ikeda</name><affiliations><json:string>Vision Research Unit of the Sherrington School, The Rayne Institute, St. Thomas' Hospital, London, U.K.</json:string></affiliations></json:item></author><articleId><json:string>86913648</json:string></articleId><arkIstex>ark:/67375/6H6-MNXGMCV3-7</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Fast and slow axonal transport of protein have been studied in the optic nerves of mice infected with Semliki Forest Virus (SFV) that causes patchy demyelination throughout the CNS. Intravitreal injections of [3H]proline were given at regular intervals after virus inoculation, the labelled protein in the superior colliculi was then measured after survival periods of 18 h or 10 days, for fast and slow axonal transport studies, respectively. Fast transport studies showed an enhanced amount of protein arriving at the optic nerve terminals (superior colliculus) of the SFV-infected mice prior to the onset of demyelination. In contrast, the slow transport studies showed an enhanced amount of protein at the superior colliculus of the SFV-infected mice during the demyelination period. There was no concomitant increase in labelled protein in the retina at any time after the SFV infection. 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Ikeda, Vision Research Unit of the Sherrington School, The Rayne Institute, St. Thomas' Hospital, London SE1 7EH, U.K.</p></note><affiliation>Vision Research Unit of the Sherrington School, The Rayne Institute, St. Thomas' Hospital, London, U.K.</affiliation></author><idno type="istex">ED968AD88C6101AC2657186E4503F8EFE8B80825</idno><idno type="ark">ark:/67375/6H6-MNXGMCV3-7</idno><idno type="DOI">10.1016/0006-8993(86)91364-8</idno><idno type="PII">0006-8993(86)91364-8</idno><idno type="article-id">86913648</idno></analytic><monogr><title level="j">Brain Research</title><title level="j" type="abbrev">BRES</title><idno type="pISSN">0006-8993</idno><idno type="PII">S0006-8993(00)X1307-8</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1986"></date><biblScope unit="volume">397</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="9">9</biblScope><biblScope unit="page" to="15">15</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1986</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Fast and slow axonal transport of protein have been studied in the optic nerves of mice infected with Semliki Forest Virus (SFV) that causes patchy demyelination throughout the CNS. Intravitreal injections of [3H]proline were given at regular intervals after virus inoculation, the labelled protein in the superior colliculi was then measured after survival periods of 18 h or 10 days, for fast and slow axonal transport studies, respectively. Fast transport studies showed an enhanced amount of protein arriving at the optic nerve terminals (superior colliculus) of the SFV-infected mice prior to the onset of demyelination. In contrast, the slow transport studies showed an enhanced amount of protein at the superior colliculus of the SFV-infected mice during the demyelination period. There was no concomitant increase in labelled protein in the retina at any time after the SFV infection. It is proposed that alteration in the transport of the protein constituents other than major myelin specific components may cause disruption of myelin maintenance in SFV infection.</p></abstract></profileDesc><revisionDesc><change when="1986">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-MNXGMCV3-7/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier doc found" wicri:toSee="Elsevier, no converted or simple article"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 5.0.1//EN//XML" URI="art501.dtd" name="istex:docType"></istex:docType><istex:document><article version="5.0" xml:lang="en" docsubtype="fla"><item-info><jid>BRES</jid><aid>86913648</aid><ce:pii>0006-8993(86)91364-8</ce:pii><ce:doi>10.1016/0006-8993(86)91364-8</ce:doi><ce:copyright type="unknown" year="1986">Elsevier Science Publishers B.V. (Biomedical Division)</ce:copyright></item-info><head><ce:title>The relationship between axonal transport of protein and demyelination in the optic nerves of mice infected with Semliki Forest Virus</ce:title><ce:author-group><ce:author><ce:given-name>E.M.</ce:given-name><ce:surname>Tansey</ce:surname></ce:author><ce:author><ce:given-name>Hisako</ce:given-name><ce:surname>Ikeda</ce:surname><ce:cross-ref refid="cor1"><ce:sup loc="post">*</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>Vision Research Unit of the Sherrington School, The Rayne Institute, St. Thomas' Hospital, London, U.K.</ce:textfn></ce:affiliation><ce:correspondence id="cor1"><ce:label>*</ce:label><ce:text><ce:italic>Correspondence:</ce:italic> H. Ikeda, Vision Research Unit of the Sherrington School, The Rayne Institute, St. Thomas' Hospital, London SE1 7EH, U.K.</ce:text></ce:correspondence></ce:author-group><ce:date-accepted day="8" month="4" year="1986"></ce:date-accepted><ce:abstract id="ab1" class="author" xml:lang="en"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">Fast and slow axonal transport of protein have been studied in the optic nerves of mice infected with Semliki Forest Virus (SFV) that causes patchy demyelination throughout the CNS. Intravitreal injections of [<ce:sup loc="pre">3</ce:sup>H]proline were given at regular intervals after virus inoculation, the labelled protein in the superior colliculi was then measured after survival periods of 18 h or 10 days, for fast and slow axonal transport studies, respectively. Fast transport studies showed an enhanced amount of protein arriving at the optic nerve terminals (superior colliculus) of the SFV-infected mice prior to the onset of demyelination. In contrast, the slow transport studies showed an enhanced amount of protein at the superior colliculus of the SFV-infected mice during the demyelination period. There was no concomitant increase in labelled protein in the retina at any time after the SFV infection. It is proposed that alteration in the transport of the protein constituents other than major myelin specific components may cause disruption of myelin maintenance in SFV infection.</ce:simple-para></ce:abstract-sec></ce:abstract></head><tail view="all"><ce:bibliography view="all" id="bibliography.0010"><ce:section-title>Reference</ce:section-title><ce:bibliography-sec id="bibliography-sec.0010"><ce:bib-reference id="bib1"><ce:label>1</ce:label><sb:reference><sb:contribution langtype="en"><sb:authors><sb:author><ce:surname>Allen</ce:surname><ce:given-name>T.G.J.</ce:given-name></sb:author><sb:author><ce:surname>Ikeda</ce:surname><ce:given-name>H.</ce:given-name></sb:author><sb:author><ce:surname>Tansey</ce:surname><ce:given-name>E.M.</ce:given-name></sb:author></sb:authors><sb:title><sb:maintitle>An increase in axoplasmic flow precedes demyelination of optic nerve fibres in mice infected with Semliki Forest Virus</sb:maintitle></sb:title></sb:contribution><sb:host><sb:issue><sb:series><sb:title><sb:maintitle>J. 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Ikeda, Vision Research Unit of the Sherrington School, The Rayne Institute, St. Thomas' Hospital, London SE1 7EH, U.K.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1986</dateIssued><copyrightDate encoding="w3cdtf">1986</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Fast and slow axonal transport of protein have been studied in the optic nerves of mice infected with Semliki Forest Virus (SFV) that causes patchy demyelination throughout the CNS. Intravitreal injections of [3H]proline were given at regular intervals after virus inoculation, the labelled protein in the superior colliculi was then measured after survival periods of 18 h or 10 days, for fast and slow axonal transport studies, respectively. Fast transport studies showed an enhanced amount of protein arriving at the optic nerve terminals (superior colliculus) of the SFV-infected mice prior to the onset of demyelination. In contrast, the slow transport studies showed an enhanced amount of protein at the superior colliculus of the SFV-infected mice during the demyelination period. There was no concomitant increase in labelled protein in the retina at any time after the SFV infection. It is proposed that alteration in the transport of the protein constituents other than major myelin specific components may cause disruption of myelin maintenance in SFV infection.</abstract><relatedItem type="host"><titleInfo><title>Brain Research</title></titleInfo><titleInfo type="abbreviated"><title>BRES</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1986</dateIssued></originInfo><identifier type="ISSN">0006-8993</identifier><identifier type="PII">S0006-8993(00)X1307-8</identifier><part><date>1986</date><detail type="volume"><number>397</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue-pages"><start>1</start><end>204</end></extent><extent unit="pages"><start>9</start><end>15</end></extent></part></relatedItem><identifier type="istex">ED968AD88C6101AC2657186E4503F8EFE8B80825</identifier><identifier type="ark">ark:/67375/6H6-MNXGMCV3-7</identifier><identifier type="DOI">10.1016/0006-8993(86)91364-8</identifier><identifier type="PII">0006-8993(86)91364-8</identifier><identifier type="ArticleID">86913648</identifier><accessCondition type="use and reproduction" contentType="copyright">©1986 Elsevier Science Publishers B.V. 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