Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system
Identifieur interne : 000465 ( Istex/Corpus ); précédent : 000464; suivant : 000466Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system
Auteurs : I. Dusart ; S. Marty ; M. PeschanskiSource :
- Neuroscience [ 0306-4522 ] ; 1992.
English descriptors
- Teeft :
- Afferent, Afferent fibers, Astrocyte, Axon, Axonal, Axonal ensheathment, Axonoglial, Axonoglial interactions, Axonoglial relationships, Axons myelinated, Basal lamina, Collagen fibrils, Degeneration, Demyelinated, Demyelinating, Demyelination, Demyelination process, Dorsal column nuclei, Ensheathed, Excitotoxic, Excitotoxic lesion, First weeks, Glia limitans, Glial, Horseradish peroxidase, Internal capsule, Kainate, Kainate injection, Kainate lesion, Kainic, Kainic acid, Lemniscal, Lesion, Macrophage, Multiple sclerosis, Myelin, Myelin debris, Myelin sheaths, Myelinated, Neuronal, Neuronal depletion, Neuropile, Numerous schwann cells, Oligodendrocyte, Peschanski, Present study, Reactive astrocytes, Remyelination, Schwann, Schwann cell, Schwann cells, Spinal, Spinal cord, Thalamus, Ultrastructural, Ultrastructural study, Unmyelinated, Unmyelinated axons, Wallerian degeneration, Wheatgerm agglutinin.
Abstract
Abstract: Excitotoxins are thought to kill neurons while sparing afferent fibers and axons of passage. The validity of this classical conclusion has recently been questioned by the demonstration of axonal demyelination. In addition, axons are submitted to a profound alteration of their glial environment. This work was, therefore, undertaken to reassess axonoglial interactions over time after an excitotoxic lesion in the rat. Ultrastructural studies were carried out in the ventrobasal thalamus two days to 18 months after neuronal depletion by in situ injections of kainic acid. In some cases, lemniscal afferents were identified by using anterograde transport of wheatgerm agglutinin conjugated to horseradish peroxidase from the dorsal column nuclei. Two and four days after kainate injection, numerous dying axons displaying typical signs of Wallerian degeneration were observed in a neuropile characterized by the loss of neuronal somata and dendrites, an increase in number of microglia/macrophages and the disappearance of astrocytes. Ten and 12 days after kainate injection, degenerating axons were no longer observed although myelin degeneration of otherwise unaltered axons was ongoing with an accumulation of myelin remnants in the neuropile. At 16 and 20 days, the demyelination process was apparently complete and axons of different diameters were sometimes packed together. One and two months after kainate injection, the axonal environment changed again: remyelination of large-caliber axons occurred at the same time as reactive astrocytes, oligodendrocytes and numerous Schwann cells appeared in the tissue. Schwann cell processes surrounded aggregates of axons of diverse calibers, ensheathed small ones and myelinated larger ones. Axons were also remyelinated by oligodendrocytes. Horseradish peroxidase-labeled lemniscal afferents could be myelinated by either of the two cell types. After three months, the neuropile exhibited an increase in number of hypertrophied astrocytes and the progressive loss of any other cellular or axonal element. At this stage, remaining Schwann cells were surrounded by a glia limitans formed by astrocytic processes. These data indicate that although excitotoxins are sparing the axons, they are having a profound and complex effect on the axonal environment. Demyelination occurs over the first weeks, accompanying the loss of astrocytes and oligodendrocytes. Axonal ensheathment and remyelination takes place in a second period, associated with the reappearance of oligodendrocytes and recruitment of numerous Schwann cells, while reactive astrocytes appear in the tissue at a slightly later time. Over the following months, astrocytes occupy a greater proportion of the neuron-depleted territory and other elements decrease in number. These successive stages in alteration of axonoglial interactions seem to evolve in parallel to the changes in density and terminal morphology that we described earlier for myelinated afferent fibers to the excitotoxic lesion.
Url:
DOI: 10.1016/0306-4522(92)90478-K
Links to Exploration step
ISTEX:8C76FC7748C09806679BEA4601EB11B9E629FC86Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system</title>
<author><name sortKey="Dusart, I" sort="Dusart, I" uniqKey="Dusart I" first="I." last="Dusart">I. Dusart</name>
<affiliation><mods:affiliation>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</mods:affiliation>
</affiliation>
</author>
<author><name sortKey="Marty, S" sort="Marty, S" uniqKey="Marty S" first="S." last="Marty">S. Marty</name>
<affiliation><mods:affiliation>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</mods:affiliation>
</affiliation>
</author>
<author><name sortKey="Peschanski, M" sort="Peschanski, M" uniqKey="Peschanski M" first="M." last="Peschanski">M. Peschanski</name>
<affiliation><mods:affiliation>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</mods:affiliation>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:8C76FC7748C09806679BEA4601EB11B9E629FC86</idno>
<date when="1992" year="1992">1992</date>
<idno type="doi">10.1016/0306-4522(92)90478-K</idno>
<idno type="url">https://api.istex.fr/ark:/67375/6H6-SDG85FX3-D/fulltext.pdf</idno>
<idno type="wicri:Area/Istex/Corpus">000465</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000465</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title level="a">Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system</title>
<author><name sortKey="Dusart, I" sort="Dusart, I" uniqKey="Dusart I" first="I." last="Dusart">I. Dusart</name>
<affiliation><mods:affiliation>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</mods:affiliation>
</affiliation>
</author>
<author><name sortKey="Marty, S" sort="Marty, S" uniqKey="Marty S" first="S." last="Marty">S. Marty</name>
<affiliation><mods:affiliation>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</mods:affiliation>
</affiliation>
</author>
<author><name sortKey="Peschanski, M" sort="Peschanski, M" uniqKey="Peschanski M" first="M." last="Peschanski">M. Peschanski</name>
<affiliation><mods:affiliation>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</mods:affiliation>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series><title level="j">Neuroscience</title>
<title level="j" type="abbrev">NSC</title>
<idno type="ISSN">0306-4522</idno>
<imprint><publisher>ELSEVIER</publisher>
<date type="published" when="1992">1992</date>
<biblScope unit="volume">51</biblScope>
<biblScope unit="issue">1</biblScope>
<biblScope unit="page" from="137">137</biblScope>
<biblScope unit="page" to="148">148</biblScope>
</imprint>
<idno type="ISSN">0306-4522</idno>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><idno type="ISSN">0306-4522</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Afferent</term>
<term>Afferent fibers</term>
<term>Astrocyte</term>
<term>Axon</term>
<term>Axonal</term>
<term>Axonal ensheathment</term>
<term>Axonoglial</term>
<term>Axonoglial interactions</term>
<term>Axonoglial relationships</term>
<term>Axons myelinated</term>
<term>Basal lamina</term>
<term>Collagen fibrils</term>
<term>Degeneration</term>
<term>Demyelinated</term>
<term>Demyelinating</term>
<term>Demyelination</term>
<term>Demyelination process</term>
<term>Dorsal column nuclei</term>
<term>Ensheathed</term>
<term>Excitotoxic</term>
<term>Excitotoxic lesion</term>
<term>First weeks</term>
<term>Glia limitans</term>
<term>Glial</term>
<term>Horseradish peroxidase</term>
<term>Internal capsule</term>
<term>Kainate</term>
<term>Kainate injection</term>
<term>Kainate lesion</term>
<term>Kainic</term>
<term>Kainic acid</term>
<term>Lemniscal</term>
<term>Lesion</term>
<term>Macrophage</term>
<term>Multiple sclerosis</term>
<term>Myelin</term>
<term>Myelin debris</term>
<term>Myelin sheaths</term>
<term>Myelinated</term>
<term>Neuronal</term>
<term>Neuronal depletion</term>
<term>Neuropile</term>
<term>Numerous schwann cells</term>
<term>Oligodendrocyte</term>
<term>Peschanski</term>
<term>Present study</term>
<term>Reactive astrocytes</term>
<term>Remyelination</term>
<term>Schwann</term>
<term>Schwann cell</term>
<term>Schwann cells</term>
<term>Spinal</term>
<term>Spinal cord</term>
<term>Thalamus</term>
<term>Ultrastructural</term>
<term>Ultrastructural study</term>
<term>Unmyelinated</term>
<term>Unmyelinated axons</term>
<term>Wallerian degeneration</term>
<term>Wheatgerm agglutinin</term>
</keywords>
</textClass>
<langUsage><language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Abstract: Excitotoxins are thought to kill neurons while sparing afferent fibers and axons of passage. The validity of this classical conclusion has recently been questioned by the demonstration of axonal demyelination. In addition, axons are submitted to a profound alteration of their glial environment. This work was, therefore, undertaken to reassess axonoglial interactions over time after an excitotoxic lesion in the rat. Ultrastructural studies were carried out in the ventrobasal thalamus two days to 18 months after neuronal depletion by in situ injections of kainic acid. In some cases, lemniscal afferents were identified by using anterograde transport of wheatgerm agglutinin conjugated to horseradish peroxidase from the dorsal column nuclei. Two and four days after kainate injection, numerous dying axons displaying typical signs of Wallerian degeneration were observed in a neuropile characterized by the loss of neuronal somata and dendrites, an increase in number of microglia/macrophages and the disappearance of astrocytes. Ten and 12 days after kainate injection, degenerating axons were no longer observed although myelin degeneration of otherwise unaltered axons was ongoing with an accumulation of myelin remnants in the neuropile. At 16 and 20 days, the demyelination process was apparently complete and axons of different diameters were sometimes packed together. One and two months after kainate injection, the axonal environment changed again: remyelination of large-caliber axons occurred at the same time as reactive astrocytes, oligodendrocytes and numerous Schwann cells appeared in the tissue. Schwann cell processes surrounded aggregates of axons of diverse calibers, ensheathed small ones and myelinated larger ones. Axons were also remyelinated by oligodendrocytes. Horseradish peroxidase-labeled lemniscal afferents could be myelinated by either of the two cell types. After three months, the neuropile exhibited an increase in number of hypertrophied astrocytes and the progressive loss of any other cellular or axonal element. At this stage, remaining Schwann cells were surrounded by a glia limitans formed by astrocytic processes. These data indicate that although excitotoxins are sparing the axons, they are having a profound and complex effect on the axonal environment. Demyelination occurs over the first weeks, accompanying the loss of astrocytes and oligodendrocytes. Axonal ensheathment and remyelination takes place in a second period, associated with the reappearance of oligodendrocytes and recruitment of numerous Schwann cells, while reactive astrocytes appear in the tissue at a slightly later time. Over the following months, astrocytes occupy a greater proportion of the neuron-depleted territory and other elements decrease in number. These successive stages in alteration of axonoglial interactions seem to evolve in parallel to the changes in density and terminal morphology that we described earlier for myelinated afferent fibers to the excitotoxic lesion.</div>
</front>
</TEI>
<istex><corpusName>elsevier</corpusName>
<keywords><teeft><json:string>axon</json:string>
<json:string>schwann</json:string>
<json:string>schwann cells</json:string>
<json:string>myelin</json:string>
<json:string>kainate</json:string>
<json:string>demyelination</json:string>
<json:string>oligodendrocyte</json:string>
<json:string>astrocyte</json:string>
<json:string>neuropile</json:string>
<json:string>myelinated</json:string>
<json:string>axonal</json:string>
<json:string>thalamus</json:string>
<json:string>spinal</json:string>
<json:string>axonoglial</json:string>
<json:string>kainate injection</json:string>
<json:string>remyelination</json:string>
<json:string>ultrastructural</json:string>
<json:string>spinal cord</json:string>
<json:string>kainic</json:string>
<json:string>excitotoxic</json:string>
<json:string>unmyelinated</json:string>
<json:string>peschanski</json:string>
<json:string>glial</json:string>
<json:string>macrophage</json:string>
<json:string>ensheathed</json:string>
<json:string>lesion</json:string>
<json:string>kainic acid</json:string>
<json:string>axonoglial interactions</json:string>
<json:string>excitotoxic lesion</json:string>
<json:string>schwann cell</json:string>
<json:string>lemniscal</json:string>
<json:string>demyelinating</json:string>
<json:string>demyelinated</json:string>
<json:string>neuronal</json:string>
<json:string>myelin sheaths</json:string>
<json:string>kainate lesion</json:string>
<json:string>afferent</json:string>
<json:string>wallerian degeneration</json:string>
<json:string>reactive astrocytes</json:string>
<json:string>degeneration</json:string>
<json:string>internal capsule</json:string>
<json:string>axonoglial relationships</json:string>
<json:string>unmyelinated axons</json:string>
<json:string>first weeks</json:string>
<json:string>axons myelinated</json:string>
<json:string>numerous schwann cells</json:string>
<json:string>basal lamina</json:string>
<json:string>neuronal depletion</json:string>
<json:string>demyelination process</json:string>
<json:string>wheatgerm agglutinin</json:string>
<json:string>horseradish peroxidase</json:string>
<json:string>present study</json:string>
<json:string>collagen fibrils</json:string>
<json:string>dorsal column nuclei</json:string>
<json:string>glia limitans</json:string>
<json:string>afferent fibers</json:string>
<json:string>axonal ensheathment</json:string>
<json:string>myelin debris</json:string>
<json:string>multiple sclerosis</json:string>
<json:string>ultrastructural study</json:string>
</teeft>
</keywords>
<author><json:item><name>I. Dusart</name>
<affiliations><json:string>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</json:string>
</affiliations>
</json:item>
<json:item><name>S. Marty</name>
<affiliations><json:string>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</json:string>
</affiliations>
</json:item>
<json:item><name>M. Peschanski</name>
<affiliations><json:string>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</json:string>
</affiliations>
</json:item>
</author>
<subject><json:item><lang><json:string>eng</json:string>
</lang>
<value>BDHC : benzidine di-hydrochloride</value>
</json:item>
<json:item><lang><json:string>eng</json:string>
</lang>
<value>HRP : horseradish peroxidase</value>
</json:item>
<json:item><lang><json:string>eng</json:string>
</lang>
<value>PNS : peripheral nervous system</value>
</json:item>
</subject>
<arkIstex>ark:/67375/6H6-SDG85FX3-D</arkIstex>
<language><json:string>eng</json:string>
</language>
<originalGenre><json:string>Full-length article</json:string>
</originalGenre>
<abstract>Abstract: Excitotoxins are thought to kill neurons while sparing afferent fibers and axons of passage. The validity of this classical conclusion has recently been questioned by the demonstration of axonal demyelination. In addition, axons are submitted to a profound alteration of their glial environment. This work was, therefore, undertaken to reassess axonoglial interactions over time after an excitotoxic lesion in the rat. Ultrastructural studies were carried out in the ventrobasal thalamus two days to 18 months after neuronal depletion by in situ injections of kainic acid. In some cases, lemniscal afferents were identified by using anterograde transport of wheatgerm agglutinin conjugated to horseradish peroxidase from the dorsal column nuclei. Two and four days after kainate injection, numerous dying axons displaying typical signs of Wallerian degeneration were observed in a neuropile characterized by the loss of neuronal somata and dendrites, an increase in number of microglia/macrophages and the disappearance of astrocytes. Ten and 12 days after kainate injection, degenerating axons were no longer observed although myelin degeneration of otherwise unaltered axons was ongoing with an accumulation of myelin remnants in the neuropile. At 16 and 20 days, the demyelination process was apparently complete and axons of different diameters were sometimes packed together. One and two months after kainate injection, the axonal environment changed again: remyelination of large-caliber axons occurred at the same time as reactive astrocytes, oligodendrocytes and numerous Schwann cells appeared in the tissue. Schwann cell processes surrounded aggregates of axons of diverse calibers, ensheathed small ones and myelinated larger ones. Axons were also remyelinated by oligodendrocytes. Horseradish peroxidase-labeled lemniscal afferents could be myelinated by either of the two cell types. After three months, the neuropile exhibited an increase in number of hypertrophied astrocytes and the progressive loss of any other cellular or axonal element. At this stage, remaining Schwann cells were surrounded by a glia limitans formed by astrocytic processes. These data indicate that although excitotoxins are sparing the axons, they are having a profound and complex effect on the axonal environment. Demyelination occurs over the first weeks, accompanying the loss of astrocytes and oligodendrocytes. Axonal ensheathment and remyelination takes place in a second period, associated with the reappearance of oligodendrocytes and recruitment of numerous Schwann cells, while reactive astrocytes appear in the tissue at a slightly later time. Over the following months, astrocytes occupy a greater proportion of the neuron-depleted territory and other elements decrease in number. These successive stages in alteration of axonoglial interactions seem to evolve in parallel to the changes in density and terminal morphology that we described earlier for myelinated afferent fibers to the excitotoxic lesion.</abstract>
<qualityIndicators><score>10</score>
<pdfWordCount>5520</pdfWordCount>
<pdfCharCount>37228</pdfCharCount>
<pdfVersion>1.2</pdfVersion>
<pdfPageCount>12</pdfPageCount>
<pdfPageSize>504 x 756 pts</pdfPageSize>
<refBibsNative>true</refBibsNative>
<abstractWordCount>432</abstractWordCount>
<abstractCharCount>3019</abstractCharCount>
<keywordCount>3</keywordCount>
</qualityIndicators>
<title>Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system</title>
<pmid><json:string>1465177</json:string>
</pmid>
<pii><json:string>0306-4522(92)90478-K</json:string>
</pii>
<genre><json:string>research-article</json:string>
</genre>
<serie><title>Proc. natn. Acad. Sci. U.S.A.</title>
<language><json:string>unknown</json:string>
</language>
<volume>75</volume>
<pages><first>1554</first>
<last>1558</last>
</pages>
</serie>
<host><title>Neuroscience</title>
<language><json:string>unknown</json:string>
</language>
<publicationDate>1992</publicationDate>
<issn><json:string>0306-4522</json:string>
</issn>
<pii><json:string>S0306-4522(00)X0513-1</json:string>
</pii>
<volume>51</volume>
<issue>1</issue>
<pages><first>137</first>
<last>148</last>
</pages>
<genre><json:string>journal</json:string>
</genre>
</host>
<namedEntities><unitex><date><json:string>1992</json:string>
<json:string>10s</json:string>
</date>
<geogName></geogName>
<orgName><json:string>Brain Research Institute, University of Zurich, Switzerland</json:string>
</orgName>
<orgName_funder></orgName_funder>
<orgName_provider></orgName_provider>
<persName></persName>
<placeName></placeName>
<ref_url></ref_url>
<ref_bibl></ref_bibl>
<bibl></bibl>
</unitex>
</namedEntities>
<ark><json:string>ark:/67375/6H6-SDG85FX3-D</json:string>
</ark>
<categories><wos><json:string>1 - science</json:string>
<json:string>2 - neurosciences</json:string>
</wos>
<scienceMetrix><json:string>1 - health sciences</json:string>
<json:string>2 - clinical medicine</json:string>
<json:string>3 - neurology & neurosurgery</json:string>
</scienceMetrix>
<scopus><json:string>1 - Life Sciences</json:string>
<json:string>2 - Neuroscience</json:string>
<json:string>3 - General Neuroscience</json:string>
</scopus>
<inist><json:string>1 - sciences appliquees, technologies et medecines</json:string>
<json:string>2 - sciences biologiques et medicales</json:string>
<json:string>3 - sciences biologiques fondamentales et appliquees. psychologie</json:string>
</inist>
</categories>
<publicationDate>1992</publicationDate>
<copyrightDate>1992</copyrightDate>
<doi><json:string>10.1016/0306-4522(92)90478-K</json:string>
</doi>
<id>8C76FC7748C09806679BEA4601EB11B9E629FC86</id>
<score>1</score>
<fulltext><json:item><extension>pdf</extension>
<original>true</original>
<mimetype>application/pdf</mimetype>
<uri>https://api.istex.fr/ark:/67375/6H6-SDG85FX3-D/fulltext.pdf</uri>
</json:item>
<json:item><extension>zip</extension>
<original>false</original>
<mimetype>application/zip</mimetype>
<uri>https://api.istex.fr/ark:/67375/6H6-SDG85FX3-D/bundle.zip</uri>
</json:item>
<istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-SDG85FX3-D/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system</title>
</titleStmt>
<publicationStmt><authority>ISTEX</authority>
<publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher>
<availability><licence><p>elsevier</p>
</licence>
</availability>
<p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M"></p>
<date>1992</date>
</publicationStmt>
<notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note>
<note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note>
<note type="content">Section title: Research paper</note>
</notesStmt>
<sourceDesc><biblStruct type="inbook"><analytic><title level="a">Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system</title>
<author xml:id="author-0000"><persName><forename type="first">I.</forename>
<surname>Dusart</surname>
</persName>
<note type="biography">Present address: Brain Research Institute, University of Zurich, Switzerland.</note>
<affiliation>Present address: Brain Research Institute, University of Zurich, Switzerland.</affiliation>
<affiliation>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</affiliation>
</author>
<author xml:id="author-0001"><persName><forename type="first">S.</forename>
<surname>Marty</surname>
</persName>
<affiliation>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</affiliation>
</author>
<author xml:id="author-0002"><persName><forename type="first">M.</forename>
<surname>Peschanski</surname>
</persName>
<affiliation>To whom correspondence should be addressed.</affiliation>
<affiliation>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</affiliation>
</author>
<idno type="istex">8C76FC7748C09806679BEA4601EB11B9E629FC86</idno>
<idno type="ark">ark:/67375/6H6-SDG85FX3-D</idno>
<idno type="DOI">10.1016/0306-4522(92)90478-K</idno>
<idno type="PII">0306-4522(92)90478-K</idno>
</analytic>
<monogr><title level="j">Neuroscience</title>
<title level="j" type="abbrev">NSC</title>
<idno type="pISSN">0306-4522</idno>
<idno type="PII">S0306-4522(00)X0513-1</idno>
<imprint><publisher>ELSEVIER</publisher>
<date type="published" when="1992"></date>
<biblScope unit="volume">51</biblScope>
<biblScope unit="issue">1</biblScope>
<biblScope unit="page" from="137">137</biblScope>
<biblScope unit="page" to="148">148</biblScope>
</imprint>
</monogr>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><creation><date>1992</date>
</creation>
<langUsage><language ident="en">en</language>
</langUsage>
<abstract xml:lang="en"><p>Abstract: Excitotoxins are thought to kill neurons while sparing afferent fibers and axons of passage. The validity of this classical conclusion has recently been questioned by the demonstration of axonal demyelination. In addition, axons are submitted to a profound alteration of their glial environment. This work was, therefore, undertaken to reassess axonoglial interactions over time after an excitotoxic lesion in the rat. Ultrastructural studies were carried out in the ventrobasal thalamus two days to 18 months after neuronal depletion by in situ injections of kainic acid. In some cases, lemniscal afferents were identified by using anterograde transport of wheatgerm agglutinin conjugated to horseradish peroxidase from the dorsal column nuclei. Two and four days after kainate injection, numerous dying axons displaying typical signs of Wallerian degeneration were observed in a neuropile characterized by the loss of neuronal somata and dendrites, an increase in number of microglia/macrophages and the disappearance of astrocytes. Ten and 12 days after kainate injection, degenerating axons were no longer observed although myelin degeneration of otherwise unaltered axons was ongoing with an accumulation of myelin remnants in the neuropile. At 16 and 20 days, the demyelination process was apparently complete and axons of different diameters were sometimes packed together. One and two months after kainate injection, the axonal environment changed again: remyelination of large-caliber axons occurred at the same time as reactive astrocytes, oligodendrocytes and numerous Schwann cells appeared in the tissue. Schwann cell processes surrounded aggregates of axons of diverse calibers, ensheathed small ones and myelinated larger ones. Axons were also remyelinated by oligodendrocytes. Horseradish peroxidase-labeled lemniscal afferents could be myelinated by either of the two cell types. After three months, the neuropile exhibited an increase in number of hypertrophied astrocytes and the progressive loss of any other cellular or axonal element. At this stage, remaining Schwann cells were surrounded by a glia limitans formed by astrocytic processes. These data indicate that although excitotoxins are sparing the axons, they are having a profound and complex effect on the axonal environment. Demyelination occurs over the first weeks, accompanying the loss of astrocytes and oligodendrocytes. Axonal ensheathment and remyelination takes place in a second period, associated with the reappearance of oligodendrocytes and recruitment of numerous Schwann cells, while reactive astrocytes appear in the tissue at a slightly later time. Over the following months, astrocytes occupy a greater proportion of the neuron-depleted territory and other elements decrease in number. These successive stages in alteration of axonoglial interactions seem to evolve in parallel to the changes in density and terminal morphology that we described earlier for myelinated afferent fibers to the excitotoxic lesion.</p>
</abstract>
<textClass><keywords scheme="keyword"><list><head>Abbreviations</head>
<item><term>BDHC</term>
<term>benzidine di-hydrochloride</term>
</item>
<item><term>HRP</term>
<term>horseradish peroxidase</term>
</item>
<item><term>PNS</term>
<term>peripheral nervous system</term>
</item>
</list>
</keywords>
</textClass>
</profileDesc>
<revisionDesc><change when="1992">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-SDG85FX3-D/fulltext.txt</uri>
</json:item>
</fulltext>
<metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration>
<istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType>
<istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>NSC</jid>
<aid>9290478K</aid>
<ce:pii>0306-4522(92)90478-K</ce:pii>
<ce:doi>10.1016/0306-4522(92)90478-K</ce:doi>
<ce:copyright type="unknown" year="1992"></ce:copyright>
</item-info>
<head><ce:dochead><ce:textfn>Research paper</ce:textfn>
</ce:dochead>
<ce:title>Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system</ce:title>
<ce:author-group><ce:author><ce:given-name>I.</ce:given-name>
<ce:surname>Dusart</ce:surname>
<ce:cross-ref refid="FN1"><ce:sup>∗</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author><ce:given-name>S.</ce:given-name>
<ce:surname>Marty</ce:surname>
</ce:author>
<ce:author><ce:given-name>M.</ce:given-name>
<ce:surname>Peschanski</ce:surname>
<ce:cross-ref refid="COR1"><ce:sup>†</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:affiliation><ce:textfn>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</ce:textfn>
</ce:affiliation>
<ce:correspondence id="COR1"><ce:label>†</ce:label>
<ce:text>To whom correspondence should be addressed.</ce:text>
</ce:correspondence>
<ce:footnote id="FN1"><ce:label>∗</ce:label>
<ce:note-para>Present address: Brain Research Institute, University of Zurich, Switzerland.</ce:note-para>
</ce:footnote>
</ce:author-group>
<ce:date-accepted day="1" month="6" year="1992"></ce:date-accepted>
<ce:abstract><ce:section-title>Abstract</ce:section-title>
<ce:abstract-sec><ce:simple-para>Excitotoxins are thought to kill neurons while sparing afferent fibers and axons of passage. The validity of this classical conclusion has recently been questioned by the demonstration of axonal demyelination. In addition, axons are submitted to a profound alteration of their glial environment. This work was, therefore, undertaken to reassess axonoglial interactions over time after an excitotoxic lesion in the rat. Ultrastructural studies were carried out in the ventrobasal thalamus two days to 18 months after neuronal depletion by <ce:italic>in situ</ce:italic>
injections of kainic acid. In some cases, lemniscal afferents were identified by using anterograde transport of wheatgerm agglutinin conjugated to horseradish peroxidase from the dorsal column nuclei.</ce:simple-para>
<ce:simple-para>Two and four days after kainate injection, numerous dying axons displaying typical signs of Wallerian degeneration were observed in a neuropile characterized by the loss of neuronal somata and dendrites, an increase in number of microglia/macrophages and the disappearance of astrocytes. Ten and 12 days after kainate injection, degenerating axons were no longer observed although myelin degeneration of otherwise unaltered axons was ongoing with an accumulation of myelin remnants in the neuropile. At 16 and 20 days, the demyelination process was apparently complete and axons of different diameters were sometimes packed together. One and two months after kainate injection, the axonal environment changed again: remyelination of large-caliber axons occurred at the same time as reactive astrocytes, oligodendrocytes and numerous Schwann cells appeared in the tissue. Schwann cell processes surrounded aggregates of axons of diverse calibers, ensheathed small ones and myelinated larger ones. Axons were also remyelinated by oligodendrocytes. Horseradish peroxidase-labeled lemniscal afferents could be myelinated by either of the two cell types. After three months, the neuropile exhibited an increase in number of hypertrophied astrocytes and the progressive loss of any other cellular or axonal element. At this stage, remaining Schwann cells were surrounded by a glia limitans formed by astrocytic processes.</ce:simple-para>
<ce:simple-para>These data indicate that although excitotoxins are sparing the axons, they are having a profound and complex effect on the axonal environment. Demyelination occurs over the first weeks, accompanying the loss of astrocytes and oligodendrocytes. Axonal ensheathment and remyelination takes place in a second period, associated with the reappearance of oligodendrocytes and recruitment of numerous Schwann cells, while reactive astrocytes appear in the tissue at a slightly later time.</ce:simple-para>
<ce:simple-para>Over the following months, astrocytes occupy a greater proportion of the neuron-depleted territory and other elements decrease in number. These successive stages in alteration of axonoglial interactions seem to evolve in parallel to the changes in density and terminal morphology that we described earlier for myelinated afferent fibers to the excitotoxic lesion.</ce:simple-para>
</ce:abstract-sec>
</ce:abstract>
<ce:keywords class="abr"><ce:section-title>Abbreviations</ce:section-title>
<ce:keyword><ce:text>BDHC</ce:text>
<ce:keyword><ce:text>benzidine di-hydrochloride</ce:text>
</ce:keyword>
</ce:keyword>
<ce:keyword><ce:text>HRP</ce:text>
<ce:keyword><ce:text>horseradish peroxidase</ce:text>
</ce:keyword>
</ce:keyword>
<ce:keyword><ce:text>PNS</ce:text>
<ce:keyword><ce:text>peripheral nervous system</ce:text>
</ce:keyword>
</ce:keyword>
</ce:keywords>
</head>
</converted-article>
</istex:document>
</istex:metadataXml>
<mods version="3.6"><titleInfo><title>Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system</title>
</titleInfo>
<titleInfo type="alternative" contentType="CDATA"><title>Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system</title>
</titleInfo>
<name type="personal"><namePart type="given">I.</namePart>
<namePart type="family">Dusart</namePart>
<affiliation>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</affiliation>
<description>Present address: Brain Research Institute, University of Zurich, Switzerland.</description>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">S.</namePart>
<namePart type="family">Marty</namePart>
<affiliation>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">M.</namePart>
<namePart type="family">Peschanski</namePart>
<affiliation>INSERM CJF 91-02, Neuroplasticité et Greffes Intracérébrales, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil, France</affiliation>
<description>To whom correspondence should be addressed.</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">1992</dateIssued>
<copyrightDate encoding="w3cdtf">1992</copyrightDate>
</originInfo>
<language><languageTerm type="code" authority="iso639-2b">eng</languageTerm>
<languageTerm type="code" authority="rfc3066">en</languageTerm>
</language>
<abstract lang="en">Abstract: Excitotoxins are thought to kill neurons while sparing afferent fibers and axons of passage. The validity of this classical conclusion has recently been questioned by the demonstration of axonal demyelination. In addition, axons are submitted to a profound alteration of their glial environment. This work was, therefore, undertaken to reassess axonoglial interactions over time after an excitotoxic lesion in the rat. Ultrastructural studies were carried out in the ventrobasal thalamus two days to 18 months after neuronal depletion by in situ injections of kainic acid. In some cases, lemniscal afferents were identified by using anterograde transport of wheatgerm agglutinin conjugated to horseradish peroxidase from the dorsal column nuclei. Two and four days after kainate injection, numerous dying axons displaying typical signs of Wallerian degeneration were observed in a neuropile characterized by the loss of neuronal somata and dendrites, an increase in number of microglia/macrophages and the disappearance of astrocytes. Ten and 12 days after kainate injection, degenerating axons were no longer observed although myelin degeneration of otherwise unaltered axons was ongoing with an accumulation of myelin remnants in the neuropile. At 16 and 20 days, the demyelination process was apparently complete and axons of different diameters were sometimes packed together. One and two months after kainate injection, the axonal environment changed again: remyelination of large-caliber axons occurred at the same time as reactive astrocytes, oligodendrocytes and numerous Schwann cells appeared in the tissue. Schwann cell processes surrounded aggregates of axons of diverse calibers, ensheathed small ones and myelinated larger ones. Axons were also remyelinated by oligodendrocytes. Horseradish peroxidase-labeled lemniscal afferents could be myelinated by either of the two cell types. After three months, the neuropile exhibited an increase in number of hypertrophied astrocytes and the progressive loss of any other cellular or axonal element. At this stage, remaining Schwann cells were surrounded by a glia limitans formed by astrocytic processes. These data indicate that although excitotoxins are sparing the axons, they are having a profound and complex effect on the axonal environment. Demyelination occurs over the first weeks, accompanying the loss of astrocytes and oligodendrocytes. Axonal ensheathment and remyelination takes place in a second period, associated with the reappearance of oligodendrocytes and recruitment of numerous Schwann cells, while reactive astrocytes appear in the tissue at a slightly later time. Over the following months, astrocytes occupy a greater proportion of the neuron-depleted territory and other elements decrease in number. These successive stages in alteration of axonoglial interactions seem to evolve in parallel to the changes in density and terminal morphology that we described earlier for myelinated afferent fibers to the excitotoxic lesion.</abstract>
<note type="content">Section title: Research paper</note>
<subject><genre>Abbreviations</genre>
<topic>BDHC : benzidine di-hydrochloride</topic>
<topic>HRP : horseradish peroxidase</topic>
<topic>PNS : peripheral nervous system</topic>
</subject>
<relatedItem type="host"><titleInfo><title>Neuroscience</title>
</titleInfo>
<titleInfo type="abbreviated"><title>NSC</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">1992</dateIssued>
</originInfo>
<identifier type="ISSN">0306-4522</identifier>
<identifier type="PII">S0306-4522(00)X0513-1</identifier>
<part><date>1992</date>
<detail type="volume"><number>51</number>
<caption>vol.</caption>
</detail>
<detail type="issue"><number>1</number>
<caption>no.</caption>
</detail>
<extent unit="issue-pages"><start>1</start>
<end>244</end>
</extent>
<extent unit="pages"><start>137</start>
<end>148</end>
</extent>
</part>
</relatedItem>
<identifier type="istex">8C76FC7748C09806679BEA4601EB11B9E629FC86</identifier>
<identifier type="ark">ark:/67375/6H6-SDG85FX3-D</identifier>
<identifier type="DOI">10.1016/0306-4522(92)90478-K</identifier>
<identifier type="PII">0306-4522(92)90478-K</identifier>
<recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource>
</recordInfo>
</mods>
<json:item><extension>json</extension>
<original>false</original>
<mimetype>application/json</mimetype>
<uri>https://api.istex.fr/ark:/67375/6H6-SDG85FX3-D/record.json</uri>
</json:item>
</metadata>
</istex>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/CovidV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000465 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 000465 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Sante |area= CovidV1 |flux= Istex |étape= Corpus |type= RBID |clé= ISTEX:8C76FC7748C09806679BEA4601EB11B9E629FC86 |texte= Demyelination, and remyelination by Schwann cells and oligodendrocytes after kainate-induced neuronal depletion in the central nervous system }}
![]() | This area was generated with Dilib version V0.6.33. | ![]() |