Synaptic Plasticity in the Caudate Nucleus of Patients with Parkinson's Disease
Identifieur interne : 002B73 ( Main/Corpus ); précédent : 002B72; suivant : 002B74Synaptic Plasticity in the Caudate Nucleus of Patients with Parkinson's Disease
Auteurs : Philippe Anglade ; Annick Mouatt-Prigent ; Yves Agid ; Etienne C. HirschSource :
- Neurodegeneration [ 1055-8330 ] ; 1996.
English descriptors
Abstract
The loss of dopaminergic neurons from the substantia nigra in Parkinson's disease (PD) may provoke a reorganization of cellular interactions in the nigrostriatal pathway. Indeed, a plasticity of putative corticostriatal synapses has been evidenced in the striatum of rats with a 6-hydroxydopamine-induced lesion of the substantia nigra. However, to our knowledge, synaptic plasticity in the striatum has not previously been investigated in human PD. In this study, we have analysed, at electron microscope level, the morphological characteristics of the synapses formed by afferents in asymmetric contact with dendritic spines of neurons in the caudate nucleus of three patients with PD and three matched controls. The length of the postsynaptic densities and the number of perforated synapses were both significantly increased (24 and 88%, respectively) in the PD patients; the size of these afferents and the surface area occupied by their mitochondria also showed an increase (24 and 50%, respectively), although not statistically significant. The size and density of dendritic spines and the size of postsynaptic density perforations were unchanged. These data indicate the presence of plasticity of the putative corticostriatal synapses in PD and suggest a hyperactivity of cortical afferents to GABAergic neurons.
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DOI: 10.1006/neur.1996.0018
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ISTEX:3D8F746019577AEF87F6A1E58BB80DADECBCC54ALe document en format XML
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Indeed, a plasticity of putative corticostriatal synapses has been evidenced in the striatum of rats with a 6-hydroxydopamine-induced lesion of the substantia nigra. However, to our knowledge, synaptic plasticity in the striatum has not previously been investigated in human PD. In this study, we have analysed, at electron microscope level, the morphological characteristics of the synapses formed by afferents in asymmetric contact with dendritic spines of neurons in the caudate nucleus of three patients with PD and three matched controls. The length of the postsynaptic densities and the number of perforated synapses were both significantly increased (24 and 88%, respectively) in the PD patients; the size of these afferents and the surface area occupied by their mitochondria also showed an increase (24 and 50%, respectively), although not statistically significant. The size and density of dendritic spines and the size of postsynaptic density perforations were unchanged. These data indicate the presence of plasticity of the putative corticostriatal synapses in PD and suggest a hyperactivity of cortical afferents to GABAergic neurons.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Philippe Anglade</name><affiliations><json:string>INSERM U289, Hôpital de la Salpêtrière, 47 bd de l'Hôpital, Paris, 75013, France</json:string></affiliations></json:item><json:item><name>Annick Mouatt-Prigent</name><affiliations><json:string>INSERM U289, Hôpital de la Salpêtrière, 47 bd de l'Hôpital, Paris, 75013, France</json:string></affiliations></json:item><json:item><name>Yves Agid</name><affiliations><json:string>INSERM U289, Hôpital de la Salpêtrière, 47 bd de l'Hôpital, Paris, 75013, France</json:string></affiliations></json:item><json:item><name>Etienne C. Hirsch</name><affiliations><json:string>INSERM U289, Hôpital de la Salpêtrière, 47 bd de l'Hôpital, Paris, 75013, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>caudate nucleus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dendritic spines</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>plasticity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>postsynaptic densities</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The loss of dopaminergic neurons from the substantia nigra in Parkinson's disease (PD) may provoke a reorganization of cellular interactions in the nigrostriatal pathway. Indeed, a plasticity of putative corticostriatal synapses has been evidenced in the striatum of rats with a 6-hydroxydopamine-induced lesion of the substantia nigra. However, to our knowledge, synaptic plasticity in the striatum has not previously been investigated in human PD. In this study, we have analysed, at electron microscope level, the morphological characteristics of the synapses formed by afferents in asymmetric contact with dendritic spines of neurons in the caudate nucleus of three patients with PD and three matched controls. The length of the postsynaptic densities and the number of perforated synapses were both significantly increased (24 and 88%, respectively) in the PD patients; the size of these afferents and the surface area occupied by their mitochondria also showed an increase (24 and 50%, respectively), although not statistically significant. The size and density of dendritic spines and the size of postsynaptic density perforations were unchanged. 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Indeed, a plasticity of putative corticostriatal synapses has been evidenced in the striatum of rats with a 6-hydroxydopamine-induced lesion of the substantia nigra. However, to our knowledge, synaptic plasticity in the striatum has not previously been investigated in human PD. In this study, we have analysed, at electron microscope level, the morphological characteristics of the synapses formed by afferents in asymmetric contact with dendritic spines of neurons in the caudate nucleus of three patients with PD and three matched controls. The length of the postsynaptic densities and the number of perforated synapses were both significantly increased (24 and 88%, respectively) in the PD patients; the size of these afferents and the surface area occupied by their mitochondria also showed an increase (24 and 50%, respectively), although not statistically significant. The size and density of dendritic spines and the size of postsynaptic density perforations were unchanged. These data indicate the presence of plasticity of the putative corticostriatal synapses in PD and suggest a hyperactivity of cortical afferents to GABAergic neurons.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>caudate nucleus</term></item><item><term>dendritic spines</term></item><item><term>Parkinson's disease</term></item><item><term>plasticity</term></item><item><term>postsynaptic densities</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996-02-07">Registration</change><change when="1996-02-07">Modified</change><change when="1996">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-5">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/3D8F746019577AEF87F6A1E58BB80DADECBCC54A/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier converted-article found"><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" xml:lang="en"><item-info><jid>YNEUR</jid><aid>90018</aid><ce:pii>S1055-8330(96)90018-5</ce:pii><ce:doi>10.1006/neur.1996.0018</ce:doi><ce:copyright type="full-transfer" year="1996">Academic Press</ce:copyright></item-info><head><ce:dochead><ce:textfn>Regular article</ce:textfn></ce:dochead><ce:title>Synaptic Plasticity in the Caudate Nucleus of Patients with Parkinson's Disease</ce:title><ce:author-group><ce:author><ce:given-name>Philippe</ce:given-name><ce:surname>Anglade</ce:surname></ce:author><ce:author><ce:given-name>Annick</ce:given-name><ce:surname>Mouatt-Prigent</ce:surname></ce:author><ce:author><ce:given-name>Yves</ce:given-name><ce:surname>Agid</ce:surname></ce:author><ce:author><ce:given-name>Etienne C.</ce:given-name><ce:surname>Hirsch</ce:surname></ce:author><ce:affiliation><ce:textfn>INSERM U289, Hôpital de la Salpêtrière, 47 bd de l'Hôpital, Paris, 75013, France</ce:textfn></ce:affiliation></ce:author-group><ce:date-received day="30" month="10" year="1995"></ce:date-received><ce:date-revised day="7" month="2" year="1996"></ce:date-revised><ce:date-accepted day="7" month="2" year="1996"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>The loss of dopaminergic neurons from the substantia nigra in Parkinson's disease (PD) may provoke a reorganization of cellular interactions in the nigrostriatal pathway. Indeed, a plasticity of putative corticostriatal synapses has been evidenced in the striatum of rats with a 6-hydroxydopamine-induced lesion of the substantia nigra. However, to our knowledge, synaptic plasticity in the striatum has not previously been investigated in human PD. In this study, we have analysed, at electron microscope level, the morphological characteristics of the synapses formed by afferents in asymmetric contact with dendritic spines of neurons in the caudate nucleus of three patients with PD and three matched controls. The length of the postsynaptic densities and the number of perforated synapses were both significantly increased (24 and 88%, respectively) in the PD patients; the size of these afferents and the surface area occupied by their mitochondria also showed an increase (24 and 50%, respectively), although not statistically significant. The size and density of dendritic spines and the size of postsynaptic density perforations were unchanged. These data indicate the presence of plasticity of the putative corticostriatal synapses in PD and suggest a hyperactivity of cortical afferents to GABAergic neurons.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>caudate nucleus</ce:text></ce:keyword><ce:keyword><ce:text>dendritic spines</ce:text></ce:keyword><ce:keyword><ce:text>Parkinson's disease</ce:text></ce:keyword><ce:keyword><ce:text>plasticity</ce:text></ce:keyword><ce:keyword><ce:text>postsynaptic densities</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Synaptic Plasticity in the Caudate Nucleus of Patients with Parkinson's Disease</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Synaptic Plasticity in the Caudate Nucleus of Patients with Parkinson's Disease</title></titleInfo><name type="personal"><namePart type="given">Philippe</namePart><namePart type="family">Anglade</namePart><affiliation>INSERM U289, Hôpital de la Salpêtrière, 47 bd de l'Hôpital, Paris, 75013, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Annick</namePart><namePart type="family">Mouatt-Prigent</namePart><affiliation>INSERM U289, Hôpital de la Salpêtrière, 47 bd de l'Hôpital, Paris, 75013, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yves</namePart><namePart type="family">Agid</namePart><affiliation>INSERM U289, Hôpital de la Salpêtrière, 47 bd de l'Hôpital, Paris, 75013, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Etienne C.</namePart><namePart type="family">Hirsch</namePart><affiliation>INSERM U289, Hôpital de la Salpêtrière, 47 bd de l'Hôpital, Paris, 75013, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1996</dateIssued><dateValid encoding="w3cdtf">1996-02-07</dateValid><dateModified encoding="w3cdtf">1996-02-07</dateModified><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">The loss of dopaminergic neurons from the substantia nigra in Parkinson's disease (PD) may provoke a reorganization of cellular interactions in the nigrostriatal pathway. Indeed, a plasticity of putative corticostriatal synapses has been evidenced in the striatum of rats with a 6-hydroxydopamine-induced lesion of the substantia nigra. However, to our knowledge, synaptic plasticity in the striatum has not previously been investigated in human PD. In this study, we have analysed, at electron microscope level, the morphological characteristics of the synapses formed by afferents in asymmetric contact with dendritic spines of neurons in the caudate nucleus of three patients with PD and three matched controls. The length of the postsynaptic densities and the number of perforated synapses were both significantly increased (24 and 88%, respectively) in the PD patients; the size of these afferents and the surface area occupied by their mitochondria also showed an increase (24 and 50%, respectively), although not statistically significant. The size and density of dendritic spines and the size of postsynaptic density perforations were unchanged. These data indicate the presence of plasticity of the putative corticostriatal synapses in PD and suggest a hyperactivity of cortical afferents to GABAergic neurons.</abstract><note type="content">Section title: Regular article</note><subject lang="en"><genre>Keywords</genre><topic>caudate nucleus</topic><topic>dendritic spines</topic><topic>Parkinson's disease</topic><topic>plasticity</topic><topic>postsynaptic densities</topic></subject><relatedItem type="host"><titleInfo><title>Neurodegeneration</title></titleInfo><titleInfo type="abbreviated"><title>YNEUR</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">199606</dateIssued></originInfo><identifier type="ISSN">1055-8330</identifier><identifier type="PII">S1055-8330(00)X0002-5</identifier><part><date>199606</date><detail type="volume"><number>5</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>115</start><end>195</end></extent><extent unit="pages"><start>121</start><end>128</end></extent></part></relatedItem><identifier type="istex">3D8F746019577AEF87F6A1E58BB80DADECBCC54A</identifier><identifier type="DOI">10.1006/neur.1996.0018</identifier><identifier type="PII">S1055-8330(96)90018-5</identifier><accessCondition type="use and reproduction" contentType="">© 1996Academic Press</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Academic Press, ©1996</recordOrigin></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/3D8F746019577AEF87F6A1E58BB80DADECBCC54A/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI><istex:refBibTEI uri="https://api.istex.fr/document/3D8F746019577AEF87F6A1E58BB80DADECBCC54A/enrichments/refBib"><teiHeader></teiHeader><text><front></front><body></body><back><listBibl><biblStruct><monogr><title level="m" type="main">The efficacy of Levodopa treatment declines in the course of Parkinson's disease: do non dopaminergic lesions play a role? 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