Synaptic plasticity in the caudate nucleus of patients with Parkinson's disease.
Identifieur interne : 001577 ( PubMed/Corpus ); précédent : 001576; suivant : 001578Synaptic plasticity in the caudate nucleus of patients with Parkinson's disease.
Auteurs : P. Anglade ; A. Mouatt-Prigent ; Y. Agid ; E. HirschSource :
- Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration [ 1055-8330 ] ; 1996.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Animals, Autopsy, Caudate Nucleus (cytology), Caudate Nucleus (pathology), Dendrites (pathology), Dendrites (ultrastructure), Female, Humans, Male, Microscopy, Electron, Neuronal Plasticity, Oxidopamine, Parkinson Disease (pathology), Rats, Reference Values, Substantia Nigra (pathology), Synapses (pathology), Synapses (ultrastructure), Synaptic Vesicles (pathology), Synaptic Vesicles (ultrastructure), Tyrosine 3-Monooxygenase (analysis).
- MESH :
- chemical , analysis : Tyrosine 3-Monooxygenase.
- chemical : Oxidopamine.
- cytology : Caudate Nucleus.
- pathology : Caudate Nucleus, Dendrites, Parkinson Disease, Substantia Nigra, Synapses, Synaptic Vesicles.
- ultrastructure : Dendrites, Synapses, Synaptic Vesicles.
- Aged, Aged, 80 and over, Animals, Autopsy, Female, Humans, Male, Microscopy, Electron, Neuronal Plasticity, Rats, Reference Values.
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-hydroxy-dopamine-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.
PubMed: 8819132
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pubmed:8819132Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Synaptic plasticity in the caudate nucleus of patients with Parkinson's disease.</title><author><name sortKey="Anglade, P" sort="Anglade, P" uniqKey="Anglade P" first="P" last="Anglade">P. Anglade</name><affiliation><nlm:affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Mouatt Prigent, A" sort="Mouatt Prigent, A" uniqKey="Mouatt Prigent A" first="A" last="Mouatt-Prigent">A. Mouatt-Prigent</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Y. Agid</name></author><author><name sortKey="Hirsch, E" sort="Hirsch, E" uniqKey="Hirsch E" first="E" last="Hirsch">E. Hirsch</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1996">1996</date><idno type="RBID">pubmed:8819132</idno><idno type="pmid">8819132</idno><idno type="wicri:Area/PubMed/Corpus">001577</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001577</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Synaptic plasticity in the caudate nucleus of patients with Parkinson's disease.</title><author><name sortKey="Anglade, P" sort="Anglade, P" uniqKey="Anglade P" first="P" last="Anglade">P. Anglade</name><affiliation><nlm:affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Mouatt Prigent, A" sort="Mouatt Prigent, A" uniqKey="Mouatt Prigent A" first="A" last="Mouatt-Prigent">A. Mouatt-Prigent</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Y. Agid</name></author><author><name sortKey="Hirsch, E" sort="Hirsch, E" uniqKey="Hirsch E" first="E" last="Hirsch">E. Hirsch</name></author></analytic><series><title level="j">Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration</title><idno type="ISSN">1055-8330</idno><imprint><date when="1996" type="published">1996</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Animals</term><term>Autopsy</term><term>Caudate Nucleus (cytology)</term><term>Caudate Nucleus (pathology)</term><term>Dendrites (pathology)</term><term>Dendrites (ultrastructure)</term><term>Female</term><term>Humans</term><term>Male</term><term>Microscopy, Electron</term><term>Neuronal Plasticity</term><term>Oxidopamine</term><term>Parkinson Disease (pathology)</term><term>Rats</term><term>Reference Values</term><term>Substantia Nigra (pathology)</term><term>Synapses (pathology)</term><term>Synapses (ultrastructure)</term><term>Synaptic Vesicles (pathology)</term><term>Synaptic Vesicles (ultrastructure)</term><term>Tyrosine 3-Monooxygenase (analysis)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Oxidopamine</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Caudate Nucleus</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Caudate Nucleus</term><term>Dendrites</term><term>Parkinson Disease</term><term>Substantia Nigra</term><term>Synapses</term><term>Synaptic Vesicles</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Dendrites</term><term>Synapses</term><term>Synaptic Vesicles</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Animals</term><term>Autopsy</term><term>Female</term><term>Humans</term><term>Male</term><term>Microscopy, Electron</term><term>Neuronal Plasticity</term><term>Rats</term><term>Reference Values</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml: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-hydroxy-dopamine-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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8819132</PMID><DateCreated><Year>1996</Year><Month>12</Month><Day>03</Day></DateCreated><DateCompleted><Year>1996</Year><Month>12</Month><Day>03</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1055-8330</ISSN><JournalIssue CitedMedium="Print"><Volume>5</Volume><Issue>2</Issue><PubDate><Year>1996</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration</Title><ISOAbbreviation>Neurodegeneration</ISOAbbreviation></Journal><ArticleTitle>Synaptic plasticity in the caudate nucleus of patients with Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>121-8</MedlinePgn></Pagination><Abstract><AbstractText>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-hydroxy-dopamine-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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Anglade</LastName><ForeName>P</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mouatt-Prigent</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Agid</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>E</ForeName><Initials>E</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Neurodegeneration</MedlineTA><NlmUniqueID>9209022</NlmUniqueID><ISSNLinking>1055-8330</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>8HW4YBZ748</RegistryNumber><NameOfSubstance UI="D016627">Oxidopamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.16.2</RegistryNumber><NameOfSubstance UI="D014446">Tyrosine 3-Monooxygenase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001344" MajorTopicYN="N">Autopsy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002421" MajorTopicYN="N">Caudate Nucleus</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003712" MajorTopicYN="N">Dendrites</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008854" MajorTopicYN="N">Microscopy, Electron</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009473" MajorTopicYN="Y">Neuronal Plasticity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016627" MajorTopicYN="N">Oxidopamine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012016" MajorTopicYN="N">Reference Values</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013569" MajorTopicYN="N">Synapses</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013572" MajorTopicYN="N">Synaptic Vesicles</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014446" MajorTopicYN="N">Tyrosine 3-Monooxygenase</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1996</Year><Month>6</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1996</Year><Month>6</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1996</Year><Month>6</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8819132</ArticleId><ArticleId IdType="pii">S1055-8330(96)90018-5</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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