Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease.
Identifieur interne : 003D51 ( PubMed/Corpus ); précédent : 003D50; suivant : 003D52Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease.
Auteurs : M P Muriel ; Y. Agid ; E. HirschSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2001.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Basal Ganglia (ultrastructure), Brain (pathology), Case-Control Studies, Caudate Nucleus (chemistry), Caudate Nucleus (ultrastructure), Corpus Striatum (ultrastructure), Humans, Immunohistochemistry, In Vitro Techniques, Microscopy, Electron, Middle Aged, Neural Pathways, Neuronal Plasticity, Neurons, Afferent (ultrastructure), Parkinson Disease (pathology), Receptors, Dopamine D1 (chemistry), Synapses (ultrastructure).
- MESH :
- chemical , chemistry : Receptors, Dopamine D1.
- chemistry : Caudate Nucleus.
- pathology : Brain, Parkinson Disease.
- ultrastructure : Basal Ganglia, Caudate Nucleus, Corpus Striatum, Neurons, Afferent, Synapses.
- Aged, Aged, 80 and over, Case-Control Studies, Humans, Immunohistochemistry, In Vitro Techniques, Microscopy, Electron, Middle Aged, Neural Pathways, Neuronal Plasticity.
Abstract
The loss of dopaminergic neurons in the substantia nigra provokes a plasticity of corticostriatal synapses in Parkinson's disease (PD). The corticostriatal pathway nevertheless makes synapses with neurons bearing D1 dopamine receptors (D1R) and/or D2 dopamine receptors. At the ultrastructural level, we analyzed the morphological characteristics of synapses formed by afferent fibers making asymmetric contacts with the dendritic spines of neurons identified by D1R immunoreactivity, in the striatum of control subjects and PD patients. A quantitative analysis of the morphological characteristics of the synapses and of the number of perforated synapses (considered to be very active) was performed. In PD, a 50% increase in the number of perforated synapses making contact with D1R dendritic spines was observed, whereas no change in the number of perforated synapses on non-D1R spines was observed. The change in the number of perforated synapses on D1R dendrites was associated with a slight but nonsignificant increase in the surface area of the corticostriatal afferent fibers and the surface of the mitochondria in these fibers (+29.0% and +34.6%, respectively). This suggests a hyperactivity of corticostriatal fibers in contact with D1R-bearing neurons of the direct pathway in the basal ganglia circuitry. Since stimulation of the direct pathway is thought to alleviate the clinical symptoms of PD, this suggests that the differences observed may be involved in compensatory mechanisms.
PubMed: 11391736
Links to Exploration step
pubmed:11391736Le document en format XML
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Hirsch</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2001">2001</date><idno type="RBID">pubmed:11391736</idno><idno type="pmid">11391736</idno><idno type="wicri:Area/PubMed/Corpus">003D51</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease.</title><author><name sortKey="Muriel, M P" sort="Muriel, M P" uniqKey="Muriel M" first="M P" last="Muriel">M P Muriel</name><affiliation><nlm:affiliation>INSERM U 289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 75013 Paris, France.</nlm:affiliation></affiliation></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">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2001" type="published">2001</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Basal Ganglia (ultrastructure)</term><term>Brain (pathology)</term><term>Case-Control Studies</term><term>Caudate Nucleus (chemistry)</term><term>Caudate Nucleus (ultrastructure)</term><term>Corpus Striatum (ultrastructure)</term><term>Humans</term><term>Immunohistochemistry</term><term>In Vitro Techniques</term><term>Microscopy, Electron</term><term>Middle Aged</term><term>Neural Pathways</term><term>Neuronal Plasticity</term><term>Neurons, Afferent (ultrastructure)</term><term>Parkinson Disease (pathology)</term><term>Receptors, Dopamine D1 (chemistry)</term><term>Synapses (ultrastructure)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Receptors, Dopamine D1</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Caudate Nucleus</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Basal Ganglia</term><term>Caudate Nucleus</term><term>Corpus Striatum</term><term>Neurons, Afferent</term><term>Synapses</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Case-Control Studies</term><term>Humans</term><term>Immunohistochemistry</term><term>In Vitro Techniques</term><term>Microscopy, Electron</term><term>Middle Aged</term><term>Neural Pathways</term><term>Neuronal Plasticity</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The loss of dopaminergic neurons in the substantia nigra provokes a plasticity of corticostriatal synapses in Parkinson's disease (PD). The corticostriatal pathway nevertheless makes synapses with neurons bearing D1 dopamine receptors (D1R) and/or D2 dopamine receptors. At the ultrastructural level, we analyzed the morphological characteristics of synapses formed by afferent fibers making asymmetric contacts with the dendritic spines of neurons identified by D1R immunoreactivity, in the striatum of control subjects and PD patients. A quantitative analysis of the morphological characteristics of the synapses and of the number of perforated synapses (considered to be very active) was performed. In PD, a 50% increase in the number of perforated synapses making contact with D1R dendritic spines was observed, whereas no change in the number of perforated synapses on non-D1R spines was observed. The change in the number of perforated synapses on D1R dendrites was associated with a slight but nonsignificant increase in the surface area of the corticostriatal afferent fibers and the surface of the mitochondria in these fibers (+29.0% and +34.6%, respectively). This suggests a hyperactivity of corticostriatal fibers in contact with D1R-bearing neurons of the direct pathway in the basal ganglia circuitry. Since stimulation of the direct pathway is thought to alleviate the clinical symptoms of PD, this suggests that the differences observed may be involved in compensatory mechanisms.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">11391736</PMID><DateCreated><Year>2001</Year><Month>06</Month><Day>06</Day></DateCreated><DateCompleted><Year>2001</Year><Month>08</Month><Day>16</Day></DateCompleted><DateRevised><Year>2014</Year><Month>11</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>16</Volume><Issue>3</Issue><PubDate><Year>2001</Year><Month>May</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>435-41</MedlinePgn></Pagination><Abstract><AbstractText>The loss of dopaminergic neurons in the substantia nigra provokes a plasticity of corticostriatal synapses in Parkinson's disease (PD). The corticostriatal pathway nevertheless makes synapses with neurons bearing D1 dopamine receptors (D1R) and/or D2 dopamine receptors. At the ultrastructural level, we analyzed the morphological characteristics of synapses formed by afferent fibers making asymmetric contacts with the dendritic spines of neurons identified by D1R immunoreactivity, in the striatum of control subjects and PD patients. A quantitative analysis of the morphological characteristics of the synapses and of the number of perforated synapses (considered to be very active) was performed. In PD, a 50% increase in the number of perforated synapses making contact with D1R dendritic spines was observed, whereas no change in the number of perforated synapses on non-D1R spines was observed. The change in the number of perforated synapses on D1R dendrites was associated with a slight but nonsignificant increase in the surface area of the corticostriatal afferent fibers and the surface of the mitochondria in these fibers (+29.0% and +34.6%, respectively). This suggests a hyperactivity of corticostriatal fibers in contact with D1R-bearing neurons of the direct pathway in the basal ganglia circuitry. Since stimulation of the direct pathway is thought to alleviate the clinical symptoms of PD, this suggests that the differences observed may be involved in compensatory mechanisms.</AbstractText><CopyrightInformation>Copyright 2001 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Muriel</LastName><ForeName>M P</ForeName><Initials>MP</Initials><AffiliationInfo><Affiliation>INSERM U 289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 75013 Paris, France.</Affiliation></AffiliationInfo></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>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017447">Receptors, Dopamine D1</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000369">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001479">Basal Ganglia</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000648">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001921">Brain</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016022">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002421">Caudate Nucleus</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000737">chemistry</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000648">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003342">Corpus Striatum</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000648">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007150">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D066298">In Vitro Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008854">Microscopy, Electron</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009434">Neural Pathways</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D009473">Neuronal Plasticity</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009475">Neurons, Afferent</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000648">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017447">Receptors, Dopamine D1</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000737">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013569">Synapses</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000648">ultrastructure</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2001</Year><Month>6</Month><Day>8</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2001</Year><Month>8</Month><Day>17</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2001</Year><Month>6</Month><Day>8</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">11391736</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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