Movement Disorders (revue)

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Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease

Identifieur interne : 000954 ( Istex/Corpus ); précédent : 000953; suivant : 000955

Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease

Auteurs : Marie-Paule Muriel ; Yves Agid ; Etienne Hirsch

Source :

RBID : ISTEX:F08BA412500E87376349EF77A6BFA0B59E5FF1DD

English descriptors

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. © 2001 Movement Disorder Society.

Url:
DOI: 10.1002/mds.1103

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ISTEX:F08BA412500E87376349EF77A6BFA0B59E5FF1DD

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<affiliation>INSERM U 289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, Paris, France</affiliation>
<description>Correspondence: INSERM U289, Hôpital de la Salpêtrière, 47 boulevard de l' Hôpital, 75013 Paris, France.</description>
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<publisher>John Wiley & Sons, Inc.</publisher>
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<placeTerm type="text">New York</placeTerm>
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<dateIssued encoding="w3cdtf">2001-05</dateIssued>
<dateCaptured encoding="w3cdtf">2000-07-14</dateCaptured>
<dateValid encoding="w3cdtf">2000-11-30</dateValid>
<copyrightDate encoding="w3cdtf">2001</copyrightDate>
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<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<abstract 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. © 2001 Movement Disorder Society.</abstract>
<subject lang="en">
<genre>Keywords</genre>
<topic>basal ganglia</topic>
<topic>plasticity</topic>
<topic>dopamine receptor</topic>
<topic>Parkinson</topic>
</subject>
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<titleInfo>
<title>Movement Disorders</title>
<subTitle>Official Journal of the Movement Disorder Society</subTitle>
</titleInfo>
<titleInfo type="abbreviated">
<title>Mov. Disord.</title>
</titleInfo>
<subject>
<genre>article category</genre>
<topic>Article</topic>
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<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
<identifier type="PublisherID">MDS</identifier>
<part>
<date>2001</date>
<detail type="volume">
<caption>vol.</caption>
<number>16</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>3</number>
</detail>
<extent unit="pages">
<start>435</start>
<end>441</end>
<total>7</total>
</extent>
</part>
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<identifier type="DOI">10.1002/mds.1103</identifier>
<identifier type="ArticleID">MDS1103</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2001 Movement Disorder Society</accessCondition>
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<recordOrigin>John Wiley & Sons, Inc.</recordOrigin>
<recordContentSource>WILEY</recordContentSource>
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