Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease
Identifieur interne : 006E28 ( Main/Merge ); précédent : 006E27; suivant : 006E29Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease
Auteurs : Marie-Paule Muriel [France] ; Yves Agid [France] ; Etienne Hirsch [France]Source :
- Movement disorders [ 0885-3185 ] ; 2001.
Descripteurs français
- Pascal (Inist)
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- topic : Homme.
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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 Dl 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-DIR 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 DIR-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.
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Pascal:01-0378507Le document en format XML
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type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>INSERM U 289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>France</country><placeName><settlement type="city">Paris</settlement></placeName><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName></affiliation></author><author><name sortKey="Hirsch, Etienne" sort="Hirsch, Etienne" uniqKey="Hirsch E" first="Etienne" last="Hirsch">Etienne Hirsch</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>INSERM U 289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>France</country><placeName><settlement type="city">Paris</settlement></placeName></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2001">2001</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Corpus striatum</term><term>D1 Dopamine receptor</term><term>Human</term><term>Immunohistochemistry</term><term>Parkinson disease</term><term>Pathophysiology</term><term>Postmortem</term><term>Synaptic plasticity</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Parkinson maladie</term><term>Corps strié</term><term>Récepteur dopaminergique D1</term><term>Immunohistochimie</term><term>Plasticité synaptique</term><term>Physiopathologie</term><term>Homme</term><term>Postmortem</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</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 Dl 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-DIR 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 DIR-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><affiliations><list><country><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Paris</li></settlement><orgName><li>Hôpital de la Salpêtrière</li></orgName></list><tree><country name="France"><noRegion><name sortKey="Muriel, Marie Paule" sort="Muriel, Marie Paule" uniqKey="Muriel M" first="Marie-Paule" last="Muriel">Marie-Paule Muriel</name></noRegion><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name><name sortKey="Hirsch, Etienne" sort="Hirsch, Etienne" uniqKey="Hirsch E" first="Etienne" last="Hirsch">Etienne Hirsch</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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