Movement Disorders (revue)

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

Identifieur interne : 000338 ( PascalFrancis/Curation ); précédent : 000337; suivant : 000339

Plasticity 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 :

RBID : Pascal:01-0378507

Descripteurs français

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 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.
pA  
A01 01  1    @0 0885-3185
A03   1    @0 Mov. disord.
A05       @2 16
A06       @2 3
A08 01  1  ENG  @1 Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease
A11 01  1    @1 MURIEL (Marie-Paule)
A11 02  1    @1 AGID (Yves)
A11 03  1    @1 HIRSCH (Etienne)
A14 01      @1 INSERM U 289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière @2 Paris @3 FRA @Z 1 aut. @Z 2 aut. @Z 3 aut.
A20       @1 435-441
A21       @1 2001
A23 01      @0 ENG
A43 01      @1 INIST @2 20953 @5 354000099011180050
A44       @0 0000 @1 © 2001 INIST-CNRS. All rights reserved.
A45       @0 45 ref.
A47 01  1    @0 01-0378507
A60       @1 P
A61       @0 A
A64 01  1    @0 Movement disorders
A66 01      @0 USA
C01 01    ENG  @0 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.
C02 01  X    @0 002B17G
C03 01  X  FRE  @0 Parkinson maladie @5 01
C03 01  X  ENG  @0 Parkinson disease @5 01
C03 01  X  SPA  @0 Parkinson enfermedad @5 01
C03 02  X  FRE  @0 Corps strié @5 04
C03 02  X  ENG  @0 Corpus striatum @5 04
C03 02  X  SPA  @0 Cuerpo estriado @5 04
C03 03  X  FRE  @0 Récepteur dopaminergique D1 @5 07
C03 03  X  ENG  @0 D1 Dopamine receptor @5 07 @6 «D1» Dopamine receptor
C03 03  X  SPA  @0 Receptor dopaminérgico D1 @5 07
C03 04  X  FRE  @0 Immunohistochimie @5 10
C03 04  X  ENG  @0 Immunohistochemistry @5 10
C03 04  X  SPA  @0 Inmunohistoquímica @5 10
C03 05  X  FRE  @0 Plasticité synaptique @5 13
C03 05  X  ENG  @0 Synaptic plasticity @5 13
C03 05  X  SPA  @0 Plasticidad sináptica @5 13
C03 06  X  FRE  @0 Physiopathologie @5 17
C03 06  X  ENG  @0 Pathophysiology @5 17
C03 06  X  SPA  @0 Fisiopatología @5 17
C03 07  X  FRE  @0 Homme @5 20
C03 07  X  ENG  @0 Human @5 20
C03 07  X  SPA  @0 Hombre @5 20
C03 08  X  FRE  @0 Postmortem @5 21
C03 08  X  ENG  @0 Postmortem @5 21
C03 08  X  SPA  @0 Postmortem @5 21
C07 01  X  FRE  @0 Système nerveux pathologie @5 37
C07 01  X  ENG  @0 Nervous system diseases @5 37
C07 01  X  SPA  @0 Sistema nervioso patología @5 37
C07 02  X  FRE  @0 Système nerveux central pathologie @5 38
C07 02  X  ENG  @0 Central nervous system disease @5 38
C07 02  X  SPA  @0 Sistema nervosio central patología @5 38
C07 03  X  FRE  @0 Encéphale pathologie @5 39
C07 03  X  ENG  @0 Cerebral disorder @5 39
C07 03  X  SPA  @0 Encéfalo patología @5 39
C07 04  X  FRE  @0 Extrapyramidal syndrome @5 40
C07 04  X  ENG  @0 Extrapyramidal syndrome @5 40
C07 04  X  SPA  @0 Extrapiramidal síndrome @5 40
C07 05  X  FRE  @0 Maladie dégénérative @5 41
C07 05  X  ENG  @0 Degenerative disease @5 41
C07 05  X  SPA  @0 Enfermedad degenerativa @5 41
C07 06  X  FRE  @0 Encéphale @5 45
C07 06  X  ENG  @0 Brain (vertebrata) @5 45
C07 06  X  SPA  @0 Encéfalo @5 45
C07 07  X  FRE  @0 Anatomopathologie @5 61
C07 07  X  ENG  @0 Pathology @5 61
C07 07  X  SPA  @0 Anatomía patológica @5 61
N21       @1 267

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