Movement Disorders (revue)

Attention, ce site est en cours de développement !
Attention, site généré par des moyens informatiques à partir de corpus bruts.
Les informations ne sont donc pas validées.

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

Identifieur interne : 002983 ( PascalFrancis/Corpus ); précédent : 002982; suivant : 002984

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 : 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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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

Format Inist (serveur)

NO : PASCAL 01-0378507 INIST
ET : Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease
AU : MURIEL (Marie-Paule); AGID (Yves); HIRSCH (Etienne)
AF : INSERM U 289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière/Paris/France (1 aut., 2 aut., 3 aut.)
DT : Publication en série; Niveau analytique
SO : Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2001; Vol. 16; No. 3; Pp. 435-441; Bibl. 45 ref.
LA : Anglais
EA : 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.
CC : 002B17G
FD : Parkinson maladie; Corps strié; Récepteur dopaminergique D1; Immunohistochimie; Plasticité synaptique; Physiopathologie; Homme; Postmortem
FG : Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Encéphale; Anatomopathologie
ED : Parkinson disease; Corpus striatum; D1 Dopamine receptor; Immunohistochemistry; Synaptic plasticity; Pathophysiology; Human; Postmortem
EG : Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Brain (vertebrata); Pathology
SD : Parkinson enfermedad; Cuerpo estriado; Receptor dopaminérgico D1; Inmunohistoquímica; Plasticidad sináptica; Fisiopatología; Hombre; Postmortem
LO : INIST-20953.354000099011180050
ID : 01-0378507

Links to Exploration step

Pascal:01-0378507

Le document en format XML

<record>
<TEI>
<teiHeader>
<fileDesc>
<titleStmt>
<title xml:lang="en" level="a">Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease</title>
<author>
<name sortKey="Muriel, Marie Paule" sort="Muriel, Marie Paule" uniqKey="Muriel M" first="Marie-Paule" last="Muriel">Marie-Paule Muriel</name>
<affiliation>
<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>
</affiliation>
</author>
<author>
<name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name>
<affiliation>
<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>
</affiliation>
</author>
<author>
<name sortKey="Hirsch, Etienne" sort="Hirsch, Etienne" uniqKey="Hirsch E" first="Etienne" last="Hirsch">Etienne Hirsch</name>
<affiliation>
<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>
</affiliation>
</author>
</titleStmt>
<publicationStmt>
<idno type="wicri:source">INIST</idno>
<idno type="inist">01-0378507</idno>
<date when="2001">2001</date>
<idno type="stanalyst">PASCAL 01-0378507 INIST</idno>
<idno type="RBID">Pascal:01-0378507</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">002983</idno>
</publicationStmt>
<sourceDesc>
<biblStruct>
<analytic>
<title xml:lang="en" level="a">Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease</title>
<author>
<name sortKey="Muriel, Marie Paule" sort="Muriel, Marie Paule" uniqKey="Muriel M" first="Marie-Paule" last="Muriel">Marie-Paule Muriel</name>
<affiliation>
<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>
</affiliation>
</author>
<author>
<name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name>
<affiliation>
<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>
</affiliation>
</author>
<author>
<name sortKey="Hirsch, Etienne" sort="Hirsch, Etienne" uniqKey="Hirsch E" first="Etienne" last="Hirsch">Etienne Hirsch</name>
<affiliation>
<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>
</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>
</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>
<inist>
<standard h6="B">
<pA>
<fA01 i1="01" i2="1">
<s0>0885-3185</s0>
</fA01>
<fA03 i2="1">
<s0>Mov. disord.</s0>
</fA03>
<fA05>
<s2>16</s2>
</fA05>
<fA06>
<s2>3</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG">
<s1>Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease</s1>
</fA08>
<fA11 i1="01" i2="1">
<s1>MURIEL (Marie-Paule)</s1>
</fA11>
<fA11 i1="02" i2="1">
<s1>AGID (Yves)</s1>
</fA11>
<fA11 i1="03" i2="1">
<s1>HIRSCH (Etienne)</s1>
</fA11>
<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>
</fA14>
<fA20>
<s1>435-441</s1>
</fA20>
<fA21>
<s1>2001</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>20953</s2>
<s5>354000099011180050</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2001 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>45 ref.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>01-0378507</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Movement disorders</s0>
</fA64>
<fA66 i1="01">
<s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>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.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Parkinson maladie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Parkinson disease</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Parkinson enfermedad</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Corps strié</s0>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Corpus striatum</s0>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Cuerpo estriado</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Récepteur dopaminergique D1</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>D1 Dopamine receptor</s0>
<s5>07</s5>
<s6>«D1» Dopamine receptor</s6>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Receptor dopaminérgico D1</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Immunohistochimie</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Immunohistochemistry</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Inmunohistoquímica</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Plasticité synaptique</s0>
<s5>13</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Synaptic plasticity</s0>
<s5>13</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Plasticidad sináptica</s0>
<s5>13</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Physiopathologie</s0>
<s5>17</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Pathophysiology</s0>
<s5>17</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Fisiopatología</s0>
<s5>17</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Homme</s0>
<s5>20</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Human</s0>
<s5>20</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Hombre</s0>
<s5>20</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Postmortem</s0>
<s5>21</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Postmortem</s0>
<s5>21</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Postmortem</s0>
<s5>21</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Système nerveux pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Système nerveux central pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Encéphale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Encéphale</s0>
<s5>45</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Brain (vertebrata)</s0>
<s5>45</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Encéfalo</s0>
<s5>45</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Anatomopathologie</s0>
<s5>61</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Pathology</s0>
<s5>61</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Anatomía patológica</s0>
<s5>61</s5>
</fC07>
<fN21>
<s1>267</s1>
</fN21>
</pA>
</standard>
<server>
<NO>PASCAL 01-0378507 INIST</NO>
<ET>Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease</ET>
<AU>MURIEL (Marie-Paule); AGID (Yves); HIRSCH (Etienne)</AU>
<AF>INSERM U 289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière/Paris/France (1 aut., 2 aut., 3 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2001; Vol. 16; No. 3; Pp. 435-441; Bibl. 45 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002B17G</CC>
<FD>Parkinson maladie; Corps strié; Récepteur dopaminergique D1; Immunohistochimie; Plasticité synaptique; Physiopathologie; Homme; Postmortem</FD>
<FG>Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Encéphale; Anatomopathologie</FG>
<ED>Parkinson disease; Corpus striatum; D1 Dopamine receptor; Immunohistochemistry; Synaptic plasticity; Pathophysiology; Human; Postmortem</ED>
<EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Brain (vertebrata); Pathology</EG>
<SD>Parkinson enfermedad; Cuerpo estriado; Receptor dopaminérgico D1; Inmunohistoquímica; Plasticidad sináptica; Fisiopatología; Hombre; Postmortem</SD>
<LO>INIST-20953.354000099011180050</LO>
<ID>01-0378507</ID>
</server>
</inist>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/PascalFrancis/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002983 | SxmlIndent | more

Ou

HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Corpus/biblio.hfd -nk 002983 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Santé
   |area=    MovDisordV3
   |flux=    PascalFrancis
   |étape=   Corpus
   |type=    RBID
   |clé=     Pascal:01-0378507
   |texte=   Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease
}}

Wicri

This area was generated with Dilib version V0.6.23.
Data generation: Sun Jul 3 12:29:32 2016. Site generation: Wed Feb 14 10:52:30 2024