Movement Disorders (revue)

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Aberrant Striatal Plasticity is Specifically Associated With Dyskinesia Following Levodopa Treatment

Identifieur interne : 000964 ( PascalFrancis/Corpus ); précédent : 000963; suivant : 000965

Aberrant Striatal Plasticity is Specifically Associated With Dyskinesia Following Levodopa Treatment

Auteurs : Pauline Belujon ; Daniel J. Lodge ; Anthony A. Grace

Source :

RBID : Pascal:10-0413274

Descripteurs français

English descriptors

Abstract

Chronic levodopa treatment for Parkinson's disease often results in the development of abnormal involuntary movement, known as L-dopa-induced dyskinesia (LIDs). Studies suggest that LIDs may be associated with aberrant corticostriatal plasticity. Using in vivo extracellular recordings from identified Type I and Type II medium spiny striatal neurons, chronic L-dopa treatment was found to produce abnormal corticostriatal information processing. Specifically, after chronic L-dopa treatment in dopamine-depleted rats, there was a transition from a cortically evoked long-term depression (LTD) to a complementary but opposing form of plasticity, long-term potentiation, in Type II "indirect" pathway neurons. In contrast, LTD could still be induced in Type I neurons. Interestingly, the one parameter that correlated best with dyskinesias was the inability to de-depress established LTD in Type I medium spiny striatal neurons. Taken as a whole, we propose that the induction of LIDs is due, at least in part, to an aberrant induction of plasticity within the Type II indirect pathway neurons combined with an inability to de-depress established plastic responses in Type I neurons. Such information is critical for understanding the cellular mechanisms underlying one of the major caveats to L-dopa therapy.

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 25
A06       @2 11
A08 01  1  ENG  @1 Aberrant Striatal Plasticity is Specifically Associated With Dyskinesia Following Levodopa Treatment
A11 01  1    @1 BELUJON (Pauline)
A11 02  1    @1 LODGE (Daniel J.)
A11 03  1    @1 GRACE (Anthony A.)
A14 01      @1 Departments of Neuroscience, Psychiatry, and Psychology, University of Pittsburgh @2 Pittsburgh, PA @3 USA @Z 1 aut. @Z 2 aut. @Z 3 aut.
A20       @1 1568-1576
A21       @1 2010
A23 01      @0 ENG
A43 01      @1 INIST @2 20953 @5 354000192608100060
A44       @0 0000 @1 © 2010 INIST-CNRS. All rights reserved.
A45       @0 38 ref.
A47 01  1    @0 10-0413274
A60       @1 P
A61       @0 A
A64 01  1    @0 Movement disorders
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C01 01    ENG  @0 Chronic levodopa treatment for Parkinson's disease often results in the development of abnormal involuntary movement, known as L-dopa-induced dyskinesia (LIDs). Studies suggest that LIDs may be associated with aberrant corticostriatal plasticity. Using in vivo extracellular recordings from identified Type I and Type II medium spiny striatal neurons, chronic L-dopa treatment was found to produce abnormal corticostriatal information processing. Specifically, after chronic L-dopa treatment in dopamine-depleted rats, there was a transition from a cortically evoked long-term depression (LTD) to a complementary but opposing form of plasticity, long-term potentiation, in Type II "indirect" pathway neurons. In contrast, LTD could still be induced in Type I neurons. Interestingly, the one parameter that correlated best with dyskinesias was the inability to de-depress established LTD in Type I medium spiny striatal neurons. Taken as a whole, we propose that the induction of LIDs is due, at least in part, to an aberrant induction of plasticity within the Type II indirect pathway neurons combined with an inability to de-depress established plastic responses in Type I neurons. Such information is critical for understanding the cellular mechanisms underlying one of the major caveats to L-dopa therapy.
C02 01  X    @0 002B17
C02 02  X    @0 002B02U01
C03 01  X  FRE  @0 Dyskinésie @5 01
C03 01  X  ENG  @0 Dyskinesia @5 01
C03 01  X  SPA  @0 Disquinesia @5 01
C03 02  X  FRE  @0 Pathologie du système nerveux @5 02
C03 02  X  ENG  @0 Nervous system diseases @5 02
C03 02  X  SPA  @0 Sistema nervioso patología @5 02
C03 03  X  FRE  @0 Plasticité @5 09
C03 03  X  ENG  @0 Plasticity @5 09
C03 03  X  SPA  @0 Plasticidad @5 09
C03 04  X  FRE  @0 Lévodopa @2 NK @2 FR @5 10
C03 04  X  ENG  @0 Levodopa @2 NK @2 FR @5 10
C03 04  X  SPA  @0 Levodopa @2 NK @2 FR @5 10
C03 05  X  FRE  @0 Traitement @5 11
C03 05  X  ENG  @0 Treatment @5 11
C03 05  X  SPA  @0 Tratamiento @5 11
C07 01  X  FRE  @0 Syndrome extrapyramidal @5 37
C07 01  X  ENG  @0 Extrapyramidal syndrome @5 37
C07 01  X  SPA  @0 Extrapiramidal síndrome @5 37
C07 02  X  FRE  @0 Mouvement involontaire @5 38
C07 02  X  ENG  @0 Involuntary movement @5 38
C07 02  X  SPA  @0 Movimiento involuntario @5 38
C07 03  X  FRE  @0 Trouble neurologique @5 40
C07 03  X  ENG  @0 Neurological disorder @5 40
C07 03  X  SPA  @0 Trastorno neurológico @5 40
C07 04  X  FRE  @0 Pathologie de l'encéphale @5 41
C07 04  X  ENG  @0 Cerebral disorder @5 41
C07 04  X  SPA  @0 Encéfalo patología @5 41
C07 05  X  FRE  @0 Pathologie du système nerveux central @5 42
C07 05  X  ENG  @0 Central nervous system disease @5 42
C07 05  X  SPA  @0 Sistema nervosio central patología @5 42
N21       @1 270
N44 01      @1 OTO
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Format Inist (serveur)

NO : PASCAL 10-0413274 INIST
ET : Aberrant Striatal Plasticity is Specifically Associated With Dyskinesia Following Levodopa Treatment
AU : BELUJON (Pauline); LODGE (Daniel J.); GRACE (Anthony A.)
AF : Departments of Neuroscience, Psychiatry, and Psychology, University of Pittsburgh/Pittsburgh, PA/Etats-Unis (1 aut., 2 aut., 3 aut.)
DT : Publication en série; Niveau analytique
SO : Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2010; Vol. 25; No. 11; Pp. 1568-1576; Bibl. 38 ref.
LA : Anglais
EA : Chronic levodopa treatment for Parkinson's disease often results in the development of abnormal involuntary movement, known as L-dopa-induced dyskinesia (LIDs). Studies suggest that LIDs may be associated with aberrant corticostriatal plasticity. Using in vivo extracellular recordings from identified Type I and Type II medium spiny striatal neurons, chronic L-dopa treatment was found to produce abnormal corticostriatal information processing. Specifically, after chronic L-dopa treatment in dopamine-depleted rats, there was a transition from a cortically evoked long-term depression (LTD) to a complementary but opposing form of plasticity, long-term potentiation, in Type II "indirect" pathway neurons. In contrast, LTD could still be induced in Type I neurons. Interestingly, the one parameter that correlated best with dyskinesias was the inability to de-depress established LTD in Type I medium spiny striatal neurons. Taken as a whole, we propose that the induction of LIDs is due, at least in part, to an aberrant induction of plasticity within the Type II indirect pathway neurons combined with an inability to de-depress established plastic responses in Type I neurons. Such information is critical for understanding the cellular mechanisms underlying one of the major caveats to L-dopa therapy.
CC : 002B17; 002B02U01
FD : Dyskinésie; Pathologie du système nerveux; Plasticité; Lévodopa; Traitement
FG : Syndrome extrapyramidal; Mouvement involontaire; Trouble neurologique; Pathologie de l'encéphale; Pathologie du système nerveux central
ED : Dyskinesia; Nervous system diseases; Plasticity; Levodopa; Treatment
EG : Extrapyramidal syndrome; Involuntary movement; Neurological disorder; Cerebral disorder; Central nervous system disease
SD : Disquinesia; Sistema nervioso patología; Plasticidad; Levodopa; Tratamiento
LO : INIST-20953.354000192608100060
ID : 10-0413274

Links to Exploration step

Pascal:10-0413274

Le document en format XML

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-dopa treatment was found to produce abnormal corticostriatal information processing. Specifically, after chronic
<sub>L</sub>
-dopa treatment in dopamine-depleted rats, there was a transition from a cortically evoked long-term depression (LTD) to a complementary but opposing form of plasticity, long-term potentiation, in Type II "indirect" pathway neurons. In contrast, LTD could still be induced in Type I neurons. Interestingly, the one parameter that correlated best with dyskinesias was the inability to de-depress established LTD in Type I medium spiny striatal neurons. Taken as a whole, we propose that the induction of LIDs is due, at least in part, to an aberrant induction of plasticity within the Type II indirect pathway neurons combined with an inability to de-depress established plastic responses in Type I neurons. Such information is critical for understanding the cellular mechanisms underlying one of the major caveats to
<sub>L</sub>
-dopa therapy.</EA>
<CC>002B17; 002B02U01</CC>
<FD>Dyskinésie; Pathologie du système nerveux; Plasticité; Lévodopa; Traitement</FD>
<FG>Syndrome extrapyramidal; Mouvement involontaire; Trouble neurologique; Pathologie de l'encéphale; Pathologie du système nerveux central</FG>
<ED>Dyskinesia; Nervous system diseases; Plasticity; Levodopa; Treatment</ED>
<EG>Extrapyramidal syndrome; Involuntary movement; Neurological disorder; Cerebral disorder; Central nervous system disease</EG>
<SD>Disquinesia; Sistema nervioso patología; Plasticidad; Levodopa; Tratamiento</SD>
<LO>INIST-20953.354000192608100060</LO>
<ID>10-0413274</ID>
</server>
</inist>
</record>

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