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La maladie de Parkinson au Canada (serveur d'exploration)

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Effects of oligonucleotide antisense to dopamine D1A receptor messenger RNA in a rodent model of levodopa-induced dyskinesia

Identifieur interne : 000C77 ( PascalFrancis/Corpus ); précédent : 000C76; suivant : 000C78

Effects of oligonucleotide antisense to dopamine D1A receptor messenger RNA in a rodent model of levodopa-induced dyskinesia

Auteurs : J. M. Van Kampen ; A. J. Stoessl

Source :

RBID : Pascal:00-0396300

Descripteurs français

English descriptors

Abstract

Dyskinesias are abnormal involuntary movements which develop as a side-effect of long-term treatment with levodopa in patients with Parkinson's disease. The pathophysiology underlying these dyskinesias remains unclear, although, it has been suggested that heightened activity of dopamine D1 receptor-bearing striatonigral neurons may play a key role. Chronic pulsatile levodopa administration to hemiparkinsonian rats results in sensitization of rotational responses to apomorphine. This sensitization is thought to be analogous to levodopa-induced dyskinesias in humans. In these studies, we further clarify the role of the dopamine D1A receptor in this rodent model of levodopa-induced dyskinesias using an in vivo oligonucleotide antisense approach. Hemiparkinsonian rats received twice daily injections of levodopa for three weeks followed by intrastriatal infusion of dopamine D1A receptor antisense (7 nmol/day, three days), a scrambled missense control sequence, or saline. Those animals treated with antisense displayed significantly fewer apomorphine-induced rotations than saline- or missense-treated controls. By reducing dopamine D1A receptor expression, we were able to attenuate sensitization of the response to apomorphine resulting from chronic pulsatile levodopa treatment. Thus, the dopamine D1A receptor appears to play a significant role in levodopa-induced dyskinesias and warrants further examination. These findings may have important implications for the development of selective treatment strategies designed to alleviate parkinsonian symptoms, while minimizing motor complications.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A05       @2 98
A06       @2 1
A08 01  1  ENG  @1 Effects of oligonucleotide antisense to dopamine D1A receptor messenger RNA in a rodent model of levodopa-induced dyskinesia
A11 01  1    @1 VAN KAMPEN (J. M.)
A11 02  1    @1 STOESSL (A. J.)
A14 01      @1 Neurodegenerative Disorders Centre, Faculty of Medicine, University of British Columbia, 2221 Wesbrook Mall @2 Vancouver, B.C., V6T 2B5 @3 CAN @Z 1 aut. @Z 2 aut.
A20       @1 61-67
A21       @1 2000
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A43 01      @1 INIST @2 17194 @5 354000088987520070
A44       @0 0000 @1 © 2000 INIST-CNRS. All rights reserved.
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A47 01  1    @0 00-0396300
A60       @1 P
A61       @0 A
A64 01  1    @0 Neuroscience
A66 01      @0 GBR
C01 01    ENG  @0 Dyskinesias are abnormal involuntary movements which develop as a side-effect of long-term treatment with levodopa in patients with Parkinson's disease. The pathophysiology underlying these dyskinesias remains unclear, although, it has been suggested that heightened activity of dopamine D1 receptor-bearing striatonigral neurons may play a key role. Chronic pulsatile levodopa administration to hemiparkinsonian rats results in sensitization of rotational responses to apomorphine. This sensitization is thought to be analogous to levodopa-induced dyskinesias in humans. In these studies, we further clarify the role of the dopamine D1A receptor in this rodent model of levodopa-induced dyskinesias using an in vivo oligonucleotide antisense approach. Hemiparkinsonian rats received twice daily injections of levodopa for three weeks followed by intrastriatal infusion of dopamine D1A receptor antisense (7 nmol/day, three days), a scrambled missense control sequence, or saline. Those animals treated with antisense displayed significantly fewer apomorphine-induced rotations than saline- or missense-treated controls. By reducing dopamine D1A receptor expression, we were able to attenuate sensitization of the response to apomorphine resulting from chronic pulsatile levodopa treatment. Thus, the dopamine D1A receptor appears to play a significant role in levodopa-induced dyskinesias and warrants further examination. These findings may have important implications for the development of selective treatment strategies designed to alleviate parkinsonian symptoms, while minimizing motor complications.
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N21       @1 269

Format Inist (serveur)

NO : PASCAL 00-0396300 INIST
ET : Effects of oligonucleotide antisense to dopamine D1A receptor messenger RNA in a rodent model of levodopa-induced dyskinesia
AU : VAN KAMPEN (J. M.); STOESSL (A. J.)
AF : Neurodegenerative Disorders Centre, Faculty of Medicine, University of British Columbia, 2221 Wesbrook Mall/Vancouver, B.C., V6T 2B5/Canada (1 aut., 2 aut.)
DT : Publication en série; Niveau analytique
SO : Neuroscience; ISSN 0306-4522; Coden NRSCDN; Royaume-Uni; Da. 2000; Vol. 98; No. 1; Pp. 61-67; Bibl. 62 ref.
LA : Anglais
EA : Dyskinesias are abnormal involuntary movements which develop as a side-effect of long-term treatment with levodopa in patients with Parkinson's disease. The pathophysiology underlying these dyskinesias remains unclear, although, it has been suggested that heightened activity of dopamine D1 receptor-bearing striatonigral neurons may play a key role. Chronic pulsatile levodopa administration to hemiparkinsonian rats results in sensitization of rotational responses to apomorphine. This sensitization is thought to be analogous to levodopa-induced dyskinesias in humans. In these studies, we further clarify the role of the dopamine D1A receptor in this rodent model of levodopa-induced dyskinesias using an in vivo oligonucleotide antisense approach. Hemiparkinsonian rats received twice daily injections of levodopa for three weeks followed by intrastriatal infusion of dopamine D1A receptor antisense (7 nmol/day, three days), a scrambled missense control sequence, or saline. Those animals treated with antisense displayed significantly fewer apomorphine-induced rotations than saline- or missense-treated controls. By reducing dopamine D1A receptor expression, we were able to attenuate sensitization of the response to apomorphine resulting from chronic pulsatile levodopa treatment. Thus, the dopamine D1A receptor appears to play a significant role in levodopa-induced dyskinesias and warrants further examination. These findings may have important implications for the development of selective treatment strategies designed to alleviate parkinsonian symptoms, while minimizing motor complications.
CC : 002B02U01
FD : DNA antisens; RNA messager; Récepteur dopaminergique; Modèle animal; Dyskinésie; Lévodopa; Toxicité; Antiparkinsonien; Rat
FG : Rodentia; Mammalia; Vertebrata
ED : Antisense DNA; Messenger RNA; Dopamine receptor; Animal model; Dyskinesia; Levodopa; Toxicity; Antiparkinson agent; Rat
EG : Rodentia; Mammalia; Vertebrata
SD : DNA antisentido; RNA mensajero; Receptor dopaminérgico; Modelo animal; Disquinesia; Levodopa; Toxicidad; Antiparkinsoniano; Rata
LO : INIST-17194.354000088987520070
ID : 00-0396300

Links to Exploration step

Pascal:00-0396300

Le document en format XML

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<AF>Neurodegenerative Disorders Centre, Faculty of Medicine, University of British Columbia, 2221 Wesbrook Mall/Vancouver, B.C., V6T 2B5/Canada (1 aut., 2 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neuroscience; ISSN 0306-4522; Coden NRSCDN; Royaume-Uni; Da. 2000; Vol. 98; No. 1; Pp. 61-67; Bibl. 62 ref.</SO>
<LA>Anglais</LA>
<EA>Dyskinesias are abnormal involuntary movements which develop as a side-effect of long-term treatment with levodopa in patients with Parkinson's disease. The pathophysiology underlying these dyskinesias remains unclear, although, it has been suggested that heightened activity of dopamine D
<sub>1</sub>
receptor-bearing striatonigral neurons may play a key role. Chronic pulsatile levodopa administration to hemiparkinsonian rats results in sensitization of rotational responses to apomorphine. This sensitization is thought to be analogous to levodopa-induced dyskinesias in humans. In these studies, we further clarify the role of the dopamine D
<sub>1A</sub>
receptor in this rodent model of levodopa-induced dyskinesias using an in vivo oligonucleotide antisense approach. Hemiparkinsonian rats received twice daily injections of levodopa for three weeks followed by intrastriatal infusion of dopamine D
<sub>1A</sub>
receptor antisense (7 nmol/day, three days), a scrambled missense control sequence, or saline. Those animals treated with antisense displayed significantly fewer apomorphine-induced rotations than saline- or missense-treated controls. By reducing dopamine D
<sub>1A</sub>
receptor expression, we were able to attenuate sensitization of the response to apomorphine resulting from chronic pulsatile levodopa treatment. Thus, the dopamine D
<sub>1A</sub>
receptor appears to play a significant role in levodopa-induced dyskinesias and warrants further examination. These findings may have important implications for the development of selective treatment strategies designed to alleviate parkinsonian symptoms, while minimizing motor complications.</EA>
<CC>002B02U01</CC>
<FD>DNA antisens; RNA messager; Récepteur dopaminergique; Modèle animal; Dyskinésie; Lévodopa; Toxicité; Antiparkinsonien; Rat</FD>
<FG>Rodentia; Mammalia; Vertebrata</FG>
<ED>Antisense DNA; Messenger RNA; Dopamine receptor; Animal model; Dyskinesia; Levodopa; Toxicity; Antiparkinson agent; Rat</ED>
<EG>Rodentia; Mammalia; Vertebrata</EG>
<SD>DNA antisentido; RNA mensajero; Receptor dopaminérgico; Modelo animal; Disquinesia; Levodopa; Toxicidad; Antiparkinsoniano; Rata</SD>
<LO>INIST-17194.354000088987520070</LO>
<ID>00-0396300</ID>
</server>
</inist>
</record>

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