ParkinsonFranceV1, PubMed, Corpus, bibRecord, 001034

Role of nigral lesion in the genesis of dyskinesias in a rat model of Parkinson's disease.

Identifieur interne : 001034 ( PubMed/Corpus ); précédent : 001033; suivant : 001035

Role of nigral lesion in the genesis of dyskinesias in a rat model of Parkinson's disease.

Auteurs : Vincent Paillé ; Philippe Brachet ; Philippe Damier

Source :

Neuroreport [ 0959-4965 ] ; 2004.

RBID : pubmed:15094523

English descriptors

KwdEn :
- Animals, Antiparkinson Agents (pharmacology), Behavior, Animal (drug effects), Behavior, Animal (physiology), Cell Count, Dyskinesias (physiopathology), Immunohistochemistry, Levodopa (pharmacology), Male, Oxidopamine, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (pathology), Parkinson Disease, Secondary (physiopathology), Rats, Rats, Sprague-Dawley, Substantia Nigra (pathology), Substantia Nigra (physiopathology), Sympatholytics, Tyrosine 3-Monooxygenase (metabolism).
MESH :
- chemical , metabolism : Tyrosine 3-Monooxygenase.
- chemical , pharmacology : Antiparkinson Agents, Levodopa.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Behavior, Animal.
- pathology : Parkinson Disease, Secondary, Substantia Nigra.
- physiology : Behavior, Animal.
- physiopathology : Dyskinesias, Parkinson Disease, Secondary, Substantia Nigra.
- Animals, Cell Count, Immunohistochemistry, Male, Oxidopamine, Rats, Rats, Sprague-Dawley, Sympatholytics.

Abstract

The pathogenesis of the motor fluctuations and dyskinesias that complicate levodopa treatment for Parkinson's disease (PD) remains uncertain. To evaluate the relationship between the degree of dopamine neuron loss and the severity of dyskinesias in a rodent model of PD, Sprague-Dawley rats were lesioned unilaterally using different doses of 6-hydroxydopamine injected into the substantia nigra pars compacta (SNc). All rats received two daily oral doses of levodopa for one month. In most of the animals chronic levodopa administration induced abnormal involuntary movements (AIMs), which were in some respects similar to human dyskinesias. We found that a minimum dopamine cell loss of around 95% was required for the development of dyskinesias after one-month of levodopa treatment. Moreover, we observed a positive relationship between the percentage dopaminergic cell loss in the SNc and the severity of levodopa-induced AIMs.

PubMed: 15094523

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pubmed:15094523

Le document en format XML

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<author><name sortKey="Paille, Vincent" sort="Paille, Vincent" uniqKey="Paille V" first="Vincent" last="Paillé">Vincent Paillé</name>
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<author><name sortKey="Brachet, Philippe" sort="Brachet, Philippe" uniqKey="Brachet P" first="Philippe" last="Brachet">Philippe Brachet</name>
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<author><name sortKey="Damier, Philippe" sort="Damier, Philippe" uniqKey="Damier P" first="Philippe" last="Damier">Philippe Damier</name>
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<front><div type="abstract" xml:lang="en">The pathogenesis of the motor fluctuations and dyskinesias that complicate levodopa treatment for Parkinson's disease (PD) remains uncertain. To evaluate the relationship between the degree of dopamine neuron loss and the severity of dyskinesias in a rodent model of PD, Sprague-Dawley rats were lesioned unilaterally using different doses of 6-hydroxydopamine injected into the substantia nigra pars compacta (SNc). All rats received two daily oral doses of levodopa for one month. In most of the animals chronic levodopa administration induced abnormal involuntary movements (AIMs), which were in some respects similar to human dyskinesias. We found that a minimum dopamine cell loss of around 95% was required for the development of dyskinesias after one-month of levodopa treatment. Moreover, we observed a positive relationship between the percentage dopaminergic cell loss in the SNc and the severity of levodopa-induced AIMs.</div>
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<Abstract><AbstractText>The pathogenesis of the motor fluctuations and dyskinesias that complicate levodopa treatment for Parkinson's disease (PD) remains uncertain. To evaluate the relationship between the degree of dopamine neuron loss and the severity of dyskinesias in a rodent model of PD, Sprague-Dawley rats were lesioned unilaterally using different doses of 6-hydroxydopamine injected into the substantia nigra pars compacta (SNc). All rats received two daily oral doses of levodopa for one month. In most of the animals chronic levodopa administration induced abnormal involuntary movements (AIMs), which were in some respects similar to human dyskinesias. We found that a minimum dopamine cell loss of around 95% was required for the development of dyskinesias after one-month of levodopa treatment. Moreover, we observed a positive relationship between the percentage dopaminergic cell loss in the SNc and the severity of levodopa-induced AIMs.</AbstractText>
<CopyrightInformation>Copyright 2004 Lippincott Williams & Wilkins</CopyrightInformation>
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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

Role of nigral lesion in the genesis of dyskinesias in a rat model of Parkinson's disease.

Role of nigral lesion in the genesis of dyskinesias in a rat model of Parkinson's disease.

Source :

English descriptors

Abstract

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki