MovDisordV3, Main, Merge, bibRecord, 007518

Relationship among nigrostriatal denervation, parkinsonism, and dyskinesias in the MPTP primate model

Identifieur interne : 007518 ( Main/Merge ); précédent : 007517; suivant : 007519

Relationship among nigrostriatal denervation, parkinsonism, and dyskinesias in the MPTP primate model

Auteurs : D. A. Di Monte [États-Unis] ; A. Mccormack [États-Unis, Suède] ; G. Petzinger [États-Unis] ; A. M. Janson [États-Unis, Suède] ; M. Quik [États-Unis] ; W. J. Langston [États-Unis]

Source :

Movement disorders [ 0885-3185 ] ; 2000.

RBID : Pascal:00-0269462

Descripteurs français

Pascal (Inist)
- Parkinson maladie, Dyskinésie, Voie nigrostriatale, Modèle animal, Physiopathologie, Animal, Singe, Enervation.
Wicri :
- topic : Singe.

English descriptors

KwdEn :
- Animal, Animal model, Denervation, Dyskinesia, Monkey, Nigrostriatal pathway, Parkinson disease, Pathophysiology.

Abstract

Presynaptic denervation is likely to play an important role in the pathophysiology of dyskinesias that develop after levodopa administration to patients with Parkinson's disease. In this study, the thresholds of nigrostriatal damage necessary for the occurrence of parkinsonism and levodopa-induced involuntary movements were compared in squirrel monkeys lesioned with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Animals treated with a regimen of MPTP that caused parkinsonism displayed ≥95% striatal dopamine depletion, 90% reduction of striatal dopamine uptake sites, and 70% nigral neuronal loss. Levodopa administration ameliorated the parkinsonian signs of these monkeys but also induced dyskinesias. A separate group of animals was treated with a milder MPTP regimen that caused 60%-70% striatal dopamine depletion, a 50% decrease in dopamine transporter, and 40% loss of dopaminergic nigral neurons. While these monkeys displayed no behavioral signs of parkinsonism, they all became dyskinetic after levodopa administration. The priming effect of levodopa, that is, the recurrence of dyskinesias in animals previously exposed to the drug, was compared in severely versus mildly lesioned monkeys. When severely injured parkinsonian animals underwent a second cycle of levodopa treatment, they immediately and consistently developed involuntary movements. In contrast, the recurrence of dyskinesias in primed monkeys with a partial nigrostriatal lesion required several levodopa administrations and remained relatively sporadic. The data indicate that moderate nigrostriatal damage which does not induce clinical parkinsonism predisposes to levodopa-induced dyskinesias. Once dyskinesias have been induced, the severity of denervation may enhance the sensitivity to subsequent levodopa exposures.

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Pascal:00-0269462

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term>
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<front><div type="abstract" xml:lang="en">Presynaptic denervation is likely to play an important role in the pathophysiology of dyskinesias that develop after levodopa administration to patients with Parkinson's disease. In this study, the thresholds of nigrostriatal damage necessary for the occurrence of parkinsonism and levodopa-induced involuntary movements were compared in squirrel monkeys lesioned with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Animals treated with a regimen of MPTP that caused parkinsonism displayed ≥95% striatal dopamine depletion, 90% reduction of striatal dopamine uptake sites, and 70% nigral neuronal loss. Levodopa administration ameliorated the parkinsonian signs of these monkeys but also induced dyskinesias. A separate group of animals was treated with a milder MPTP regimen that caused 60%-70% striatal dopamine depletion, a 50% decrease in dopamine transporter, and 40% loss of dopaminergic nigral neurons. While these monkeys displayed no behavioral signs of parkinsonism, they all became dyskinetic after levodopa administration. The priming effect of levodopa, that is, the recurrence of dyskinesias in animals previously exposed to the drug, was compared in severely versus mildly lesioned monkeys. When severely injured parkinsonian animals underwent a second cycle of levodopa treatment, they immediately and consistently developed involuntary movements. In contrast, the recurrence of dyskinesias in primed monkeys with a partial nigrostriatal lesion required several levodopa administrations and remained relatively sporadic. The data indicate that moderate nigrostriatal damage which does not induce clinical parkinsonism predisposes to levodopa-induced dyskinesias. Once dyskinesias have been induced, the severity of denervation may enhance the sensitivity to subsequent levodopa exposures.</div>
</front>
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<name sortKey="Quik, M" sort="Quik, M" uniqKey="Quik M" first="M." last="Quik">M. Quik</name>
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<country name="Suède"><region name="Svealand"><name sortKey="Mccormack, A" sort="Mccormack, A" uniqKey="Mccormack A" first="A." last="Mccormack">A. Mccormack</name>
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	Movement Disorders (revue)
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Movement Disorders (revue)

Relationship among nigrostriatal denervation, parkinsonism, and dyskinesias in the MPTP primate model

Relationship among nigrostriatal denervation, parkinsonism, and dyskinesias in the MPTP primate model

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

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