MovDisordV3, PascalFrancis, Corpus, bibRecord, 002C10

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

Identifieur interne : 002C10 ( PascalFrancis/Corpus ); précédent : 002C09; suivant : 002C11

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

Auteurs : D. A. Di Monte ; A. Mccormack ; G. Petzinger ; A. M. Janson ; M. Quik ; W. J. Langston

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.

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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`02`	`1`		`@1 MCCORMACK (A.)`
A11	`03`	`1`		`@1 PETZINGER (G.)`
A11	`04`	`1`		`@1 JANSON (A. M.)`
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A11	`06`	`1`		`@1 LANGSTON (W. J.)`
A14	`01`			`@1 The Parkinson's Institute @2 Sunnyvale, California @3 USA @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut.`
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C01	`01`		`ENG`	@0 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.
C02	`01`	`X`		`@0 002B17G`
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C03	`03`	`X`	`SPA`	`@0 Vía nigroestriatal @5 07`
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C03	`07`	`X`	`ENG`	`@0 Monkey @5 21`
C03	`07`	`X`	`SPA`	`@0 Mono @5 21`
C03	`08`	`X`	`FRE`	`@0 Enervation @5 23`
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C07	`01`	`X`	`FRE`	`@0 Primates @2 NS`
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C07	`03`	`X`	`FRE`	`@0 Vertebrata @2 NS`
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C07	`07`	`X`	`FRE`	`@0 Extrapyramidal syndrome @5 40`
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C07	`10`	`X`	`FRE`	`@0 Mouvement involontaire @5 47`
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N21				`@1 185`

Format Inist (serveur)

NO :	PASCAL 00-0269462 INIST
ET :	Relationship among nigrostriatal denervation, parkinsonism, and dyskinesias in the MPTP primate model
AU :	DI MONTE (D. A.); MCCORMACK (A.); PETZINGER (G.); JANSON (A. M.); QUIK (M.); LANGSTON (W. J.)
AF :	The Parkinson's Institute/Sunnyvale, California/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut.); Department of Neuroscience, Karolinska Institute/Stockholm/Suède (2 aut., 4 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2000; Vol. 15; No. 3; Pp. 459-466; Bibl. 35 ref.
LA :	Anglais
EA :	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.
CC :	002B17G
FD :	Parkinson maladie; Dyskinésie; Voie nigrostriatale; Modèle animal; Physiopathologie; Animal; Singe; Enervation
FG :	Primates; Mammalia; Vertebrata; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Trouble neurologique; Mouvement involontaire
ED :	Parkinson disease; Dyskinesia; Nigrostriatal pathway; Animal model; Pathophysiology; Animal; Monkey; Denervation
EG :	Primates; Mammalia; Vertebrata; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Neurological disorder; Involuntary movement
SD :	Parkinson enfermedad; Disquinesia; Vía nigroestriatal; Modelo animal; Fisiopatología; Animal; Mono; Denervación
LO :	INIST-20953.354000087348900050
ID :	00-0269462

Links to Exploration step

Pascal:00-0269462

Le document en format XML

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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>
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<fA08 i1="01" i2="1" l="ENG"><s1>Relationship among nigrostriatal denervation, parkinsonism, and dyskinesias in the MPTP primate model</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>DI MONTE (D. A.)</s1>
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<fA11 i1="02" i2="1"><s1>MCCORMACK (A.)</s1>
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<fA11 i1="03" i2="1"><s1>PETZINGER (G.)</s1>
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<fA11 i1="04" i2="1"><s1>JANSON (A. M.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>QUIK (M.)</s1>
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<fA11 i1="06" i2="1"><s1>LANGSTON (W. J.)</s1>
</fA11>
<fA14 i1="01"><s1>The Parkinson's Institute</s1>
<s2>Sunnyvale, California</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Neuroscience, Karolinska Institute</s1>
<s2>Stockholm</s2>
<s3>SWE</s3>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
</fA14>
<fA20><s1>459-466</s1>
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<fC01 i1="01" l="ENG"><s0>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.</s0>
</fC01>
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</fC02>
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<s5>01</s5>
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<s5>04</s5>
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<s5>07</s5>
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<s5>07</s5>
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<s5>07</s5>
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<s5>16</s5>
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<s5>16</s5>
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<s5>21</s5>
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<s5>23</s5>
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<s5>23</s5>
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<s5>23</s5>
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<s2>NS</s2>
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<s2>NS</s2>
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<s2>NS</s2>
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<fC07 i1="04" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>37</s5>
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<s5>37</s5>
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<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>37</s5>
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<s5>38</s5>
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<s5>38</s5>
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<s5>39</s5>
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<s5>39</s5>
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<s5>39</s5>
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<fC07 i1="07" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
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<fC07 i1="07" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
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<fC07 i1="07" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
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<s5>41</s5>
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<s5>41</s5>
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<fC07 i1="08" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>41</s5>
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<s5>46</s5>
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<s5>46</s5>
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<s5>46</s5>
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<s5>47</s5>
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<fC07 i1="10" i2="X" l="ENG"><s0>Involuntary movement</s0>
<s5>47</s5>
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<s5>47</s5>
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<server><NO>PASCAL 00-0269462 INIST</NO>
<ET>Relationship among nigrostriatal denervation, parkinsonism, and dyskinesias in the MPTP primate model</ET>
<AU>DI MONTE (D. A.); MCCORMACK (A.); PETZINGER (G.); JANSON (A. M.); QUIK (M.); LANGSTON (W. J.)</AU>
<AF>The Parkinson's Institute/Sunnyvale, California/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut.); Department of Neuroscience, Karolinska Institute/Stockholm/Suède (2 aut., 4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2000; Vol. 15; No. 3; Pp. 459-466; Bibl. 35 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002B17G</CC>
<FD>Parkinson maladie; Dyskinésie; Voie nigrostriatale; Modèle animal; Physiopathologie; Animal; Singe; Enervation</FD>
<FG>Primates; Mammalia; Vertebrata; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Trouble neurologique; Mouvement involontaire</FG>
<ED>Parkinson disease; Dyskinesia; Nigrostriatal pathway; Animal model; Pathophysiology; Animal; Monkey; Denervation</ED>
<EG>Primates; Mammalia; Vertebrata; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Neurological disorder; Involuntary movement</EG>
<SD>Parkinson enfermedad; Disquinesia; Vía nigroestriatal; Modelo animal; Fisiopatología; Animal; Mono; Denervación</SD>
<LO>INIST-20953.354000087348900050</LO>
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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

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