Toward a primate model of l‐dopa‐unresponsive parkinsonism mimicking striatonigral degeneration
Identifieur interne : 004931 ( Main/Exploration ); précédent : 004930; suivant : 004932Toward a primate model of l‐dopa‐unresponsive parkinsonism mimicking striatonigral degeneration
Auteurs : Imad Ghorayeb [France] ; Pierre O. Fernagut [France] ; Incarnation Aubert [France] ; Erwan Bezard [France] ; Werner Poewe [Autriche] ; Gregor K. Wenning [Autriche] ; François Tison [France]Source :
- Movement Disorders [ 0885-3185 ] ; 2000-05.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Singe.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Animal, Animal model, Animals, Antiparkinson Agents (pharmacology), Brain Mapping, Corpus Striatum (drug effects), Corpus Striatum (pathology), Corpus Striatum (physiopathology), Diagnosis, Differential, Disease Models, Animal, Dopamine (metabolism), Levodopa (pharmacology), MPTP—3 nitropropionic acid, Macaca fascicularis, Male, Monkey, Multiple System Atrophy (chemically induced), Multiple System Atrophy (pathology), Multiple System Atrophy (physiopathology), Multiple system atrophy, Nerve Degeneration (chemically induced), Nerve Degeneration (pathology), Nerve Degeneration (physiopathology), Neurotoxins, Nigrostriatal pathway, Nitro Compounds, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (pathology), Parkinson Disease, Secondary (physiopathology), Parkinsonism, Pathophysiology, Primate model, Propionates, Striatonigral Degeneration (chemically induced), Striatonigral Degeneration (pathology), Striatonigral Degeneration (physiopathology), Striatonigral degeneration.
- MESH :
- chemical , metabolism : Dopamine.
- chemical , pharmacology : Antiparkinson Agents, Levodopa.
- chemical : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Neurotoxins, Nitro Compounds, Propionates.
- chemically induced : Multiple System Atrophy, Nerve Degeneration, Parkinson Disease, Secondary, Striatonigral Degeneration.
- drug effects : Corpus Striatum.
- pathology : Corpus Striatum, Multiple System Atrophy, Nerve Degeneration, Parkinson Disease, Secondary, Striatonigral Degeneration.
- physiopathology : Corpus Striatum, Multiple System Atrophy, Nerve Degeneration, Parkinson Disease, Secondary, Striatonigral Degeneration.
- Animals, Brain Mapping, Diagnosis, Differential, Disease Models, Animal, Macaca fascicularis, Male.
Abstract
We developed a primate model of striatonigral degeneration (SND), the neuropathology underlying levodopa‐unresponsive parkinsonism associated with multiple systemic atrophy (MSA‐P), by sequential systemic administration of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) and 3‐nitropropionic acid (3NP) in a Macaca fascicularis monkey. l‐Dopa‐responsive parkinsonian features emerged after MPTP injections. Subsequent chronic 3NP administration aggravated the motor symptoms and abolished the l‐dopa response. In vivo magnetic resonance imaging revealed bilateral striatal lesions. Histopathologically, there was severe dopaminergic cell loss in the substantia nigra pars compacta compared with the control monkey. Furthermore, we observed circumscribed areas of severe neuronal degeneration in the motor striatum. These changes were absent in the control monkey, and they were associated with diffuse metabolic failure as demonstrated by cytochrome oxidase histochemistry. The striatal pathology predominantly involved output pre‐pro‐enkephalin A‐ and substance P‐containing cells, whereas somatostatin (NADPH‐diaphorase)‐containing interneurons were relatively spared. Our model therefore reproduced levodopa‐unresponsive parkinsonism and SND‐like pathologic changes characteristic of MSA‐P. The double‐lesion primate model of SND may serve as a preclinical test‐bed for the evaluation of novel therapeutic strategies in MSA‐P.
Url:
DOI: 10.1002/1531-8257(200005)15:3<531::AID-MDS1017>3.0.CO;2-C
Affiliations:
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2000-05">2000-05</date><biblScope unit="vol">15</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="531">531</biblScope><biblScope unit="page" to="536">536</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">4D6E85DF3EC76EB51B1CC83F44AD782982A427DB</idno><idno type="DOI">10.1002/1531-8257(200005)15:3<531::AID-MDS1017>3.0.CO;2-C</idno><idno type="ArticleID">MDS1017</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Animal</term><term>Animal model</term><term>Animals</term><term>Antiparkinson Agents (pharmacology)</term><term>Brain Mapping</term><term>Corpus Striatum (drug effects)</term><term>Corpus Striatum (pathology)</term><term>Corpus Striatum (physiopathology)</term><term>Diagnosis, Differential</term><term>Disease Models, Animal</term><term>Dopamine (metabolism)</term><term>Levodopa (pharmacology)</term><term>MPTP—3 nitropropionic acid</term><term>Macaca fascicularis</term><term>Male</term><term>Monkey</term><term>Multiple System Atrophy (chemically induced)</term><term>Multiple System Atrophy (pathology)</term><term>Multiple System Atrophy (physiopathology)</term><term>Multiple system atrophy</term><term>Nerve Degeneration (chemically induced)</term><term>Nerve Degeneration (pathology)</term><term>Nerve Degeneration (physiopathology)</term><term>Neurotoxins</term><term>Nigrostriatal pathway</term><term>Nitro Compounds</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (pathology)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Parkinsonism</term><term>Pathophysiology</term><term>Primate model</term><term>Propionates</term><term>Striatonigral Degeneration (chemically induced)</term><term>Striatonigral Degeneration (pathology)</term><term>Striatonigral Degeneration (physiopathology)</term><term>Striatonigral degeneration</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Neurotoxins</term><term>Nitro Compounds</term><term>Propionates</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Multiple System Atrophy</term><term>Nerve Degeneration</term><term>Parkinson Disease, Secondary</term><term>Striatonigral Degeneration</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Corpus Striatum</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term><term>Multiple System Atrophy</term><term>Nerve Degeneration</term><term>Parkinson Disease, Secondary</term><term>Striatonigral Degeneration</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Corpus Striatum</term><term>Multiple System Atrophy</term><term>Nerve Degeneration</term><term>Parkinson Disease, Secondary</term><term>Striatonigral Degeneration</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Brain Mapping</term><term>Diagnosis, Differential</term><term>Disease Models, Animal</term><term>Macaca fascicularis</term><term>Male</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Animal</term><term>Atrophie multisystématisée</term><term>Modèle animal</term><term>Parkinsonisme</term><term>Physiopathologie</term><term>Singe</term><term>Voie nigrostriatale</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Singe</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We developed a primate model of striatonigral degeneration (SND), the neuropathology underlying levodopa‐unresponsive parkinsonism associated with multiple systemic atrophy (MSA‐P), by sequential systemic administration of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) and 3‐nitropropionic acid (3NP) in a Macaca fascicularis monkey. l‐Dopa‐responsive parkinsonian features emerged after MPTP injections. Subsequent chronic 3NP administration aggravated the motor symptoms and abolished the l‐dopa response. In vivo magnetic resonance imaging revealed bilateral striatal lesions. Histopathologically, there was severe dopaminergic cell loss in the substantia nigra pars compacta compared with the control monkey. Furthermore, we observed circumscribed areas of severe neuronal degeneration in the motor striatum. These changes were absent in the control monkey, and they were associated with diffuse metabolic failure as demonstrated by cytochrome oxidase histochemistry. The striatal pathology predominantly involved output pre‐pro‐enkephalin A‐ and substance P‐containing cells, whereas somatostatin (NADPH‐diaphorase)‐containing interneurons were relatively spared. Our model therefore reproduced levodopa‐unresponsive parkinsonism and SND‐like pathologic changes characteristic of MSA‐P. The double‐lesion primate model of SND may serve as a preclinical test‐bed for the evaluation of novel therapeutic strategies in MSA‐P.</div></front></TEI><affiliations><list><country><li>Autriche</li><li>France</li></country><region><li>Tyrol (Land)</li></region><settlement><li>Bordeaux</li><li>Innsbruck</li></settlement><orgName><li>Université de médecine d'Innsbruck</li></orgName></list><tree><country name="France"><noRegion><name sortKey="Ghorayeb, Imad" sort="Ghorayeb, Imad" uniqKey="Ghorayeb I" first="Imad" last="Ghorayeb">Imad Ghorayeb</name></noRegion><name sortKey="Aubert, Incarnation" sort="Aubert, Incarnation" uniqKey="Aubert I" first="Incarnation" last="Aubert">Incarnation Aubert</name><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name><name sortKey="Fernagut, Pierre O" sort="Fernagut, Pierre O" uniqKey="Fernagut P" first="Pierre O." last="Fernagut">Pierre O. Fernagut</name><name sortKey="Tison, Francois" sort="Tison, Francois" uniqKey="Tison F" first="François" last="Tison">François Tison</name></country><country name="Autriche"><region name="Tyrol (Land)"><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name></region><name sortKey="Wenning, Gregor K" sort="Wenning, Gregor K" uniqKey="Wenning G" first="Gregor K." last="Wenning">Gregor K. Wenning</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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