Toward a primate model of L-dopa-unresponsive parkinsonism mimicking striatonigral degeneration.
Identifieur interne : 001320 ( PubMed/Corpus ); précédent : 001319; suivant : 001321Toward a primate model of L-dopa-unresponsive parkinsonism mimicking striatonigral degeneration.
Auteurs : I. Ghorayeb ; P O Fernagut ; I. Aubert ; E. Bezard ; W. Poewe ; G K Wenning ; F. TisonSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2000.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, 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), Macaca fascicularis, Male, Multiple System Atrophy (chemically induced), Multiple System Atrophy (pathology), Multiple System Atrophy (physiopathology), Nerve Degeneration (chemically induced), Nerve Degeneration (pathology), Nerve Degeneration (physiopathology), Neurotoxins, Nitro Compounds, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (pathology), Parkinson Disease, Secondary (physiopathology), Propionates, Striatonigral Degeneration (chemically induced), Striatonigral Degeneration (pathology), Striatonigral Degeneration (physiopathology).
- 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.
PubMed: 10830420
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Poewe</name></author><author><name sortKey="Wenning, G K" sort="Wenning, G K" uniqKey="Wenning G" first="G K" last="Wenning">G K Wenning</name></author><author><name sortKey="Tison, F" sort="Tison, F" uniqKey="Tison F" first="F" last="Tison">F. Tison</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2000">2000</date><idno type="RBID">pubmed:10830420</idno><idno type="pmid">10830420</idno><idno type="wicri:Area/PubMed/Corpus">001320</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001320</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Toward a primate model of L-dopa-unresponsive parkinsonism mimicking striatonigral degeneration.</title><author><name sortKey="Ghorayeb, I" sort="Ghorayeb, I" uniqKey="Ghorayeb I" first="I" last="Ghorayeb">I. Ghorayeb</name><affiliation><nlm:affiliation>CNRS-UMR 5543, Université Victor Segalen Bordeaux 2, France.</nlm:affiliation></affiliation></author><author><name sortKey="Fernagut, P O" sort="Fernagut, P O" uniqKey="Fernagut P" first="P O" last="Fernagut">P O Fernagut</name></author><author><name sortKey="Aubert, I" sort="Aubert, I" uniqKey="Aubert I" first="I" last="Aubert">I. Aubert</name></author><author><name sortKey="Bezard, E" sort="Bezard, E" uniqKey="Bezard E" first="E" last="Bezard">E. Bezard</name></author><author><name sortKey="Poewe, W" sort="Poewe, W" uniqKey="Poewe W" first="W" last="Poewe">W. Poewe</name></author><author><name sortKey="Wenning, G K" sort="Wenning, G K" uniqKey="Wenning G" first="G K" last="Wenning">G K Wenning</name></author><author><name sortKey="Tison, F" sort="Tison, F" uniqKey="Tison F" first="F" last="Tison">F. Tison</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2000" type="published">2000</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</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>Macaca fascicularis</term><term>Male</term><term>Multiple System Atrophy (chemically induced)</term><term>Multiple System Atrophy (pathology)</term><term>Multiple System Atrophy (physiopathology)</term><term>Nerve Degeneration (chemically induced)</term><term>Nerve Degeneration (pathology)</term><term>Nerve Degeneration (physiopathology)</term><term>Neurotoxins</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>Propionates</term><term>Striatonigral Degeneration (chemically induced)</term><term>Striatonigral Degeneration (pathology)</term><term>Striatonigral Degeneration (physiopathology)</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></textClass></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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10830420</PMID><DateCreated><Year>2000</Year><Month>10</Month><Day>02</Day></DateCreated><DateCompleted><Year>2000</Year><Month>10</Month><Day>02</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>15</Volume><Issue>3</Issue><PubDate><Year>2000</Year><Month>May</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Toward a primate model of L-dopa-unresponsive parkinsonism mimicking striatonigral degeneration.</ArticleTitle><Pagination><MedlinePgn>531-6</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ghorayeb</LastName><ForeName>I</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>CNRS-UMR 5543, Université Victor Segalen Bordeaux 2, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fernagut</LastName><ForeName>P O</ForeName><Initials>PO</Initials></Author><Author ValidYN="Y"><LastName>Aubert</LastName><ForeName>I</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Bezard</LastName><ForeName>E</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Poewe</LastName><ForeName>W</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Wenning</LastName><ForeName>G K</ForeName><Initials>GK</Initials></Author><Author ValidYN="Y"><LastName>Tison</LastName><ForeName>F</ForeName><Initials>F</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009498">Neurotoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009574">Nitro Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011422">Propionates</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>9P21XSP91P</RegistryNumber><NameOfSubstance UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</NameOfSubstance></Chemical><Chemical><RegistryNumber>QY4L0FOX0D</RegistryNumber><NameOfSubstance UI="C015392">3-nitropropionic acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D015632" MajorTopicYN="N">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName 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UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008252" MajorTopicYN="N">Macaca fascicularis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019578" MajorTopicYN="N">Multiple System Atrophy</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009410" MajorTopicYN="N">Nerve Degeneration</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009498" MajorTopicYN="N">Neurotoxins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009574" MajorTopicYN="N">Nitro Compounds</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011422" MajorTopicYN="N">Propionates</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020955" MajorTopicYN="N">Striatonigral Degeneration</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2000</Year><Month>6</Month><Day>1</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2000</Year><Month>10</Month><Day>7</Day><Hour>11</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2000</Year><Month>6</Month><Day>1</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10830420</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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