A chronic MPTP model reproducing the slow evolution of Parkinson's disease: evolution of motor symptoms in the monkey.
Identifieur interne : 001517 ( PubMed/Corpus ); précédent : 001516; suivant : 001518A chronic MPTP model reproducing the slow evolution of Parkinson's disease: evolution of motor symptoms in the monkey.
Auteurs : E. Bezard ; C. Imbert ; X. Deloire ; B. Bioulac ; C E GrossSource :
- Brain research [ 0006-8993 ] ; 1997.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Animals, Antiparkinson Agents (pharmacology), Cell Count, Chronic Disease, Disease Models, Animal, Disease Progression, Dopamine Agents, Levodopa (pharmacology), Macaca fascicularis, Movement (physiology), Neurons (cytology), Neurons (enzymology), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (drug therapy), Parkinson Disease, Secondary (physiopathology), Tyrosine 3-Monooxygenase (analysis).
- MESH :
- chemical , analysis : Tyrosine 3-Monooxygenase.
- chemical , pharmacology : Antiparkinson Agents, Levodopa.
- chemical : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Dopamine Agents.
- chemically induced : Parkinson Disease, Secondary.
- cytology : Neurons.
- drug therapy : Parkinson Disease, Secondary.
- enzymology : Neurons.
- physiology : Movement.
- physiopathology : Parkinson Disease, Secondary.
- Animals, Cell Count, Chronic Disease, Disease Models, Animal, Disease Progression, Macaca fascicularis.
Abstract
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown to induce parkinsonism both in man and non-human primates. Several models have now been developed, but acute MPTP administration does not consistently reproduce all the clinical features of the disease. To mirror the slow evolution observed in human pathology, a chronic model of intoxication is necessary. The present study describes a chronic MPTP protocol in the monkey. Six monkeys received daily injections of MPTP (0.2 mg/kg i.v.) until they reached a score over 8 on the clinical rating scale (15.5 days +/- 1.1). Full parkinsonism was first obtained on the 22nd day. Levodopa testing (20 mg/kg per os) alleviated motor abnormalities (51%), proving the parkinsonian nature of these disturbances. Histological lesions reproduced those observed in Parkinson's disease with a decrease in tyrosine hydroxylase immunoreactivity of 90%. This model so could be of great interest for the study of the dynamic physiopathological changes which occur in Parkinson's disease and consequently for research on new neuroprotective therapies.
PubMed: 9359593
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Bioulac</name></author><author><name sortKey="Gross, C E" sort="Gross, C E" uniqKey="Gross C" first="C E" last="Gross">C E Gross</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1997">1997</date><idno type="RBID">pubmed:9359593</idno><idno type="pmid">9359593</idno><idno type="wicri:Area/PubMed/Corpus">001517</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001517</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">A chronic MPTP model reproducing the slow evolution of Parkinson's disease: evolution of motor symptoms in the monkey.</title><author><name sortKey="Bezard, E" sort="Bezard, E" uniqKey="Bezard E" first="E" last="Bezard">E. Bezard</name><affiliation><nlm:affiliation>Laboratoire de Neurophysiologie, CNRS UMR 5543, Université de Bordeaux II, France. erwan.bezard@umr5543.u-bordeaux2.fr</nlm:affiliation></affiliation></author><author><name sortKey="Imbert, C" sort="Imbert, C" uniqKey="Imbert C" first="C" last="Imbert">C. Imbert</name></author><author><name sortKey="Deloire, X" sort="Deloire, X" uniqKey="Deloire X" first="X" last="Deloire">X. Deloire</name></author><author><name sortKey="Bioulac, B" sort="Bioulac, B" uniqKey="Bioulac B" first="B" last="Bioulac">B. Bioulac</name></author><author><name sortKey="Gross, C E" sort="Gross, C E" uniqKey="Gross C" first="C E" last="Gross">C E Gross</name></author></analytic><series><title level="j">Brain research</title><idno type="ISSN">0006-8993</idno><imprint><date when="1997" type="published">1997</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>Cell Count</term><term>Chronic Disease</term><term>Disease Models, Animal</term><term>Disease Progression</term><term>Dopamine Agents</term><term>Levodopa (pharmacology)</term><term>Macaca fascicularis</term><term>Movement (physiology)</term><term>Neurons (cytology)</term><term>Neurons (enzymology)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (drug therapy)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Tyrosine 3-Monooxygenase (analysis)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Tyrosine 3-Monooxygenase</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>Dopamine Agents</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Movement</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Count</term><term>Chronic Disease</term><term>Disease Models, Animal</term><term>Disease Progression</term><term>Macaca fascicularis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown to induce parkinsonism both in man and non-human primates. Several models have now been developed, but acute MPTP administration does not consistently reproduce all the clinical features of the disease. To mirror the slow evolution observed in human pathology, a chronic model of intoxication is necessary. The present study describes a chronic MPTP protocol in the monkey. Six monkeys received daily injections of MPTP (0.2 mg/kg i.v.) until they reached a score over 8 on the clinical rating scale (15.5 days +/- 1.1). Full parkinsonism was first obtained on the 22nd day. Levodopa testing (20 mg/kg per os) alleviated motor abnormalities (51%), proving the parkinsonian nature of these disturbances. Histological lesions reproduced those observed in Parkinson's disease with a decrease in tyrosine hydroxylase immunoreactivity of 90%. This model so could be of great interest for the study of the dynamic physiopathological changes which occur in Parkinson's disease and consequently for research on new neuroprotective therapies.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9359593</PMID><DateCreated><Year>1998</Year><Month>01</Month><Day>02</Day></DateCreated><DateCompleted><Year>1998</Year><Month>01</Month><Day>02</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0006-8993</ISSN><JournalIssue CitedMedium="Print"><Volume>766</Volume><Issue>1-2</Issue><PubDate><Year>1997</Year><Month>Aug</Month><Day>22</Day></PubDate></JournalIssue><Title>Brain research</Title><ISOAbbreviation>Brain Res.</ISOAbbreviation></Journal><ArticleTitle>A chronic MPTP model reproducing the slow evolution of Parkinson's disease: evolution of motor symptoms in the monkey.</ArticleTitle><Pagination><MedlinePgn>107-12</MedlinePgn></Pagination><Abstract><AbstractText>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown to induce parkinsonism both in man and non-human primates. Several models have now been developed, but acute MPTP administration does not consistently reproduce all the clinical features of the disease. To mirror the slow evolution observed in human pathology, a chronic model of intoxication is necessary. The present study describes a chronic MPTP protocol in the monkey. Six monkeys received daily injections of MPTP (0.2 mg/kg i.v.) until they reached a score over 8 on the clinical rating scale (15.5 days +/- 1.1). Full parkinsonism was first obtained on the 22nd day. Levodopa testing (20 mg/kg per os) alleviated motor abnormalities (51%), proving the parkinsonian nature of these disturbances. Histological lesions reproduced those observed in Parkinson's disease with a decrease in tyrosine hydroxylase immunoreactivity of 90%. This model so could be of great interest for the study of the dynamic physiopathological changes which occur in Parkinson's disease and consequently for research on new neuroprotective therapies.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bezard</LastName><ForeName>E</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Laboratoire de Neurophysiologie, CNRS UMR 5543, Université de Bordeaux II, France. erwan.bezard@umr5543.u-bordeaux2.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Imbert</LastName><ForeName>C</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Deloire</LastName><ForeName>X</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Bioulac</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Gross</LastName><ForeName>C E</ForeName><Initials>CE</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>Netherlands</Country><MedlineTA>Brain Res</MedlineTA><NlmUniqueID>0045503</NlmUniqueID><ISSNLinking>0006-8993</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015259">Dopamine Agents</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>EC 1.14.16.2</RegistryNumber><NameOfSubstance UI="D014446">Tyrosine 3-Monooxygenase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D015632" MajorTopicYN="Y">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 UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002452" MajorTopicYN="N">Cell Count</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002908" MajorTopicYN="N">Chronic Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015259" MajorTopicYN="Y">Dopamine Agents</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008252" MajorTopicYN="N">Macaca fascicularis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009068" MajorTopicYN="N">Movement</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014446" MajorTopicYN="N">Tyrosine 3-Monooxygenase</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1997</Year><Month>8</Month><Day>22</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1997</Year><Month>11</Month><Day>14</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1997</Year><Month>8</Month><Day>22</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9359593</ArticleId><ArticleId IdType="pii">S0006-8993(97)00531-3</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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