Loss of dopaminergic responsiveness in a double lesion rat model of the Parkinson variant of multiple system atrophy.
Identifieur interne : 002737 ( PubMed/Checkpoint ); précédent : 002736; suivant : 002738Loss of dopaminergic responsiveness in a double lesion rat model of the Parkinson variant of multiple system atrophy.
Auteurs : Martin Köllensperger [Autriche] ; Nadia Stefanova ; Markus Reindl ; Werner Poewe [Autriche] ; Gregor K. WenningSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2007.
English descriptors
- KwdEn :
- Analysis of Variance, Animals, Apomorphine (pharmacology), Behavior, Animal (drug effects), Disease Models, Animal, Functional Laterality, Levodopa (therapeutic use), Male, Multiple System Atrophy (chemically induced), Multiple System Atrophy (drug therapy), Multiple System Atrophy (pathology), Multiple System Atrophy (physiopathology), Oxidopamine, Parkinsonian Disorders (chemically induced), Parkinsonian Disorders (drug therapy), Parkinsonian Disorders (pathology), Parkinsonian Disorders (physiopathology), Rats, Rats, Wistar, Substantia Nigra (drug effects), Substantia Nigra (pathology).
- MESH :
- chemical , pharmacology : Apomorphine.
- chemically induced : Multiple System Atrophy, Parkinsonian Disorders.
- drug effects : Behavior, Animal, Substantia Nigra.
- drug therapy : Multiple System Atrophy, Parkinsonian Disorders.
- pathology : Multiple System Atrophy, Parkinsonian Disorders, Substantia Nigra.
- physiopathology : Multiple System Atrophy, Parkinsonian Disorders.
- chemical , therapeutic use : Levodopa.
- Analysis of Variance, Animals, Disease Models, Animal, Functional Laterality, Male, Oxidopamine, Rats, Rats, Wistar.
Abstract
The Parkinson variant of multiple system atrophy (MSA-P) is a distinct atypical parkinsonian disorder with a loss of dopaminergic neurons comparable to that found in Parkinson's disease (PD). The additional loss of striatopallidal projections is thought to account for levodopa unresponsiveness in MSA-P. Whereas histological features of MSA-P have been successfully reproduced in the double lesion rat model, loss of levodopa responsiveness has so far not been demonstrated. In the current study, 6-hydroxydopamine (6-OHDA) induced unilateral lesions of the substantia nigra produced a marked contralateral forelimb stepping deficit, which improved significantly after challenge with levodopa (P < 0.001). This response was abolished by the subsequent striatal quinolinic acid (QA) lesion. In the cylinder test, the marked asymmetry observed after 6-OHDA lesioning was reversed by levodopa to baseline levels. After QA, cylinder test performance under levodopa failed to reach baseline (P = 0.001) or 6-OHDA + levodopa (P = 0.002) levels. Nigral cell loss (90% +/- 5%) correlated with both stepping test (r = 0.608; P = 0.008) and cylinder test results (r = 0.656; P = 0.005). Lesion extent of the dorsal striatum correlated significantly with the loss of levodopa response (r = 0.593; P = 0.01) in the stepping test. These findings contribute further to the behavioral characterization of the double lesion rat model of MSA, improving its value in the evaluation of future neurorestorative strategies.
DOI: 10.1002/mds.21251
PubMed: 17149724
Affiliations:
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Wenning</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="doi">10.1002/mds.21251</idno><idno type="RBID">pubmed:17149724</idno><idno type="pmid">17149724</idno><idno type="wicri:Area/PubMed/Corpus">002944</idno><idno type="wicri:Area/PubMed/Curation">002944</idno><idno type="wicri:Area/PubMed/Checkpoint">002737</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Loss of dopaminergic responsiveness in a double lesion rat model of the Parkinson variant of multiple system atrophy.</title><author><name sortKey="Kollensperger, Martin" sort="Kollensperger, Martin" uniqKey="Kollensperger M" first="Martin" last="Köllensperger">Martin Köllensperger</name><affiliation wicri:level="1"><nlm:affiliation>Clinical Department of Neurology, Innsbruck Medical University, Austria.</nlm:affiliation><country xml:lang="fr">Autriche</country><wicri:regionArea>Clinical Department of Neurology, Innsbruck Medical University</wicri:regionArea><wicri:noRegion>Innsbruck Medical University</wicri:noRegion></affiliation></author><author><name sortKey="Stefanova, Nadia" sort="Stefanova, Nadia" uniqKey="Stefanova N" first="Nadia" last="Stefanova">Nadia Stefanova</name></author><author><name sortKey="Reindl, Markus" sort="Reindl, Markus" uniqKey="Reindl M" first="Markus" last="Reindl">Markus Reindl</name></author><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><affiliation><country>Autriche</country><placeName><settlement type="city">Innsbruck</settlement><region nuts="2" type="region">Tyrol (Land)</region></placeName><orgName type="university">Université de médecine d'Innsbruck</orgName></affiliation></author><author><name sortKey="Wenning, Gregor K" sort="Wenning, Gregor K" uniqKey="Wenning G" first="Gregor K" last="Wenning">Gregor K. Wenning</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="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Analysis of Variance</term><term>Animals</term><term>Apomorphine (pharmacology)</term><term>Behavior, Animal (drug effects)</term><term>Disease Models, Animal</term><term>Functional Laterality</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Multiple System Atrophy (chemically induced)</term><term>Multiple System Atrophy (drug therapy)</term><term>Multiple System Atrophy (pathology)</term><term>Multiple System Atrophy (physiopathology)</term><term>Oxidopamine</term><term>Parkinsonian Disorders (chemically induced)</term><term>Parkinsonian Disorders (drug therapy)</term><term>Parkinsonian Disorders (pathology)</term><term>Parkinsonian Disorders (physiopathology)</term><term>Rats</term><term>Rats, Wistar</term><term>Substantia Nigra (drug effects)</term><term>Substantia Nigra (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Apomorphine</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Multiple System Atrophy</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Behavior, Animal</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Multiple System Atrophy</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Multiple System Atrophy</term><term>Parkinsonian Disorders</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Multiple System Atrophy</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term><term>Animals</term><term>Disease Models, Animal</term><term>Functional Laterality</term><term>Male</term><term>Oxidopamine</term><term>Rats</term><term>Rats, Wistar</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The Parkinson variant of multiple system atrophy (MSA-P) is a distinct atypical parkinsonian disorder with a loss of dopaminergic neurons comparable to that found in Parkinson's disease (PD). The additional loss of striatopallidal projections is thought to account for levodopa unresponsiveness in MSA-P. Whereas histological features of MSA-P have been successfully reproduced in the double lesion rat model, loss of levodopa responsiveness has so far not been demonstrated. In the current study, 6-hydroxydopamine (6-OHDA) induced unilateral lesions of the substantia nigra produced a marked contralateral forelimb stepping deficit, which improved significantly after challenge with levodopa (P < 0.001). This response was abolished by the subsequent striatal quinolinic acid (QA) lesion. In the cylinder test, the marked asymmetry observed after 6-OHDA lesioning was reversed by levodopa to baseline levels. After QA, cylinder test performance under levodopa failed to reach baseline (P = 0.001) or 6-OHDA + levodopa (P = 0.002) levels. Nigral cell loss (90% +/- 5%) correlated with both stepping test (r = 0.608; P = 0.008) and cylinder test results (r = 0.656; P = 0.005). Lesion extent of the dorsal striatum correlated significantly with the loss of levodopa response (r = 0.593; P = 0.01) in the stepping test. These findings contribute further to the behavioral characterization of the double lesion rat model of MSA, improving its value in the evaluation of future neurorestorative strategies.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">17149724</PMID><DateCreated><Year>2007</Year><Month>03</Month><Day>06</Day></DateCreated><DateCompleted><Year>2007</Year><Month>05</Month><Day>01</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>22</Volume><Issue>3</Issue><PubDate><Year>2007</Year><Month>Feb</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Loss of dopaminergic responsiveness in a double lesion rat model of the Parkinson variant of multiple system atrophy.</ArticleTitle><Pagination><MedlinePgn>353-8</MedlinePgn></Pagination><Abstract><AbstractText>The Parkinson variant of multiple system atrophy (MSA-P) is a distinct atypical parkinsonian disorder with a loss of dopaminergic neurons comparable to that found in Parkinson's disease (PD). The additional loss of striatopallidal projections is thought to account for levodopa unresponsiveness in MSA-P. Whereas histological features of MSA-P have been successfully reproduced in the double lesion rat model, loss of levodopa responsiveness has so far not been demonstrated. In the current study, 6-hydroxydopamine (6-OHDA) induced unilateral lesions of the substantia nigra produced a marked contralateral forelimb stepping deficit, which improved significantly after challenge with levodopa (P < 0.001). This response was abolished by the subsequent striatal quinolinic acid (QA) lesion. In the cylinder test, the marked asymmetry observed after 6-OHDA lesioning was reversed by levodopa to baseline levels. After QA, cylinder test performance under levodopa failed to reach baseline (P = 0.001) or 6-OHDA + levodopa (P = 0.002) levels. Nigral cell loss (90% +/- 5%) correlated with both stepping test (r = 0.608; P = 0.008) and cylinder test results (r = 0.656; P = 0.005). Lesion extent of the dorsal striatum correlated significantly with the loss of levodopa response (r = 0.593; P = 0.01) in the stepping test. These findings contribute further to the behavioral characterization of the double lesion rat model of MSA, improving its value in the evaluation of future neurorestorative strategies.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Köllensperger</LastName><ForeName>Martin</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Clinical Department of Neurology, Innsbruck Medical University, Austria.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stefanova</LastName><ForeName>Nadia</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Reindl</LastName><ForeName>Markus</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Poewe</LastName><ForeName>Werner</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Wenning</LastName><ForeName>Gregor K</ForeName><Initials>GK</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P 17905-B05</GrantID><Agency>Austrian Science Fund FWF</Agency><Country>Austria</Country></Grant></GrantList><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>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>8HW4YBZ748</RegistryNumber><NameOfSubstance UI="D016627">Oxidopamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>N21FAR7B4S</RegistryNumber><NameOfSubstance UI="D001058">Apomorphine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000704">Analysis of Variance</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001058">Apomorphine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000494">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001522">Behavior, Animal</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004195">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D007839">Functional Laterality</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007980">Levodopa</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D019578">Multiple System Atrophy</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000139">chemically induced</QualifierName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016627">Oxidopamine</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020734">Parkinsonian Disorders</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000139">chemically induced</QualifierName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051381">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017208">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013378">Substantia Nigra</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>12</Month><Day>7</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>5</Month><Day>2</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>12</Month><Day>7</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.21251</ArticleId><ArticleId IdType="pubmed">17149724</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Autriche</li></country><region><li>Tyrol (Land)</li></region><settlement><li>Innsbruck</li></settlement><orgName><li>Université de médecine d'Innsbruck</li></orgName></list><tree><noCountry><name sortKey="Reindl, Markus" sort="Reindl, Markus" uniqKey="Reindl M" first="Markus" last="Reindl">Markus Reindl</name><name sortKey="Stefanova, Nadia" sort="Stefanova, Nadia" uniqKey="Stefanova N" first="Nadia" last="Stefanova">Nadia Stefanova</name><name sortKey="Wenning, Gregor K" sort="Wenning, Gregor K" uniqKey="Wenning G" first="Gregor K" last="Wenning">Gregor K. Wenning</name></noCountry><country name="Autriche"><noRegion><name sortKey="Kollensperger, Martin" sort="Kollensperger, Martin" uniqKey="Kollensperger M" first="Martin" last="Köllensperger">Martin Köllensperger</name></noRegion><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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