Rat model of Parkinson's disease with bilateral motor abnormalities, reversible with levodopa, and dyskinesias.
Identifieur interne : 002597 ( PubMed/Checkpoint ); précédent : 002596; suivant : 002598Rat model of Parkinson's disease with bilateral motor abnormalities, reversible with levodopa, and dyskinesias.
Auteurs : Vincent Paillé [France] ; Vincent Henry ; Laurent Lescaudron ; Philippe Brachet ; Philippe DamierSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2007.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (therapeutic use), Disease Models, Animal, Disease Progression, Dopamine (metabolism), Dyskinesias (diagnosis), Dyskinesias (drug therapy), Dyskinesias (physiopathology), Extremities (physiopathology), Levodopa (therapeutic use), Male, Mesencephalon (metabolism), Mesencephalon (pathology), Nerve Degeneration (metabolism), Nerve Degeneration (pathology), Nerve Degeneration (physiopathology), Parkinson Disease (drug therapy), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Prosencephalon (metabolism), Prosencephalon (pathology), Rats, Rats, Sprague-Dawley, Severity of Illness Index, Substantia Nigra (metabolism), Substantia Nigra (pathology), Tyrosine 3-Monooxygenase (metabolism).
- MESH :
- chemical , metabolism : Dopamine, Tyrosine 3-Monooxygenase.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- diagnosis : Dyskinesias.
- drug therapy : Dyskinesias, Parkinson Disease.
- metabolism : Mesencephalon, Nerve Degeneration, Prosencephalon, Substantia Nigra.
- pathology : Mesencephalon, Nerve Degeneration, Parkinson Disease, Prosencephalon, Substantia Nigra.
- physiopathology : Dyskinesias, Extremities, Nerve Degeneration, Parkinson Disease.
- Animals, Disease Models, Animal, Disease Progression, Male, Rats, Rats, Sprague-Dawley, Severity of Illness Index.
Abstract
Parkinson's disease (PD) is characterized by the bilateral degeneration of the midbrain dopamine-containing neurons with the most severe lesion in the posterolateral part of the substantia nigra pars compacta (SNpc). In humans, such lesions lead to specific motor abnormalities (i.e., akinesia, rigidity, and tremor) that are greatly improved by levodopa treatment. After a few years, the beneficial effect of the treatment is frequently offset by the development of dyskinesias. To improve treatment strategies, an animal model showing most of the histological and clinical characteristics of the human disease is mandatory. Ten rats received a bilateral injection of small doses of 6-OHDA in the medial forebrain bundle (MFB) and were compared with five sham-lesioned rats. The 6-OHDA-lesioned rats progressively developed abnormal motor behavior (assessed by the stepping test) compared with the sham-lesioned rats. The lesioned rats greatly improved under levodopa treatment, but developed concomitant dyskinesias. All 6-OHDA-lesioned animals had bilateral partial lesions of the SNpc, with the most severe lesion being in its posterolateral part. There was a significant correlation between the severity of the dopaminergic cell loss and the severity of the levodopa-induced dyskinesias. These rats constitute an interesting model of PD, sharing some of the main characteristics of the human disease.
DOI: 10.1002/mds.21308
PubMed: 17230470
Affiliations:
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last="Lescaudron">Laurent Lescaudron</name></author><author><name sortKey="Brachet, Philippe" sort="Brachet, Philippe" uniqKey="Brachet P" first="Philippe" last="Brachet">Philippe Brachet</name></author><author><name sortKey="Damier, Philippe" sort="Damier, Philippe" uniqKey="Damier P" first="Philippe" last="Damier">Philippe Damier</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="doi">10.1002/mds.21308</idno><idno type="RBID">pubmed:17230470</idno><idno type="pmid">17230470</idno><idno type="wicri:Area/PubMed/Corpus">002897</idno><idno type="wicri:Area/PubMed/Curation">002897</idno><idno type="wicri:Area/PubMed/Checkpoint">002597</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Rat model of Parkinson's disease with bilateral motor abnormalities, reversible with levodopa, and dyskinesias.</title><author><name sortKey="Paille, Vincent" sort="Paille, Vincent" uniqKey="Paille V" first="Vincent" last="Paillé">Vincent Paillé</name><affiliation wicri:level="1"><nlm:affiliation>INSERM, UMR 643 and Institut de Transplantation et de Recherche en Transplantation, CHU, Nantes, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM, UMR 643 and Institut de Transplantation et de Recherche en Transplantation, CHU, Nantes</wicri:regionArea><placeName><settlement type="city">Nantes</settlement></placeName></affiliation></author><author><name sortKey="Henry, Vincent" sort="Henry, Vincent" uniqKey="Henry V" first="Vincent" last="Henry">Vincent Henry</name></author><author><name sortKey="Lescaudron, Laurent" sort="Lescaudron, Laurent" uniqKey="Lescaudron L" first="Laurent" last="Lescaudron">Laurent Lescaudron</name></author><author><name sortKey="Brachet, Philippe" sort="Brachet, Philippe" uniqKey="Brachet P" first="Philippe" last="Brachet">Philippe Brachet</name></author><author><name sortKey="Damier, Philippe" sort="Damier, Philippe" uniqKey="Damier P" first="Philippe" last="Damier">Philippe Damier</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>Animals</term><term>Antiparkinson Agents (therapeutic use)</term><term>Disease Models, Animal</term><term>Disease Progression</term><term>Dopamine (metabolism)</term><term>Dyskinesias (diagnosis)</term><term>Dyskinesias (drug therapy)</term><term>Dyskinesias (physiopathology)</term><term>Extremities (physiopathology)</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Mesencephalon (metabolism)</term><term>Mesencephalon (pathology)</term><term>Nerve Degeneration (metabolism)</term><term>Nerve Degeneration (pathology)</term><term>Nerve Degeneration 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scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mesencephalon</term><term>Nerve Degeneration</term><term>Prosencephalon</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Mesencephalon</term><term>Nerve Degeneration</term><term>Parkinson Disease</term><term>Prosencephalon</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Dyskinesias</term><term>Extremities</term><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Disease Progression</term><term>Male</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Severity of Illness Index</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is characterized by the bilateral degeneration of the midbrain dopamine-containing neurons with the most severe lesion in the posterolateral part of the substantia nigra pars compacta (SNpc). In humans, such lesions lead to specific motor abnormalities (i.e., akinesia, rigidity, and tremor) that are greatly improved by levodopa treatment. After a few years, the beneficial effect of the treatment is frequently offset by the development of dyskinesias. To improve treatment strategies, an animal model showing most of the histological and clinical characteristics of the human disease is mandatory. Ten rats received a bilateral injection of small doses of 6-OHDA in the medial forebrain bundle (MFB) and were compared with five sham-lesioned rats. The 6-OHDA-lesioned rats progressively developed abnormal motor behavior (assessed by the stepping test) compared with the sham-lesioned rats. The lesioned rats greatly improved under levodopa treatment, but developed concomitant dyskinesias. All 6-OHDA-lesioned animals had bilateral partial lesions of the SNpc, with the most severe lesion being in its posterolateral part. There was a significant correlation between the severity of the dopaminergic cell loss and the severity of the levodopa-induced dyskinesias. These rats constitute an interesting model of PD, sharing some of the main characteristics of the human disease.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">17230470</PMID><DateCreated><Year>2007</Year><Month>04</Month><Day>03</Day></DateCreated><DateCompleted><Year>2007</Year><Month>06</Month><Day>22</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>4</Issue><PubDate><Year>2007</Year><Month>Mar</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. 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Ten rats received a bilateral injection of small doses of 6-OHDA in the medial forebrain bundle (MFB) and were compared with five sham-lesioned rats. The 6-OHDA-lesioned rats progressively developed abnormal motor behavior (assessed by the stepping test) compared with the sham-lesioned rats. The lesioned rats greatly improved under levodopa treatment, but developed concomitant dyskinesias. All 6-OHDA-lesioned animals had bilateral partial lesions of the SNpc, with the most severe lesion being in its posterolateral part. There was a significant correlation between the severity of the dopaminergic cell loss and the severity of the levodopa-induced dyskinesias. 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Index</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013378">Substantia Nigra</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014446">Tyrosine 3-Monooxygenase</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>1</Month><Day>19</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2007</Year><Month>6</Month><Day>23</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>1</Month><Day>19</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.21308</ArticleId><ArticleId IdType="pubmed">17230470</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><settlement><li>Nantes</li></settlement></list><tree><noCountry><name sortKey="Brachet, Philippe" sort="Brachet, Philippe" uniqKey="Brachet P" first="Philippe" last="Brachet">Philippe Brachet</name><name sortKey="Damier, Philippe" sort="Damier, Philippe" uniqKey="Damier P" first="Philippe" last="Damier">Philippe Damier</name><name sortKey="Henry, Vincent" sort="Henry, Vincent" uniqKey="Henry V" first="Vincent" last="Henry">Vincent Henry</name><name sortKey="Lescaudron, Laurent" sort="Lescaudron, Laurent" uniqKey="Lescaudron L" first="Laurent" last="Lescaudron">Laurent Lescaudron</name></noCountry><country name="France"><noRegion><name sortKey="Paille, Vincent" sort="Paille, Vincent" uniqKey="Paille V" first="Vincent" last="Paillé">Vincent Paillé</name></noRegion></country></tree></affiliations></record>Pour 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