Rat model of Parkinson's disease with bilateral motor abnormalities, reversible with levodopa, and dyskinesias
Identifieur interne : 001641 ( Main/Corpus ); précédent : 001640; suivant : 001642Rat model of Parkinson's disease with bilateral motor abnormalities, reversible with levodopa, and dyskinesias
Auteurs : Vincent Paillé ; Vincent Henry ; Laurent Lescaudron ; Philippe Brachet ; Philippe DamierSource :
- Movement Disorders [ 0885-3185 ] ; 2007-03-15.
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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. © 2006 Movement Disorder Society
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DOI: 10.1002/mds.21308
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ISTEX:E5D74CA8A007AC9F0101A7596D921ED625C80D09Le document en format XML
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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. © 2006 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Vincent Paillé PhD</name><affiliations><json:string>INSERM, UMR 643 and Institut de Transplantation et de Recherche en Transplantation, CHU, Nantes, France</json:string><json:string>UFR de Médecine,Université de Nantes, Nantes, France</json:string></affiliations></json:item><json:item><name>Vincent Henry MS</name><affiliations><json:string>INSERM, UMR 643 and Institut de Transplantation et de Recherche en Transplantation, CHU, Nantes, France</json:string><json:string>UFR de Médecine,Université de Nantes, Nantes, France</json:string></affiliations></json:item><json:item><name>Laurent Lescaudron PhD</name><affiliations><json:string>INSERM, UMR 643 and Institut de Transplantation et de Recherche en Transplantation, CHU, Nantes, France</json:string><json:string>UFR des Sciences et des Techniques,Université de Nantes, Nantes, France</json:string></affiliations></json:item><json:item><name>Philippe Brachet PhD</name><affiliations><json:string>INSERM, UMR 643 and Institut de Transplantation et de Recherche en Transplantation, CHU, Nantes, France</json:string><json:string>UFR de Médecine,Université de Nantes, Nantes, France</json:string></affiliations></json:item><json:item><name>Philippe Damier MD, PhD</name><affiliations><json:string>INSERM, UMR 643 and Institut de Transplantation et de Recherche en Transplantation, CHU, Nantes, France</json:string><json:string>CHU Nantes, Clinique Neurologique and Centre d'Investigation Clinique, Nantes, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>6‐OHDA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dyskinesias</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>levodopa</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>substantia nigra</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>akinesia</value></json:item></subject><articleId><json:string>MDS21308</json:string></articleId><language><json:string>eng</json:string></language><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. 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type="organization"><unparsedAffiliation>UFR de Médecine,Université de Nantes, Nantes, France</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FR" type="organization"><unparsedAffiliation>UFR des Sciences et des Techniques,Université de Nantes, Nantes, France</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="FR" type="organization"><unparsedAffiliation>CHU Nantes, Clinique Neurologique and Centre d'Investigation Clinique, Nantes, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">6‐OHDA</keyword><keyword xml:id="kwd2">dyskinesias</keyword><keyword xml:id="kwd3">levodopa</keyword><keyword xml:id="kwd4">Parkinson's disease</keyword><keyword xml:id="kwd5">substantia nigra</keyword><keyword xml:id="kwd6">akinesia</keyword></keywordGroup><fundingInfo><fundingAgency>INSERM (AVENIR 2001)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Association de parkinsoniens de Loire‐Atlantique (ADPLA)</fundingAgency></fundingInfo><supportingInformation><p> This article contains Supplementary Video, available online at <url href="http://www.interscience.wiley.com/jpages/0885-3185/suppmat"> http://www.interscience.wiley.com/jpages/0885‐3185/suppmat </url></p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds21308:jws-mds"></mediaResource><caption>Forelimb abnormal motor behavior following bilateral lesion assessed by a modified version of the stepping test and improvement of performance during L‐dopa treatment:Segment 1. Stepping test performed by a sham‐lesioned rat (6th day of L‐dopa treatment).Segment 2. Stepping test performed by a rat with bilateral partial lesion (before L‐dopa treatment).Segment 3. Stepping test performed by the same lesioned‐rat during L‐dopa treatment (6th day of treatment).Bilateral dyskinesiasSegment 4. Rat with bilateral 6‐OHDA lesion presenting bilateral forelimb dyskinesias with unilateral dystonia following 6 days of L‐dopa treatment.Segment 5. Orolingual dyskinesias in a 6‐OHDA‐lesioned rat.Segment 6. Unilateral forelimb dyskinesias in a 6‐OHDA‐lesioned rat.</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>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. © 2006 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Rat model of Parkinson's disease with bilateral motor abnormalities, reversible with levodopa, and dyskinesias</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Bilateral Rat Model of Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Rat model of Parkinson's disease with bilateral motor abnormalities, reversible with levodopa, and dyskinesias</title></titleInfo><name type="personal"><namePart type="given">Vincent</namePart><namePart type="family">Paillé</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>INSERM, UMR 643 and Institut de Transplantation et de Recherche en Transplantation, CHU, Nantes, France</affiliation><affiliation>UFR de Médecine,Université de Nantes, Nantes, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Vincent</namePart><namePart type="family">Henry</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>INSERM, UMR 643 and Institut de Transplantation et de Recherche en Transplantation, CHU, Nantes, France</affiliation><affiliation>UFR de Médecine,Université de Nantes, Nantes, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Laurent</namePart><namePart type="family">Lescaudron</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>INSERM, UMR 643 and Institut de Transplantation et de Recherche en Transplantation, CHU, Nantes, France</affiliation><affiliation>UFR des Sciences et des Techniques,Université de Nantes, Nantes, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Philippe</namePart><namePart type="family">Brachet</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>INSERM, UMR 643 and Institut de Transplantation et de Recherche en Transplantation, CHU, Nantes, France</affiliation><affiliation>UFR de Médecine,Université de Nantes, Nantes, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Philippe</namePart><namePart type="family">Damier</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>INSERM, UMR 643 and Institut de Transplantation et de Recherche en Transplantation, CHU, Nantes, France</affiliation><affiliation>CHU Nantes, Clinique Neurologique and Centre d'Investigation Clinique, Nantes, France</affiliation><description>Correspondence: Clinique Neurologique, Hôpital Guillaume et René Laënnec, Boulevard Jacques Monod, F‐44093 Nantes Cedex 01, France</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2007-03-15</dateIssued><dateCaptured encoding="w3cdtf">2006-06-18</dateCaptured><dateValid encoding="w3cdtf">2006-10-04</dateValid><copyrightDate encoding="w3cdtf">2007</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">4</extent><extent unit="references">42</extent><extent unit="words">5251</extent></physicalDescription><abstract 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. © 2006 Movement Disorder Society</abstract><note type="funding">INSERM (AVENIR 2001)</note><note type="funding">Association de parkinsoniens de Loire‐Atlantique (ADPLA)</note><subject lang="en"><genre>Keywords</genre><topic>6‐OHDA</topic><topic>dyskinesias</topic><topic>levodopa</topic><topic>Parkinson's disease</topic><topic>substantia nigra</topic><topic>akinesia</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><note type="content"> This article contains Supplementary Video, available online at http://www.interscience.wiley.com/jpages/0885‐3185/suppmatSupporting Info Item: Forelimb abnormal motor behavior following bilateral lesion assessed by a modified version of the stepping test and improvement of performance during L‐dopa treatment:Segment 1. Stepping test performed by a sham‐lesioned rat (6th day of L‐dopa treatment).Segment 2. Stepping test performed by a rat with bilateral partial lesion (before L‐dopa treatment).Segment 3. Stepping test performed by the same lesioned‐rat during L‐dopa treatment (6th day of treatment).Bilateral dyskinesiasSegment 4. Rat with bilateral 6‐OHDA lesion presenting bilateral forelimb dyskinesias with unilateral dystonia following 6 days of L‐dopa treatment.Segment 5. Orolingual dyskinesias in a 6‐OHDA‐lesioned rat.Segment 6. Unilateral forelimb dyskinesias in a 6‐OHDA‐lesioned rat. - </note><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>533</start><end>539</end><total>7</total></extent></part></relatedItem><identifier type="istex">E5D74CA8A007AC9F0101A7596D921ED625C80D09</identifier><identifier type="DOI">10.1002/mds.21308</identifier><identifier type="ArticleID">MDS21308</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2006 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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