The unilateral 6‐OHDA rat model of Parkinson's disease revisited: an electromyographic and behavioural analysis
Identifieur interne : 002832 ( Main/Corpus ); précédent : 002831; suivant : 002833The unilateral 6‐OHDA rat model of Parkinson's disease revisited: an electromyographic and behavioural analysis
Auteurs : Gerlinde A. Metz ; Arthur Tse ; Mark Ballermann ; Lori K. Smith ; Karim FouadSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2005-08.
English descriptors
- KwdEn :
Abstract
The characteristic locomotor disturbances of Parkinson's disease (PD) include shuffling gait, short steps and low walking velocity. In this study we investigated features of walking and turning in a rat model of PD caused by unilateral infusion of the neurotoxin 6‐hydroxydopamine (6‐OHDA). We assessed gait and electromyographic (EMG) patterns of the ankle flexor tibialis anterior and the knee extensor vastus lateralis of the hindlimb, and triceps brachii of the forelimb, during overgound locomotion, spontaneous rotation (turning) and apomorphine‐induced rotation. When compared with control rats, rats with unilateral dopamine depletion displayed a shuffling gait and short stride lengths. This locomotor pattern was accompanied by prolonged ankle flexor activity on the ipsilateral side, and prolonged activity of knee extensors on the contralateral side. The dopamine depletion also led to enhanced contraversive rotations after an apomorphine challenge. The EMG recordings during drug‐induced rotation suggested that hindlimb stepping was a reflective response to an active drive produced by forelimbs. The EMG recordings of the contralateral side during rotation were marked by reduced ankle flexor activity and increased knee extensor activity. Furthermore, EMG recordings indicated that dopamine‐agonists induce rotational bias by altering the coupling between ipsi‐ and contralateral hindlimbs, and between forelimbs. In straight walking, however, the gait of 6‐OHDA lesion animals reflected normal, coupled hindlimb stepping as controlled by spinal pattern generators. The data suggest that the unilateral rat model of PD resembles key features of human parkinsonian gait, and that asymmetric descending input may underlie the observed changes in gait patterns.
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DOI: 10.1111/j.1460-9568.2005.04238.x
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Metz</name><affiliation><mods:affiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge AB, Canada T1K 3M4</mods:affiliation></affiliation></author><author><name sortKey="Tse, Arthur" sort="Tse, Arthur" uniqKey="Tse A" first="Arthur" last="Tse">Arthur Tse</name><affiliation><mods:affiliation>Centre for Neuroscience</mods:affiliation></affiliation></author><author><name sortKey="Ballermann, Mark" sort="Ballermann, Mark" uniqKey="Ballermann M" first="Mark" last="Ballermann">Mark Ballermann</name><affiliation><mods:affiliation>Centre for Neuroscience</mods:affiliation></affiliation><affiliation><mods:affiliation>Faculty of Rehabilitation Medicine, University of Alberta, Edmonton AB, Canada T6G 2G4</mods:affiliation></affiliation></author><author><name sortKey="Smith, Lori K" sort="Smith, Lori K" uniqKey="Smith L" first="Lori K." last="Smith">Lori K. 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Smith</name><affiliation><mods:affiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge AB, Canada T1K 3M4</mods:affiliation></affiliation></author><author><name sortKey="Fouad, Karim" sort="Fouad, Karim" uniqKey="Fouad K" first="Karim" last="Fouad">Karim Fouad</name><affiliation><mods:affiliation>Centre for Neuroscience</mods:affiliation></affiliation><affiliation><mods:affiliation>Faculty of Rehabilitation Medicine, University of Alberta, Edmonton AB, Canada T6G 2G4</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Neuroscience</title><idno type="ISSN">0953-816X</idno><idno type="eISSN">1460-9568</idno><imprint><publisher>Blackwell Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2005-08">2005-08</date><biblScope unit="volume">22</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="735">735</biblScope><biblScope unit="page" to="744">744</biblScope></imprint><idno type="ISSN">0953-816X</idno></series><idno type="istex">5E8B9F886AFD20959EF0DE88F4249C82871EBFAB</idno><idno type="DOI">10.1111/j.1460-9568.2005.04238.x</idno><idno type="ArticleID">EJN4238</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0953-816X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>EMG</term><term>dopamine depletion</term><term>gait</term><term>locomotion</term><term>movement</term><term>walking</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The characteristic locomotor disturbances of Parkinson's disease (PD) include shuffling gait, short steps and low walking velocity. In this study we investigated features of walking and turning in a rat model of PD caused by unilateral infusion of the neurotoxin 6‐hydroxydopamine (6‐OHDA). We assessed gait and electromyographic (EMG) patterns of the ankle flexor tibialis anterior and the knee extensor vastus lateralis of the hindlimb, and triceps brachii of the forelimb, during overgound locomotion, spontaneous rotation (turning) and apomorphine‐induced rotation. When compared with control rats, rats with unilateral dopamine depletion displayed a shuffling gait and short stride lengths. This locomotor pattern was accompanied by prolonged ankle flexor activity on the ipsilateral side, and prolonged activity of knee extensors on the contralateral side. The dopamine depletion also led to enhanced contraversive rotations after an apomorphine challenge. The EMG recordings during drug‐induced rotation suggested that hindlimb stepping was a reflective response to an active drive produced by forelimbs. The EMG recordings of the contralateral side during rotation were marked by reduced ankle flexor activity and increased knee extensor activity. Furthermore, EMG recordings indicated that dopamine‐agonists induce rotational bias by altering the coupling between ipsi‐ and contralateral hindlimbs, and between forelimbs. In straight walking, however, the gait of 6‐OHDA lesion animals reflected normal, coupled hindlimb stepping as controlled by spinal pattern generators. The data suggest that the unilateral rat model of PD resembles key features of human parkinsonian gait, and that asymmetric descending input may underlie the observed changes in gait patterns.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Gerlinde A. 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In this study we investigated features of walking and turning in a rat model of PD caused by unilateral infusion of the neurotoxin 6‐hydroxydopamine (6‐OHDA). We assessed gait and electromyographic (EMG) patterns of the ankle flexor tibialis anterior and the knee extensor vastus lateralis of the hindlimb, and triceps brachii of the forelimb, during overgound locomotion, spontaneous rotation (turning) and apomorphine‐induced rotation. When compared with control rats, rats with unilateral dopamine depletion displayed a shuffling gait and short stride lengths. This locomotor pattern was accompanied by prolonged ankle flexor activity on the ipsilateral side, and prolonged activity of knee extensors on the contralateral side. The dopamine depletion also led to enhanced contraversive rotations after an apomorphine challenge. The EMG recordings during drug‐induced rotation suggested that hindlimb stepping was a reflective response to an active drive produced by forelimbs. The EMG recordings of the contralateral side during rotation were marked by reduced ankle flexor activity and increased knee extensor activity. Furthermore, EMG recordings indicated that dopamine‐agonists induce rotational bias by altering the coupling between ipsi‐ and contralateral hindlimbs, and between forelimbs. In straight walking, however, the gait of 6‐OHDA lesion animals reflected normal, coupled hindlimb stepping as controlled by spinal pattern generators. The data suggest that the unilateral rat model of PD resembles key features of human parkinsonian gait, and that asymmetric descending input may underlie the observed changes in gait patterns.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>dopamine depletion</term></item><item><term>EMG</term></item><item><term>gait</term></item><item><term>locomotion</term></item><item><term>movement</term></item><item><term>walking</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005-08">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/5E8B9F886AFD20959EF0DE88F4249C82871EBFAB/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Science Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1460-9568</doi><issn type="print">0953-816X</issn><issn type="electronic">1460-9568</issn><idGroup><id type="product" value="EJN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROSCIENCE">European Journal of Neuroscience</title></titleGroup></publicationMeta><publicationMeta level="part" position="08003"><doi origin="wiley">10.1111/ejn.2005.22.issue-3</doi><numberingGroup><numbering type="journalVolume" number="22">22</numbering><numbering type="journalIssue" number="3">3</numbering></numberingGroup><coverDate startDate="2005-08">August 2005</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="20" status="forIssue"><doi origin="wiley">10.1111/j.1460-9568.2005.04238.x</doi><idGroup><id type="unit" value="EJN4238"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="tocHeading1">Research Reports</title></titleGroup><eventGroup><event type="firstOnline" date="2005-08-11"></event><event type="publishedOnlineFinalForm" date="2005-08-11"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.5 mode:FullText source:FullText result:FullText" date="2010-04-07"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-12"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="735">735</numbering><numbering type="pageLast" number="744">744</numbering></numberingGroup><correspondenceTo>Dr G. A. Metz, as above.
E‐mail: <email>gerlinde.metz@uleth.ca</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EJN.EJN4238.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 10 February 2005, revised 28 April 2005, accepted 25 May 2005</unparsedEditorialHistory><countGroup><count type="figureTotal" number="7"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="79"></count><count type="wordTotal" number="5418"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">The unilateral 6‐OHDA rat model of Parkinson's disease revisited: an electromyographic and behavioural analysis</title><title type="shortAuthors">G. A. Metz <i>et al.</i></title><title type="short">Gait patterns after dopamine depletion</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Gerlinde A.</givenNames><familyName>Metz</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>Arthur</givenNames><familyName>Tse</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2 #a3"><personName><givenNames>Mark</givenNames><familyName>Ballermann</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>Lori K.</givenNames><familyName>Smith</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a2 #a3"><personName><givenNames>Karim</givenNames><familyName>Fouad</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="CA"><unparsedAffiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge AB, Canada T1K 3M4</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>Centre for Neuroscience</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="CA"><unparsedAffiliation>Faculty of Rehabilitation Medicine, University of Alberta, Edmonton AB, Canada T6G 2G4</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">dopamine depletion</keyword><keyword xml:id="k2">EMG</keyword><keyword xml:id="k3">gait</keyword><keyword xml:id="k4">locomotion</keyword><keyword xml:id="k5">movement</keyword><keyword xml:id="k6">walking</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The characteristic locomotor disturbances of Parkinson's disease (PD) include shuffling gait, short steps and low walking velocity. In this study we investigated features of walking and turning in a rat model of PD caused by unilateral infusion of the neurotoxin 6‐hydroxydopamine (6‐OHDA). We assessed gait and electromyographic (EMG) patterns of the ankle flexor tibialis anterior and the knee extensor vastus lateralis of the hindlimb, and triceps brachii of the forelimb, during overgound locomotion, spontaneous rotation (turning) and apomorphine‐induced rotation. When compared with control rats, rats with unilateral dopamine depletion displayed a shuffling gait and short stride lengths. This locomotor pattern was accompanied by prolonged ankle flexor activity on the ipsilateral side, and prolonged activity of knee extensors on the contralateral side. The dopamine depletion also led to enhanced contraversive rotations after an apomorphine challenge. The EMG recordings during drug‐induced rotation suggested that hindlimb stepping was a reflective response to an active drive produced by forelimbs. The EMG recordings of the contralateral side during rotation were marked by reduced ankle flexor activity and increased knee extensor activity. Furthermore, EMG recordings indicated that dopamine‐agonists induce rotational bias by altering the coupling between ipsi‐ and contralateral hindlimbs, and between forelimbs. In straight walking, however, the gait of 6‐OHDA lesion animals reflected normal, coupled hindlimb stepping as controlled by spinal pattern generators. The data suggest that the unilateral rat model of PD resembles key features of human parkinsonian gait, and that asymmetric descending input may underlie the observed changes in gait patterns.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The unilateral 6‐OHDA rat model of Parkinson's disease revisited: an electromyographic and behavioural analysis</title></titleInfo><titleInfo type="abbreviated"><title>Gait patterns after dopamine depletion</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The unilateral 6‐OHDA rat model of Parkinson's disease revisited: an electromyographic and behavioural analysis</title></titleInfo><name type="personal"><namePart type="given">Gerlinde A.</namePart><namePart type="family">Metz</namePart><affiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge AB, Canada T1K 3M4</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Arthur</namePart><namePart type="family">Tse</namePart><affiliation>Centre for Neuroscience</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mark</namePart><namePart type="family">Ballermann</namePart><affiliation>Centre for Neuroscience</affiliation><affiliation>Faculty of Rehabilitation Medicine, University of Alberta, Edmonton AB, Canada T6G 2G4</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lori K.</namePart><namePart type="family">Smith</namePart><affiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge AB, Canada T1K 3M4</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Karim</namePart><namePart type="family">Fouad</namePart><affiliation>Centre for Neuroscience</affiliation><affiliation>Faculty of Rehabilitation Medicine, University of Alberta, Edmonton AB, Canada T6G 2G4</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Science Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2005-08</dateIssued><edition>Received 10 February 2005, revised 28 April 2005, accepted 25 May 2005</edition><copyrightDate encoding="w3cdtf">2005</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">7</extent><extent unit="references">79</extent><extent unit="words">5418</extent></physicalDescription><abstract lang="en">The characteristic locomotor disturbances of Parkinson's disease (PD) include shuffling gait, short steps and low walking velocity. In this study we investigated features of walking and turning in a rat model of PD caused by unilateral infusion of the neurotoxin 6‐hydroxydopamine (6‐OHDA). We assessed gait and electromyographic (EMG) patterns of the ankle flexor tibialis anterior and the knee extensor vastus lateralis of the hindlimb, and triceps brachii of the forelimb, during overgound locomotion, spontaneous rotation (turning) and apomorphine‐induced rotation. When compared with control rats, rats with unilateral dopamine depletion displayed a shuffling gait and short stride lengths. This locomotor pattern was accompanied by prolonged ankle flexor activity on the ipsilateral side, and prolonged activity of knee extensors on the contralateral side. The dopamine depletion also led to enhanced contraversive rotations after an apomorphine challenge. The EMG recordings during drug‐induced rotation suggested that hindlimb stepping was a reflective response to an active drive produced by forelimbs. The EMG recordings of the contralateral side during rotation were marked by reduced ankle flexor activity and increased knee extensor activity. Furthermore, EMG recordings indicated that dopamine‐agonists induce rotational bias by altering the coupling between ipsi‐ and contralateral hindlimbs, and between forelimbs. In straight walking, however, the gait of 6‐OHDA lesion animals reflected normal, coupled hindlimb stepping as controlled by spinal pattern generators. The data suggest that the unilateral rat model of PD resembles key features of human parkinsonian gait, and that asymmetric descending input may underlie the observed changes in gait patterns.</abstract><subject lang="en"><genre>Keywords</genre><topic>dopamine depletion</topic><topic>EMG</topic><topic>gait</topic><topic>locomotion</topic><topic>movement</topic><topic>walking</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neuroscience</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0953-816X</identifier><identifier type="eISSN">1460-9568</identifier><identifier type="DOI">10.1111/(ISSN)1460-9568</identifier><identifier type="PublisherID">EJN</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>735</start><end>744</end><total>10</total></extent></part></relatedItem><identifier type="istex">5E8B9F886AFD20959EF0DE88F4249C82871EBFAB</identifier><identifier type="DOI">10.1111/j.1460-9568.2005.04238.x</identifier><identifier type="ArticleID">EJN4238</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Science Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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