Paroxysmal dyskinesias in mice
Identifieur interne : 002958 ( Istex/Corpus ); précédent : 002957; suivant : 002959Paroxysmal dyskinesias in mice
Auteurs : Thomas L. Shirley ; Lekha M. Rao ; Ellen J. Hess ; H. A. JinnahSource :
- Movement Disorders [ 0885-3185 ] ; 2008-01-30.
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- KwdEn :
Abstract
Animal models of human disease are important tools for revealing the underlying mechanisms of pathophysiology and developing therapeutic strategies. Several unique mouse calcium channel mutants have been identified with nonepileptic, episodic dyskinetic movements that are phenotypically similar to human paroxysmal dyskinesias. In this report, video demonstrations of these motor attacks are provided for two previously described mouse mutants, tottering and lethargic, as well as a new one, rocker. Semiquantitative comparisons using two different rating scales reveal differences in attack morphology, severity, and duration among the strains. These mice provide three independent models of paroxysmal dyskinesia and support for prior proposals that channelopathies may underlie the human disorders. © 2007 Movement Disorder Society
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DOI: 10.1002/mds.21829
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ISTEX:BC5FF097585FB0A2A2D5F037E0FDF67F796B3BB5Le document en format XML
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Several unique mouse calcium channel mutants have been identified with nonepileptic, episodic dyskinetic movements that are phenotypically similar to human paroxysmal dyskinesias. In this report, video demonstrations of these motor attacks are provided for two previously described mouse mutants, tottering and lethargic, as well as a new one, rocker. Semiquantitative comparisons using two different rating scales reveal differences in attack morphology, severity, and duration among the strains. These mice provide three independent models of paroxysmal dyskinesia and support for prior proposals that channelopathies may underlie the human disorders. © 2007 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Thomas L. Shirley PhD</name><affiliations><json:string>Department of Neurology, Johns Hopkins University, Baltimore, Maryland, USA</json:string></affiliations></json:item><json:item><name>Lekha M. Rao MD</name><affiliations><json:string>Department of Neurology, Johns Hopkins University, Baltimore, Maryland, USA</json:string></affiliations></json:item><json:item><name>Ellen J. Hess PhD</name><affiliations><json:string>Department of Neurology, Johns Hopkins University, Baltimore, Maryland, USA</json:string></affiliations></json:item><json:item><name>H. A. 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A.</givenNames> <familyName>Jinnah</familyName> <degrees>MD, PhD</degrees> </personName> <contactDetails> <email>hjinnah@jhmi.edu</email> </contactDetails> </creator> </creators> <affiliationGroup> <affiliation xml:id="af1" countryCode="US" type="organization"> <unparsedAffiliation>Department of Neurology, Johns Hopkins University, Baltimore, Maryland, USA</unparsedAffiliation> </affiliation> </affiliationGroup> <keywordGroup xml:lang="en" type="author"> <keyword xml:id="kwd1">tottering</keyword> <keyword xml:id="kwd2">lethargic</keyword> <keyword xml:id="kwd3">rocker</keyword> <keyword xml:id="kwd4">paroxysmal dyskinesia</keyword> <keyword xml:id="kwd5">dystonia</keyword> <keyword xml:id="kwd6">channelopathy</keyword> </keywordGroup> <fundingInfo> <fundingAgency>NIH</fundingAgency> <fundingNumber>F32 NS52040</fundingNumber> <fundingNumber>R01 NS40470</fundingNumber> <fundingNumber>R01 NS33592</fundingNumber> </fundingInfo> <fundingInfo> <fundingAgency>Bachmann‐Strauss Dystonia & Parkinson Foundation</fundingAgency> </fundingInfo> <supportingInformation> <p> This article includes supplementary video clips, 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:mds21829:mds21829"></mediaResource> <caption>The first of three video segments is shown as the earlyview video segment for this article. Segment 1.The first segment of this clip shows a tottering mouse at baseline. It walks and rears with a slightly tremulous and unsteady gait. The second segment shows the early phase of an attack involving predominantly the hind limbs and caudal body. The second segment shows full body involvement at the peak of an attack. The third segment shows the late phase of an attack with predominant involvement of the forelimbs, head, neck, and jaw (Adapted from Hess and Jinnah 38 ).</caption> </supportingInfoItem> </supportingInformation> <abstractGroup> <abstract type="main" xml:lang="en"> <title type="main">Abstract</title> <p>Animal models of human disease are important tools for revealing the underlying mechanisms of pathophysiology and developing therapeutic strategies. Several unique mouse calcium channel mutants have been identified with nonepileptic, episodic dyskinetic movements that are phenotypically similar to human paroxysmal dyskinesias. In this report, video demonstrations of these motor attacks are provided for two previously described mouse mutants, tottering and lethargic, as well as a new one, rocker. Semiquantitative comparisons using two different rating scales reveal differences in attack morphology, severity, and duration among the strains. These mice provide three independent models of paroxysmal dyskinesia and support for prior proposals that channelopathies may underlie the human disorders. © 2007 Movement Disorder Society</p> </abstract> </abstractGroup> </contentMeta> </header> </component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Paroxysmal dyskinesias in mice</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Paroxysmal Dyskinesias in Mice</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Paroxysmal dyskinesias in mice</title></titleInfo><name type="personal"><namePart type="given">Thomas L.</namePart><namePart type="family">Shirley</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Johns Hopkins University, Baltimore, Maryland, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lekha M.</namePart><namePart type="family">Rao</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Johns Hopkins University, Baltimore, Maryland, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ellen J.</namePart><namePart type="family">Hess</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Johns Hopkins University, Baltimore, Maryland, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H. A.</namePart><namePart type="family">Jinnah</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Johns Hopkins University, Baltimore, Maryland, USA</affiliation><description>Correspondence: Meyer 6‐181, Johns Hopkins University, Baltimore, Maryland 21287</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2008-01-30</dateIssued><dateCaptured encoding="w3cdtf">2007-07-19</dateCaptured><dateValid encoding="w3cdtf">2007-10-08</dateValid><copyrightDate encoding="w3cdtf">2008</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">2</extent><extent unit="references">38</extent><extent unit="words">3950</extent></physicalDescription><abstract lang="en">Animal models of human disease are important tools for revealing the underlying mechanisms of pathophysiology and developing therapeutic strategies. Several unique mouse calcium channel mutants have been identified with nonepileptic, episodic dyskinetic movements that are phenotypically similar to human paroxysmal dyskinesias. In this report, video demonstrations of these motor attacks are provided for two previously described mouse mutants, tottering and lethargic, as well as a new one, rocker. Semiquantitative comparisons using two different rating scales reveal differences in attack morphology, severity, and duration among the strains. These mice provide three independent models of paroxysmal dyskinesia and support for prior proposals that channelopathies may underlie the human disorders. © 2007 Movement Disorder Society</abstract><note type="funding">NIH - No. F32 NS52040; No. R01 NS40470; No. R01 NS33592; </note><note type="funding">Bachmann‐Strauss Dystonia & Parkinson Foundation</note><subject lang="en"><genre>Keywords</genre><topic>tottering</topic><topic>lethargic</topic><topic>rocker</topic><topic>paroxysmal dyskinesia</topic><topic>dystonia</topic><topic>channelopathy</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><note type="content"> This article includes supplementary video clips, available online at http://www.interscience.wiley.com/jpages/0885‐3185/suppmatSupporting Info Item: The first of three video segments is shown as the earlyview video segment for this article. Segment 1.The first segment of this clip shows a tottering mouse at baseline. It walks and rears with a slightly tremulous and unsteady gait. The second segment shows the early phase of an attack involving predominantly the hind limbs and caudal body. The second segment shows full body involvement at the peak of an attack. The third segment shows the late phase of an attack with predominant involvement of the forelimbs, head, neck, and jaw (Adapted from Hess and Jinnah 38 ). - </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>2008</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>259</start><end>264</end><total>6</total></extent></part></relatedItem><identifier type="istex">BC5FF097585FB0A2A2D5F037E0FDF67F796B3BB5</identifier><identifier type="DOI">10.1002/mds.21829</identifier><identifier type="ArticleID">MDS21829</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2007 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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