Animal models of neurological deficits: how relevant is the rat?
Identifieur interne : 000366 ( Istex/Corpus ); précédent : 000365; suivant : 000367Animal models of neurological deficits: how relevant is the rat?
Auteurs : M. Angela Cenci ; Ian Q. Whishaw ; Timothy SchallertSource :
- Nature Reviews Neuroscience [ 1471-003X ] ; 2002-07.
Abstract
Animal models of neurological deficits are essential for the assessment of new therapeutic options. It has been suggested that rats are not as appropriate as primates for the symptomatic modelling of disease, but a large body of data argues against this view. Comparative analyses of movements in rats and primates show homology of many motor patterns across species. Advances have been made in identifying rat equivalents of akinesia, tremor, postural deficits and dyskinesia, which are relevant to Parkinson's disease. Rat models of hemiplegia, neglect and tactile extinction are useful in assessing the outcome of ischaemic or traumatic brain injury, and in monitoring the effects of therapeutic interventions. Studies in rodents that emphasize careful behavioural analysis should continue to be developed as effective and inexpensive models that complement studies in primates.
Url:
DOI: 10.1038/nrn877
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Whishaw is at the Canadian Centre for Behavioral Neuroscience, University of Lethbridge, 4401 University Drive, Lethbridge, Alberta, Canada T1K 3M4.</mods:affiliation></affiliation></author><author><name sortKey="Schallert, Timothy" sort="Schallert, Timothy" uniqKey="Schallert T" first="Timothy" last="Schallert">Timothy Schallert</name><affiliation><mods:affiliation>Timothy Schallert is at the Department of Psychology and Neurobiology, University of Texas at Austin, Texas 78712, USA, and the Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan 48109, USA.</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:633ACFAA1965EF71F7C7AD3245884349C3C3C5B7</idno><date when="2002" year="2002">2002</date><idno type="doi">10.1038/nrn877</idno><idno type="url">https://api.istex.fr/document/633ACFAA1965EF71F7C7AD3245884349C3C3C5B7/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000366</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000366</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Animal models of neurological deficits: how relevant is the rat?</title><author><name sortKey="Cenci, M Angela" sort="Cenci, M Angela" uniqKey="Cenci M" first="M. 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It has been suggested that rats are not as appropriate as primates for the symptomatic modelling of disease, but a large body of data argues against this view. Comparative analyses of movements in rats and primates show homology of many motor patterns across species. Advances have been made in identifying rat equivalents of akinesia, tremor, postural deficits and dyskinesia, which are relevant to Parkinson's disease. Rat models of hemiplegia, neglect and tactile extinction are useful in assessing the outcome of ischaemic or traumatic brain injury, and in monitoring the effects of therapeutic interventions. Studies in rodents that emphasize careful behavioural analysis should continue to be developed as effective and inexpensive models that complement studies in primates.</div></front></TEI><istex><corpusName>nature</corpusName><author><json:item><name>M. Angela Cenci</name><affiliations><json:string>M. Angela Cenci is at the Wallenberg Neuroscience Centre, Neurobiology Division, University of Lund, BMC A11, S-221 84 Lund, Sweden.</json:string><json:string>E-mail: angela.cenci_nilsson@mphy.lu.se</json:string></affiliations></json:item><json:item><name>Ian Q. Whishaw</name><affiliations><json:string>Ian Q. 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Angela</forename><surname>Cenci</surname></persName><email>angela.cenci_nilsson@mphy.lu.se</email><note type="biography">Angela Cenci received a medical degree from the University of Verona, Italy, in 1986, and a degree as a specialist in neurology from the same university in 1990. She obtained her Ph.D. degree in Neurobiology at the University of Lund, Sweden, in 1993. From 1993, she has held a position as an assistant professor in neuroscience at the University of Lund. At present, her work addresses the molecular and cellular pathophysiology of parkinsonian akinesia and l-DOPA-induced dyskinesia using rodent models of Parkinson's disease.</note><affiliation>Angela Cenci received a medical degree from the University of Verona, Italy, in 1986, and a degree as a specialist in neurology from the same university in 1990. She obtained her Ph.D. degree in Neurobiology at the University of Lund, Sweden, in 1993. From 1993, she has held a position as an assistant professor in neuroscience at the University of Lund. At present, her work addresses the molecular and cellular pathophysiology of parkinsonian akinesia and l-DOPA-induced dyskinesia using rodent models of Parkinson's disease.</affiliation><affiliation>M. Angela Cenci is at the Wallenberg Neuroscience Centre, Neurobiology Division, University of Lund, BMC A11, S-221 84 Lund, Sweden.</affiliation></author><author xml:id="author-2"><persName><forename type="first">Ian Q.</forename><surname>Whishaw</surname></persName><note type="biography">Ian Whishaw received his Ph.D. from the University of Western Ontario in 1971. He moved to the University of Lethbridge in 1970, where he is now Professor of Psychology and Neuroscience, and holds a Board of Governors Chair in Neuroscience. He has had visiting appointments at the University of Texas, the University of Michigan, the University of Cambridge, UK, and the University of Strasbourg, France. He is also a Fellow of Clair Hall, Cambridge, the Canadian Psychological Association, the American Psychological Association and the Royal Society of Canada. Whishaw is a recipient of a bronze medal from the Canadian Humane Society, a recipient of the Ingrid Speaker Medal for research, and president of NeuroDetective Inc. His current research examines how injury to or disease of the motor systems of rodents and humans influences the precise details of bodily movements.</note><affiliation>Ian Whishaw received his Ph.D. from the University of Western Ontario in 1971. He moved to the University of Lethbridge in 1970, where he is now Professor of Psychology and Neuroscience, and holds a Board of Governors Chair in Neuroscience. He has had visiting appointments at the University of Texas, the University of Michigan, the University of Cambridge, UK, and the University of Strasbourg, France. He is also a Fellow of Clair Hall, Cambridge, the Canadian Psychological Association, the American Psychological Association and the Royal Society of Canada. Whishaw is a recipient of a bronze medal from the Canadian Humane Society, a recipient of the Ingrid Speaker Medal for research, and president of NeuroDetective Inc. His current research examines how injury to or disease of the motor systems of rodents and humans influences the precise details of bodily movements.</affiliation><affiliation>Ian Q. Whishaw is at the Canadian Centre for Behavioral Neuroscience, University of Lethbridge, 4401 University Drive, Lethbridge, Alberta, Canada T1K 3M4.</affiliation></author><author xml:id="author-3"><persName><forename type="first">Timothy</forename><surname>Schallert</surname></persName><note type="biography">Tim Schallert received his Ph.D. from Arizona State University in 1976. He was a postdoctoral fellow at the University of Illinois at UrbanaChampaign and the University of Lethbridge in Alberta, Canada. In 1979, he moved to The University of Texas at Austin, where he is now a professor in the Institute for Neuroscience and the Departments of Psychology and Neurobiology, and a member of the Academy of Distinguished Teachers. He is also an adjunct professor in the Department of Neurosurgery at the University of Michigan in Ann Arbor and at The Center for Human Growth and Development. He is a Fellow of the American Psychological Association, the American Psychological Society and the International Behavioral Neuroscience Society. His research is in the area of neuroplasticity, particularly brainbehaviour interactions in recovery of function after brain injury and in animal models of stroke, Parkinson's disease, brain tumours and spinal cord injury.</note><affiliation>Tim Schallert received his Ph.D. from Arizona State University in 1976. He was a postdoctoral fellow at the University of Illinois at UrbanaChampaign and the University of Lethbridge in Alberta, Canada. In 1979, he moved to The University of Texas at Austin, where he is now a professor in the Institute for Neuroscience and the Departments of Psychology and Neurobiology, and a member of the Academy of Distinguished Teachers. He is also an adjunct professor in the Department of Neurosurgery at the University of Michigan in Ann Arbor and at The Center for Human Growth and Development. He is a Fellow of the American Psychological Association, the American Psychological Society and the International Behavioral Neuroscience Society. His research is in the area of neuroplasticity, particularly brainbehaviour interactions in recovery of function after brain injury and in animal models of stroke, Parkinson's disease, brain tumours and spinal cord injury.</affiliation><affiliation>Timothy Schallert is at the Department of Psychology and Neurobiology, University of Texas at Austin, Texas 78712, USA, and the Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan 48109, USA.</affiliation></author></analytic><monogr><title level="j">Nature Reviews Neuroscience</title><idno type="pISSN">1471-003X</idno><idno type="eISSN">1471-0048</idno><imprint><publisher>Nature Publishing Group</publisher><date type="published" when="2002-07"></date><biblScope unit="volume">3</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="574">574</biblScope><biblScope unit="page" to="579">579</biblScope></imprint></monogr><idno type="istex">633ACFAA1965EF71F7C7AD3245884349C3C3C5B7</idno><idno type="DOI">10.1038/nrn877</idno><idno type="ArticleID">nrn877</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2002</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Animal models of neurological deficits are essential for the assessment of new therapeutic options. It has been suggested that rats are not as appropriate as primates for the symptomatic modelling of disease, but a large body of data argues against this view. Comparative analyses of movements in rats and primates show homology of many motor patterns across species. Advances have been made in identifying rat equivalents of akinesia, tremor, postural deficits and dyskinesia, which are relevant to Parkinson's disease. Rat models of hemiplegia, neglect and tactile extinction are useful in assessing the outcome of ischaemic or traumatic brain injury, and in monitoring the effects of therapeutic interventions. Studies in rodents that emphasize careful behavioural analysis should continue to be developed as effective and inexpensive models that complement studies in primates.</p></abstract></profileDesc><revisionDesc><change when="2002-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/633ACFAA1965EF71F7C7AD3245884349C3C3C5B7/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus nature" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0"</istex:xmlDeclaration><istex:docType PUBLIC="-//NPG//DTD XML Article//EN" URI="NPG_XML_Article.dtd" name="istex:docType"><istex:entity PUBLIC="-//NatureAmerica//FICI nrn877-t1//EN" URL="//snapple/web_d/web/npg/nrn/journal/v3/n7/images/nrn877-t1.gif" NDATA="ITEM" name="tbl1"></istex:entity></istex:docType><istex:document><article id="nrn877" language="eng" publish="issue" relation="no" origsrc="yes"><!--nrn877--><pubfm><jtl>Nature Reviews Neuroscience</jtl><vol>3</vol><iss>7</iss><idt>200207</idt><categ id="pe"></categ><subcateg id="op"></subcateg><pp><spn>574</spn><epn>579</epn><cnt>6</cnt></pp><issn type="print">1471-003X</issn><issn type="electronic">1471-0048</issn><cpg><cpy>2002</cpy><cpn>Nature Publishing Group</cpn></cpg><suppinfo id="s1"><suppobj extrefid="nrn877-s1" format="mov" filesize="722k"><descrip><p><b>Movie 1 | Skilled limb movements in an intact rat</b><newline></newline>A control rat reaches for a food pellet using normal movements. A detailed analysis of its skilled limb movements reveals very similar motor components in humans and in rats.<newline></newline><newline></newline><newline></newline></p></descrip></suppobj><suppobj extrefid="nrn877-s2" format="mov" filesize="196k"><descrip><p><b>Movie 2 | Tremor at rest</b><newline></newline>Occasional resting tremor has been observed in the wrist and the paw of rats that have been lesioned with 6-hydroxydopamine (6-OHDA). Tremor occurs when the forelimb is not being used for movement or postural support in the home cage.<newline></newline><newline></newline><newline></newline></p></descrip></suppobj><suppobj extrefid="nrn877-s3" format="mov" filesize="400k"><descrip><p><b>Movie 3 | Akinesia in a rat model of Parkinson’s disease
</b><newline></newline>Severe unilateral loss of nigrostriatal dopamine terminals in a rat 1.6 years after the infusion of 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle in the right hemisphere. The rat shows deficits in movement initiation (spontaneous stepping) with its left, but not its right, forelimb. In this test, the experimenter does not impose weight shifting; rather, the rat is allowed to initiate stepping on its own. Note that normal rats use primarily their forelimbs, rather than their hindlimbs, to initiate walking.<newline></newline><newline></newline><newline></newline></p></descrip></suppobj><suppobj extrefid="nrn877-s4" format="mov" filesize="776"><descrip><p><b>Movie 4 | The cylinder test</b><newline></newline>The cylinder test:
Limb-use asymmetry caused by unilateral loss of nigrostriatal dopamine after infusion of 6-hydroxydopamine (6-OHDA) into the nigrostriatal projections of the left hemisphere. The rat shows a preference for the left forelimb when initiating weight-shifting movements during vertical/lateral exploration. Use of the right forelimb is impaired; it is not used independently for weight shifts, support or stepping movements on the walls of the cylinder. The level of dopamine-terminal loss is correlated with percentage preferential use of the non-impaired forelimb.<newline></newline><newline></newline><newline></newline></p></descrip></suppobj><suppobj extrefid="nrn877-s5" format="mov" filesize="861k"><descrip><p><b>Movie 5 | Skilled limb movements in a 6-OHDA-lesioned rat</b><newline></newline>Rats with unilateral 6-hydroxydopamine (6-OHDA) lesions show abnormalities in both quantitative and qualitative aspects of reach-to-grasp movements on the side contralateral to dopamine depletion. When approaching a target, the impaired limb makes fragmented rather than concurrent movements, and shows incomplete pronation on the substrate. The deficits are partially compensated for using whole-body movements.<newline></newline><newline></newline><newline></newline></p></descrip></suppobj><suppobj extrefid="nrn877-s6" format="mov" filesize="921k"><descrip><p><b>Movie 6 | Minimal dyskinesia</b><newline></newline>When treated with 3,4-dihydroxyphenylalanine (<sc>l</sc>-DOPA), rats with unilateral 6-hydroxydopamine (6-OHDA) lesions can show abnormal involuntary movements (AIMs), which mainly affect the forelimb contralateral to the lesion, the trunk and the orofacial musculature. These abnormal involuntary movements can be quantified on the basis of their topographical distribution, amplitude and duration; that is, using the same criteria that are used in the clinic. This sequence of movies shows rats with <sc>l</sc>-DOPA-induced AIMs of increasing amplitude and severity.<newline></newline><newline></newline><newline></newline></p></descrip></suppobj><suppobj extrefid="nrn877-s7" format="mov" filesize="951k"><descrip><p><b>Movie 7 | Noticeable dyskinesia</b><newline></newline><newline></newline><newline></newline></p></descrip></suppobj><suppobj extrefid="nrn877-s8" format="mov" filesize="966k"><descrip><p><b>Movie 8 | Moderate dyskinesia</b><newline></newline><newline></newline><newline></newline></p></descrip></suppobj><suppobj extrefid="nrn877-s9" format="mov" filesize="1,330k"><descrip><p><b>Movie 9| Severe dyskinesia</b><newline></newline></p></descrip></suppobj></suppinfo><doi>10.1038/nrn877</doi></pubfm><fm><atl>Animal models of neurological deficits: how relevant is the rat?</atl><aug><cau><fnm>M. Angela</fnm><snm>Cenci</snm><inits>M A</inits><orf rid="a1"></orf><corf rid="c1"></corf><bio><p>Angela Cenci received a medical degree from the University of Verona, Italy, in 1986, and a degree as a specialist in neurology from the same university in 1990. She obtained her Ph.D. degree in Neurobiology at the University of Lund, Sweden, in 1993. From 1993, she has held a position as an assistant professor in neuroscience at the University of Lund. At present, her work addresses the molecular and cellular pathophysiology of parkinsonian akinesia and <sc>l</sc>-DOPA-induced dyskinesia using rodent models of Parkinson's disease.</p></bio></cau><au><fnm>Ian Q.</fnm><snm>Whishaw</snm><inits>I Q</inits><orf rid="a2"></orf><bio><p>Ian Whishaw received his Ph.D. from the University of Western Ontario in 1971. He moved to the University of Lethbridge in 1970, where he is now Professor of Psychology and Neuroscience, and holds a Board of Governors Chair in Neuroscience. He has had visiting appointments at the University of Texas, the University of Michigan, the University of Cambridge, UK, and the University of Strasbourg, France. He is also a Fellow of Clair Hall, Cambridge, the Canadian Psychological Association, the American Psychological Association and the Royal Society of Canada. Whishaw is a recipient of a bronze medal from the Canadian Humane Society, a recipient of the Ingrid Speaker Medal for research, and president of NeuroDetective Inc. His current research examines how injury to or disease of the motor systems of rodents and humans influences the precise details of bodily movements.</p></bio></au><au><fnm>Timothy</fnm><snm>Schallert</snm><inits>T</inits><orf rid="a3"></orf><bio><p>Tim Schallert received his Ph.D. from Arizona State University in 1976. He was a postdoctoral fellow at the University of Illinois at Urbana–Champaign and the University of Lethbridge in Alberta, Canada. In 1979, he moved to The University of Texas at Austin, where he is now a professor in the Institute for Neuroscience and the Departments of Psychology and Neurobiology, and a member of the Academy of Distinguished Teachers. He is also an adjunct professor in the Department of Neurosurgery at the University of Michigan in Ann Arbor and at The Center for Human Growth and Development. He is a Fellow of the American Psychological Association, the American Psychological Society and the International Behavioral Neuroscience Society. His research is in the area of neuroplasticity, particularly brain–behaviour interactions in recovery of function after brain injury and in animal models of stroke, Parkinson's disease, brain tumours and spinal cord injury.</p></bio></au><aff><oid id="a1"></oid>M. Angela Cenci is at the <org>Wallenberg Neuroscience Centre, Neurobiology Division, University of Lund</org>, <street>BMC A11</street>, <zip>S-221 84</zip> <cty>Lund</cty>, <cny>Sweden</cny>.</aff><aff><oid id="a2"></oid>Ian Q. Whishaw is at the <org>Canadian Centre for Behavioral Neuroscience, University of Lethbridge</org>, <street>4401 University Drive</street>, <cty>Lethbridge</cty>, <st>Alberta</st>, <cny>Canada</cny> <zip>T1K 3M4</zip>.</aff><aff><oid id="a3"></oid>Timothy Schallert is at the <org>Department of Psychology and Neurobiology, University of Texas at Austin</org>, <cty>Texas</cty> <zip>78712</zip>, <cny>USA</cny>, and the <org>Department of Neurosurgery, University of Michigan</org>, <cty>Ann Arbor</cty>, <st>Michigan</st> <zip>48109</zip>, <cny>USA</cny>.</aff><caff><coid id="c1"></coid><email>angela.cenci_nilsson@mphy.lu.se</email></caff></aug><abs><p>Animal models of neurological deficits are essential for the assessment of new therapeutic options. It has been suggested that rats are not as appropriate as primates for the symptomatic modelling of disease, but a large body of data argues against this view. Comparative analyses of movements in rats and primates show homology of many motor patterns across species. Advances have been made in identifying rat equivalents of akinesia, tremor, postural deficits and dyskinesia, which are relevant to Parkinson's disease. Rat models of hemiplegia, neglect and tactile extinction are useful in assessing the outcome of ischaemic or traumatic brain injury, and in monitoring the effects of therapeutic interventions. Studies in rodents that emphasize careful behavioural analysis should continue to be developed as effective and inexpensive models that complement studies in primates.</p></abs></fm><corr filename="nrn877-c1.sgm"></corr><corr filename="nrn877-c2.sgm"></corr></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="eng"><title>Animal models of neurological deficits: how relevant is the rat?</title></titleInfo><titleInfo type="alternative" lang="eng" contentType="CDATA"><title>Animal models of neurological deficits: how relevant is the rat?</title></titleInfo><name type="personal"><namePart type="given">M. Angela</namePart><namePart type="family">Cenci</namePart><affiliation>M. Angela Cenci is at the Wallenberg Neuroscience Centre, Neurobiology Division, University of Lund, BMC A11, S-221 84 Lund, Sweden.</affiliation><affiliation>E-mail: angela.cenci_nilsson@mphy.lu.se</affiliation><role><roleTerm type="text">author</roleTerm></role><description>Angela Cenci received a medical degree from the University of Verona, Italy, in 1986, and a degree as a specialist in neurology from the same university in 1990. She obtained her Ph.D. degree in Neurobiology at the University of Lund, Sweden, in 1993. From 1993, she has held a position as an assistant professor in neuroscience at the University of Lund. At present, her work addresses the molecular and cellular pathophysiology of parkinsonian akinesia and l-DOPA-induced dyskinesia using rodent models of Parkinson's disease.</description></name><name type="personal"><namePart type="given">Ian Q.</namePart><namePart type="family">Whishaw</namePart><affiliation>Ian Q. Whishaw is at the Canadian Centre for Behavioral Neuroscience, University of Lethbridge, 4401 University Drive, Lethbridge, Alberta, Canada T1K 3M4.</affiliation><role><roleTerm type="text">author</roleTerm></role><description>Ian Whishaw received his Ph.D. from the University of Western Ontario in 1971. He moved to the University of Lethbridge in 1970, where he is now Professor of Psychology and Neuroscience, and holds a Board of Governors Chair in Neuroscience. He has had visiting appointments at the University of Texas, the University of Michigan, the University of Cambridge, UK, and the University of Strasbourg, France. He is also a Fellow of Clair Hall, Cambridge, the Canadian Psychological Association, the American Psychological Association and the Royal Society of Canada. Whishaw is a recipient of a bronze medal from the Canadian Humane Society, a recipient of the Ingrid Speaker Medal for research, and president of NeuroDetective Inc. His current research examines how injury to or disease of the motor systems of rodents and humans influences the precise details of bodily movements.</description></name><name type="personal"><namePart type="given">Timothy</namePart><namePart type="family">Schallert</namePart><affiliation>Timothy Schallert is at the Department of Psychology and Neurobiology, University of Texas at Austin, Texas 78712, USA, and the Department of Neurosurgery, University of Michigan, Ann Arbor, Michigan 48109, USA.</affiliation><role><roleTerm type="text">author</roleTerm></role><description>Tim Schallert received his Ph.D. from Arizona State University in 1976. He was a postdoctoral fellow at the University of Illinois at UrbanaChampaign and the University of Lethbridge in Alberta, Canada. In 1979, he moved to The University of Texas at Austin, where he is now a professor in the Institute for Neuroscience and the Departments of Psychology and Neurobiology, and a member of the Academy of Distinguished Teachers. He is also an adjunct professor in the Department of Neurosurgery at the University of Michigan in Ann Arbor and at The Center for Human Growth and Development. He is a Fellow of the American Psychological Association, the American Psychological Society and the International Behavioral Neuroscience Society. His research is in the area of neuroplasticity, particularly brainbehaviour interactions in recovery of function after brain injury and in animal models of stroke, Parkinson's disease, brain tumours and spinal cord injury.</description></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="Perspectives"></genre><originInfo><publisher>Nature Publishing Group</publisher><dateIssued encoding="w3cdtf">2002-07</dateIssued><copyrightDate encoding="w3cdtf">2002</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="eng">Animal models of neurological deficits are essential for the assessment of new therapeutic options. It has been suggested that rats are not as appropriate as primates for the symptomatic modelling of disease, but a large body of data argues against this view. Comparative analyses of movements in rats and primates show homology of many motor patterns across species. Advances have been made in identifying rat equivalents of akinesia, tremor, postural deficits and dyskinesia, which are relevant to Parkinson's disease. Rat models of hemiplegia, neglect and tactile extinction are useful in assessing the outcome of ischaemic or traumatic brain injury, and in monitoring the effects of therapeutic interventions. Studies in rodents that emphasize careful behavioural analysis should continue to be developed as effective and inexpensive models that complement studies in primates.</abstract><relatedItem type="host"><titleInfo><title>Nature Reviews Neuroscience</title></titleInfo><genre type="journal" displayLabel="journal"></genre><identifier type="ISSN">1471-003X</identifier><identifier type="eISSN">1471-0048</identifier><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>3</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>574</start><end>579</end><total>6</total></extent></part></relatedItem><identifier type="istex">633ACFAA1965EF71F7C7AD3245884349C3C3C5B7</identifier><identifier type="DOI">10.1038/nrn877</identifier><identifier type="ArticleID">nrn877</identifier><accessCondition type="use and reproduction" contentType="copyright">©2002 Nature Publishing Group</accessCondition><recordInfo><recordContentSource>NATURE</recordContentSource></recordInfo></mods></metadata><annexes><json:item><extension>qt</extension><original>true</original><mimetype>video/quicktime</mimetype><uri>https://api.istex.fr/document/633ACFAA1965EF71F7C7AD3245884349C3C3C5B7/annexes/qt</uri></json:item><json:item><extension>gif</extension><original>true</original><mimetype>image/gif</mimetype><uri>https://api.istex.fr/document/633ACFAA1965EF71F7C7AD3245884349C3C3C5B7/annexes/gif</uri></json:item><json:item><extension>xml</extension><original>true</original><mimetype>application/xml</mimetype><uri>https://api.istex.fr/document/633ACFAA1965EF71F7C7AD3245884349C3C3C5B7/annexes/xml</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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