Stress accelerates neural degeneration and exaggerates motor symptoms in a rat model of Parkinson's disease
Identifieur interne : 000C77 ( Istex/Corpus ); précédent : 000C76; suivant : 000C78Stress accelerates neural degeneration and exaggerates motor symptoms in a rat model of Parkinson's disease
Auteurs : Lori K. Smith ; Nafisa M. Jadavji ; Keri L. Colwell ; S. Katrina Perehudoff ; Gerlinde A. MetzSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2008-04.
English descriptors
- KwdEn :
Abstract
The causes of most cases of Parkinson's disease (PD) are still poorly understood. Here we show that chronic stress and elevated corticosterone levels exaggerate motor deficits and neurodegenerative events in a Parkinson's disease rat model. Animals were tested in skilled and non‐skilled movement while being exposed to daily restraint stress or oral corticosterone treatment. Stress and corticosterone compromised normal motor function and exaggerated motor deficits caused by unilateral 6‐hydroxydopamine lesion of the nigrostriatal bundle. Moreover, stress and corticosterone treatments diminished the ability to acquire compensatory strategies in limb use during skilled reaching and skilled walking. In contrast, lesion control animals were able to significantly improve in the ability of skilled limb use during the repeated test sessions. The exaggerated motor impairments in stress‐treated animals were related to accelerated loss of midbrain dopamine‐producing neurons during the first week postlesion. Correlation analysis revealed a significant connection between loss of tyrosine hydroxylase‐positive cells and increase in Fluoro‐Jade‐positive cells only in stress‐ and corticosterone‐treated animals. Furthermore, stress and elevated corticosterone levels caused greater permanent loss of midbrain neurons than found in non‐treated lesion animals. These findings demonstrate that stress and elevated corticosterone levels can exaggerate nigral neuronal loss and motor symptoms in a rat analogue of PD. It is therefore possible that stress represents a key factor in the pathogenesis of human PD by impeding functional and structural compensation and exaggerating neurodegenerative processes.
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DOI: 10.1111/j.1460-9568.2008.06177.x
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ISTEX:B1E720EC02C7A349CC35A4FBA7DBE4DD44E3B255Le document en format XML
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Here we show that chronic stress and elevated corticosterone levels exaggerate motor deficits and neurodegenerative events in a Parkinson's disease rat model. Animals were tested in skilled and non‐skilled movement while being exposed to daily restraint stress or oral corticosterone treatment. Stress and corticosterone compromised normal motor function and exaggerated motor deficits caused by unilateral 6‐hydroxydopamine lesion of the nigrostriatal bundle. Moreover, stress and corticosterone treatments diminished the ability to acquire compensatory strategies in limb use during skilled reaching and skilled walking. In contrast, lesion control animals were able to significantly improve in the ability of skilled limb use during the repeated test sessions. The exaggerated motor impairments in stress‐treated animals were related to accelerated loss of midbrain dopamine‐producing neurons during the first week postlesion. Correlation analysis revealed a significant connection between loss of tyrosine hydroxylase‐positive cells and increase in Fluoro‐Jade‐positive cells only in stress‐ and corticosterone‐treated animals. Furthermore, stress and elevated corticosterone levels caused greater permanent loss of midbrain neurons than found in non‐treated lesion animals. These findings demonstrate that stress and elevated corticosterone levels can exaggerate nigral neuronal loss and motor symptoms in a rat analogue of PD. It is therefore possible that stress represents a key factor in the pathogenesis of human PD by impeding functional and structural compensation and exaggerating neurodegenerative processes.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Lori K. Smith</name><affiliations><json:string>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4 Canada</json:string></affiliations></json:item><json:item><name>Nafisa M. 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Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd</p></availability><date>2008</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Stress accelerates neural degeneration and exaggerates motor symptoms in a rat model of Parkinson's disease</title><author xml:id="author-1"><persName><forename type="first">Lori K.</forename><surname>Smith</surname></persName><affiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4 Canada</affiliation></author><author xml:id="author-2"><persName><forename type="first">Nafisa M.</forename><surname>Jadavji</surname></persName><affiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4 Canada</affiliation></author><author xml:id="author-3"><persName><forename type="first">Keri L.</forename><surname>Colwell</surname></persName><affiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4 Canada</affiliation></author><author xml:id="author-4"><persName><forename type="first">S.</forename><surname>Katrina Perehudoff</surname></persName><affiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4 Canada</affiliation></author><author xml:id="author-5"><persName><forename type="first">Gerlinde A.</forename><surname>Metz</surname></persName><affiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4 Canada</affiliation></author></analytic><monogr><title level="j">European Journal of Neuroscience</title><idno type="pISSN">0953-816X</idno><idno type="eISSN">1460-9568</idno><idno type="DOI">10.1111/(ISSN)1460-9568</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2008-04"></date><biblScope unit="volume">27</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="2133">2133</biblScope><biblScope unit="page" to="2146">2146</biblScope></imprint></monogr><idno type="istex">B1E720EC02C7A349CC35A4FBA7DBE4DD44E3B255</idno><idno type="DOI">10.1111/j.1460-9568.2008.06177.x</idno><idno type="ArticleID">EJN6177</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2008</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The causes of most cases of Parkinson's disease (PD) are still poorly understood. Here we show that chronic stress and elevated corticosterone levels exaggerate motor deficits and neurodegenerative events in a Parkinson's disease rat model. Animals were tested in skilled and non‐skilled movement while being exposed to daily restraint stress or oral corticosterone treatment. Stress and corticosterone compromised normal motor function and exaggerated motor deficits caused by unilateral 6‐hydroxydopamine lesion of the nigrostriatal bundle. Moreover, stress and corticosterone treatments diminished the ability to acquire compensatory strategies in limb use during skilled reaching and skilled walking. In contrast, lesion control animals were able to significantly improve in the ability of skilled limb use during the repeated test sessions. The exaggerated motor impairments in stress‐treated animals were related to accelerated loss of midbrain dopamine‐producing neurons during the first week postlesion. Correlation analysis revealed a significant connection between loss of tyrosine hydroxylase‐positive cells and increase in Fluoro‐Jade‐positive cells only in stress‐ and corticosterone‐treated animals. Furthermore, stress and elevated corticosterone levels caused greater permanent loss of midbrain neurons than found in non‐treated lesion animals. These findings demonstrate that stress and elevated corticosterone levels can exaggerate nigral neuronal loss and motor symptoms in a rat analogue of PD. It is therefore possible that stress represents a key factor in the pathogenesis of human PD by impeding functional and structural compensation and exaggerating neurodegenerative processes.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>6‐OHDA</term></item><item><term>cell death</term></item><item><term>corticosterone</term></item><item><term>medial forebrain bundle</term></item><item><term>skilled movement</term></item><item><term>tyrosine hydroxylase</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2008-04">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/B1E720EC02C7A349CC35A4FBA7DBE4DD44E3B255/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 Publishing 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="04008"><doi origin="wiley">10.1111/ejn.2008.27.issue-8</doi><numberingGroup><numbering type="journalVolume" number="27">27</numbering><numbering type="journalIssue" number="8">8</numbering></numberingGroup><coverDate startDate="2008-04">April 2008</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="23" status="forIssue"><doi origin="wiley">10.1111/j.1460-9568.2008.06177.x</doi><idGroup><id type="unit" value="EJN6177"></id></idGroup><countGroup><count type="pageTotal" number="14"></count></countGroup><titleGroup><title type="tocHeading1">Research Reports</title></titleGroup><copyright>© The Authors (2008). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd</copyright><eventGroup><event type="firstOnline" date="2008-04-11"></event><event type="publishedOnlineFinalForm" date="2008-04-11"></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="2133">2133</numbering><numbering type="pageLast" number="2146">2146</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.EJN6177.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 27 June 2007, revised 6 February 2008, accepted 26 February 2008</unparsedEditorialHistory><countGroup><count type="figureTotal" number="10"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="69"></count><count type="wordTotal" number="8291"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Stress accelerates neural degeneration and exaggerates motor symptoms in a rat model of Parkinson's disease</title><title type="shortAuthors">L. K. Smith <i>et al.</i></title><title type="short">Stress and Parkinson’s disease</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#aff-1-1"><personName><givenNames>Lori K.</givenNames><familyName>Smith</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#aff-1-1"><personName><givenNames>Nafisa M.</givenNames><familyName>Jadavji</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#aff-1-1"><personName><givenNames>Keri L.</givenNames><familyName>Colwell</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#aff-1-1"><personName><givenNames>S.</givenNames><familyName>Katrina Perehudoff</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#aff-1-1"><personName><givenNames>Gerlinde A.</givenNames><familyName>Metz</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="aff-1-1" countryCode="CA"><unparsedAffiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4 Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">6‐OHDA</keyword><keyword xml:id="k2">cell death</keyword><keyword xml:id="k3">corticosterone</keyword><keyword xml:id="k4">medial forebrain bundle</keyword><keyword xml:id="k5">skilled movement</keyword><keyword xml:id="k6">tyrosine hydroxylase </keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The causes of most cases of Parkinson's disease (PD) are still poorly understood. Here we show that chronic stress and elevated corticosterone levels exaggerate motor deficits and neurodegenerative events in a Parkinson's disease rat model. Animals were tested in skilled and non‐skilled movement while being exposed to daily restraint stress or oral corticosterone treatment. Stress and corticosterone compromised normal motor function and exaggerated motor deficits caused by unilateral 6‐hydroxydopamine lesion of the nigrostriatal bundle. Moreover, stress and corticosterone treatments diminished the ability to acquire compensatory strategies in limb use during skilled reaching and skilled walking. In contrast, lesion control animals were able to significantly improve in the ability of skilled limb use during the repeated test sessions. The exaggerated motor impairments in stress‐treated animals were related to accelerated loss of midbrain dopamine‐producing neurons during the first week postlesion. Correlation analysis revealed a significant connection between loss of tyrosine hydroxylase‐positive cells and increase in Fluoro‐Jade‐positive cells only in stress‐ and corticosterone‐treated animals. Furthermore, stress and elevated corticosterone levels caused greater permanent loss of midbrain neurons than found in non‐treated lesion animals. These findings demonstrate that stress and elevated corticosterone levels can exaggerate nigral neuronal loss and motor symptoms in a rat analogue of PD. It is therefore possible that stress represents a key factor in the pathogenesis of human PD by impeding functional and structural compensation and exaggerating neurodegenerative processes.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Stress accelerates neural degeneration and exaggerates motor symptoms in a rat model of Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Stress and Parkinson’s disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Stress accelerates neural degeneration and exaggerates motor symptoms in a rat model of Parkinson's disease</title></titleInfo><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, T1K 3M4 Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nafisa M.</namePart><namePart type="family">Jadavji</namePart><affiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4 Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Keri L.</namePart><namePart type="family">Colwell</namePart><affiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4 Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Katrina Perehudoff</namePart><affiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4 Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><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, T1K 3M4 Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2008-04</dateIssued><edition>Received 27 June 2007, revised 6 February 2008, accepted 26 February 2008</edition><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">10</extent><extent unit="references">69</extent><extent unit="words">8291</extent></physicalDescription><abstract lang="en">The causes of most cases of Parkinson's disease (PD) are still poorly understood. Here we show that chronic stress and elevated corticosterone levels exaggerate motor deficits and neurodegenerative events in a Parkinson's disease rat model. Animals were tested in skilled and non‐skilled movement while being exposed to daily restraint stress or oral corticosterone treatment. Stress and corticosterone compromised normal motor function and exaggerated motor deficits caused by unilateral 6‐hydroxydopamine lesion of the nigrostriatal bundle. Moreover, stress and corticosterone treatments diminished the ability to acquire compensatory strategies in limb use during skilled reaching and skilled walking. In contrast, lesion control animals were able to significantly improve in the ability of skilled limb use during the repeated test sessions. The exaggerated motor impairments in stress‐treated animals were related to accelerated loss of midbrain dopamine‐producing neurons during the first week postlesion. Correlation analysis revealed a significant connection between loss of tyrosine hydroxylase‐positive cells and increase in Fluoro‐Jade‐positive cells only in stress‐ and corticosterone‐treated animals. Furthermore, stress and elevated corticosterone levels caused greater permanent loss of midbrain neurons than found in non‐treated lesion animals. These findings demonstrate that stress and elevated corticosterone levels can exaggerate nigral neuronal loss and motor symptoms in a rat analogue of PD. It is therefore possible that stress represents a key factor in the pathogenesis of human PD by impeding functional and structural compensation and exaggerating neurodegenerative processes.</abstract><subject lang="en"><genre>keywords</genre><topic>6‐OHDA</topic><topic>cell death</topic><topic>corticosterone</topic><topic>medial forebrain bundle</topic><topic>skilled movement</topic><topic>tyrosine hydroxylase</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>2008</date><detail type="volume"><caption>vol.</caption><number>27</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>2133</start><end>2146</end><total>14</total></extent></part></relatedItem><identifier type="istex">B1E720EC02C7A349CC35A4FBA7DBE4DD44E3B255</identifier><identifier type="DOI">10.1111/j.1460-9568.2008.06177.x</identifier><identifier type="ArticleID">EJN6177</identifier><accessCondition type="use and reproduction" contentType="copyright">© The Authors (2008). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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