Neuroprotection in Parkinson models varies with toxin administration protocol
Identifieur interne : 000704 ( Main/Corpus ); précédent : 000703; suivant : 000705Neuroprotection in Parkinson models varies with toxin administration protocol
Auteurs : David W. Anderson ; Kristin A. Bradbury ; Jay S. SchneiderSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2006-12.
English descriptors
- KwdEn :
Abstract
Numerous factors contribute to substantia nigra pars compacta (SNc) dopamine (DA) neuron death in Parkinson's disease (PD), thus complicating the search for effective neuroprotective agents for this disease. Although the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated mouse has been widely used for assessing neuroprotective agents for PD, the pathological processes resulting from MPTP exposure can vary greatly depending upon the MPTP administration protocol. This study assessed the degree to which the neuroprotective efficacy of particular agents may depend upon the MPTP administration protocol (i.e. acute vs. subacute toxin administration). Endpoints analysed were changes in tyrosine hydroxylase (TH) and NeuN cell numbers in the SNc, striatal DA and metabolite levels, and striatal TH+ fiber density. The efficacy of putative neuroprotective agents [i.e. LIGA 20, nicotinamide and pramipexole (PPX)] varied depending upon the MPTP administration protocol. LIGA 20 spared striatal DA levels in both MPTP models, while nicotinamide was only effective in the acute toxin administration model and PPX was only effective in the subacute model. In both MPTP models, LIGA 20 and nicotinamide significantly spared DAergic neurons; PPX only spared DAergic neurons in the subacute model. Only acute MPTP‐treated mice that received nicotinamide had a significant sparing of striatal DAergic fibers. These results underscore the need to assess putative neuroprotective agents for PD in multiple animal models using multiple endpoints. This strategy may better identify compounds with broad neuroprotective/neurorestorative profiles that may be more likely to be clinically effective.
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DOI: 10.1111/j.1460-9568.2006.05192.x
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Anderson</name><affiliation><mods:affiliation>Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia PA 19107, USA</mods:affiliation></affiliation></author><author><name sortKey="Bradbury, Kristin A" sort="Bradbury, Kristin A" uniqKey="Bradbury K" first="Kristin A." last="Bradbury">Kristin A. Bradbury</name><affiliation><mods:affiliation>Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia PA 19107, USA</mods:affiliation></affiliation></author><author><name sortKey="Schneider, Jay S" sort="Schneider, Jay S" uniqKey="Schneider J" first="Jay S." last="Schneider">Jay S. Schneider</name><affiliation><mods:affiliation>Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia PA 19107, USA</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 Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2006-12">2006-12</date><biblScope unit="volume">24</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="3174">3174</biblScope><biblScope unit="page" to="3182">3182</biblScope></imprint><idno type="ISSN">0953-816X</idno></series><idno type="istex">31CAFC3DA664FAA799C02076FACA71DBA2419D5D</idno><idno type="DOI">10.1111/j.1460-9568.2006.05192.x</idno><idno type="ArticleID">EJN5192</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0953-816X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>MPTP</term><term>Parkinsonism</term><term>dopamine</term><term>mouse</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Numerous factors contribute to substantia nigra pars compacta (SNc) dopamine (DA) neuron death in Parkinson's disease (PD), thus complicating the search for effective neuroprotective agents for this disease. Although the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated mouse has been widely used for assessing neuroprotective agents for PD, the pathological processes resulting from MPTP exposure can vary greatly depending upon the MPTP administration protocol. This study assessed the degree to which the neuroprotective efficacy of particular agents may depend upon the MPTP administration protocol (i.e. acute vs. subacute toxin administration). Endpoints analysed were changes in tyrosine hydroxylase (TH) and NeuN cell numbers in the SNc, striatal DA and metabolite levels, and striatal TH+ fiber density. The efficacy of putative neuroprotective agents [i.e. LIGA 20, nicotinamide and pramipexole (PPX)] varied depending upon the MPTP administration protocol. LIGA 20 spared striatal DA levels in both MPTP models, while nicotinamide was only effective in the acute toxin administration model and PPX was only effective in the subacute model. In both MPTP models, LIGA 20 and nicotinamide significantly spared DAergic neurons; PPX only spared DAergic neurons in the subacute model. Only acute MPTP‐treated mice that received nicotinamide had a significant sparing of striatal DAergic fibers. These results underscore the need to assess putative neuroprotective agents for PD in multiple animal models using multiple endpoints. This strategy may better identify compounds with broad neuroprotective/neurorestorative profiles that may be more likely to be clinically effective.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>David W. Anderson</name><affiliations><json:string>Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia PA 19107, USA</json:string></affiliations></json:item><json:item><name>Kristin A. Bradbury</name><affiliations><json:string>Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia PA 19107, USA</json:string></affiliations></json:item><json:item><name>Jay S. Schneider</name><affiliations><json:string>Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia PA 19107, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>dopamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>mouse</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MPTP</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinsonism</value></json:item></subject><articleId><json:string>EJN5192</json:string></articleId><language><json:string>eng</json:string></language><abstract>Numerous factors contribute to substantia nigra pars compacta (SNc) dopamine (DA) neuron death in Parkinson's disease (PD), thus complicating the search for effective neuroprotective agents for this disease. Although the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated mouse has been widely used for assessing neuroprotective agents for PD, the pathological processes resulting from MPTP exposure can vary greatly depending upon the MPTP administration protocol. This study assessed the degree to which the neuroprotective efficacy of particular agents may depend upon the MPTP administration protocol (i.e. acute vs. subacute toxin administration). Endpoints analysed were changes in tyrosine hydroxylase (TH) and NeuN cell numbers in the SNc, striatal DA and metabolite levels, and striatal TH+ fiber density. The efficacy of putative neuroprotective agents [i.e. LIGA 20, nicotinamide and pramipexole (PPX)] varied depending upon the MPTP administration protocol. LIGA 20 spared striatal DA levels in both MPTP models, while nicotinamide was only effective in the acute toxin administration model and PPX was only effective in the subacute model. In both MPTP models, LIGA 20 and nicotinamide significantly spared DAergic neurons; PPX only spared DAergic neurons in the subacute model. Only acute MPTP‐treated mice that received nicotinamide had a significant sparing of striatal DAergic fibers. These results underscore the need to assess putative neuroprotective agents for PD in multiple animal models using multiple endpoints. 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Although the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated mouse has been widely used for assessing neuroprotective agents for PD, the pathological processes resulting from MPTP exposure can vary greatly depending upon the MPTP administration protocol. This study assessed the degree to which the neuroprotective efficacy of particular agents may depend upon the MPTP administration protocol (i.e. acute vs. subacute toxin administration). Endpoints analysed were changes in tyrosine hydroxylase (TH) and NeuN cell numbers in the SNc, striatal DA and metabolite levels, and striatal TH+ fiber density. The efficacy of putative neuroprotective agents [i.e. LIGA 20, nicotinamide and pramipexole (PPX)] varied depending upon the MPTP administration protocol. LIGA 20 spared striatal DA levels in both MPTP models, while nicotinamide was only effective in the acute toxin administration model and PPX was only effective in the subacute model. In both MPTP models, LIGA 20 and nicotinamide significantly spared DAergic neurons; PPX only spared DAergic neurons in the subacute model. Only acute MPTP‐treated mice that received nicotinamide had a significant sparing of striatal DAergic fibers. These results underscore the need to assess putative neuroprotective agents for PD in multiple animal models using multiple endpoints. This strategy may better identify compounds with broad neuroprotective/neurorestorative profiles that may be more likely to be clinically effective.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>dopamine</term></item><item><term>mouse</term></item><item><term>MPTP</term></item><item><term>Parkinsonism</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/31CAFC3DA664FAA799C02076FACA71DBA2419D5D/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="12011"><doi origin="wiley">10.1111/ejn.2006.24.issue-11</doi><numberingGroup><numbering type="journalVolume" number="24">24</numbering><numbering type="journalIssue" number="11">11</numbering></numberingGroup><coverDate startDate="2006-12">December 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="21" status="forIssue"><doi origin="wiley">10.1111/j.1460-9568.2006.05192.x</doi><idGroup><id type="unit" value="EJN5192"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="tocHeading1">Research Reports</title></titleGroup><eventGroup><event type="firstOnline" date="2006-12-11"></event><event type="publishedOnlineFinalForm" date="2006-12-11"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.4 mode:FullText source:FullText result:FullText" date="2010-03-29"></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="3174">3174</numbering><numbering type="pageLast" number="3182">3182</numbering></numberingGroup><correspondenceTo>Dr J.S. Schneider, as above.
E‐mail: <email>jay.schneider@jefferson.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EJN.EJN5192.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 2 August 2006, revised 20 September 2006, accepted 21 September 2006</unparsedEditorialHistory><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="2"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="47"></count><count type="wordTotal" number="7620"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Neuroprotection in Parkinson models varies with toxin administration protocol</title><title type="shortAuthors">D. W. Anderson <i>et al</i>.</title><title type="short">Neuroprotection in MPTP models</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#aff-1-1"><personName><givenNames>David W.</givenNames><familyName>Anderson</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#aff-1-1"><personName><givenNames>Kristin A.</givenNames><familyName>Bradbury</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#aff-1-1"><personName><givenNames>Jay S.</givenNames><familyName>Schneider</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="aff-1-1" countryCode="US"><unparsedAffiliation>Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia PA 19107, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">dopamine</keyword><keyword xml:id="k2">mouse</keyword><keyword xml:id="k3">MPTP</keyword><keyword xml:id="k4">Parkinsonism</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Numerous factors contribute to substantia nigra pars compacta (SNc) dopamine (DA) neuron death in Parkinson's disease (PD), thus complicating the search for effective neuroprotective agents for this disease. Although the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated mouse has been widely used for assessing neuroprotective agents for PD, the pathological processes resulting from MPTP exposure can vary greatly depending upon the MPTP administration protocol. This study assessed the degree to which the neuroprotective efficacy of particular agents may depend upon the MPTP administration protocol (i.e. acute vs. subacute toxin administration). Endpoints analysed were changes in tyrosine hydroxylase (TH) and NeuN cell numbers in the SNc, striatal DA and metabolite levels, and striatal TH<sup>+</sup> fiber density. The efficacy of putative neuroprotective agents [i.e. LIGA 20, nicotinamide and pramipexole (PPX)] varied depending upon the MPTP administration protocol. LIGA 20 spared striatal DA levels in both MPTP models, while nicotinamide was only effective in the acute toxin administration model and PPX was only effective in the subacute model. In both MPTP models, LIGA 20 and nicotinamide significantly spared DAergic neurons; PPX only spared DAergic neurons in the subacute model. Only acute MPTP‐treated mice that received nicotinamide had a significant sparing of striatal DAergic fibers. These results underscore the need to assess putative neuroprotective agents for PD in multiple animal models using multiple endpoints. This strategy may better identify compounds with broad neuroprotective/neurorestorative profiles that may be more likely to be clinically effective.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Neuroprotection in Parkinson models varies with toxin administration protocol</title></titleInfo><titleInfo type="abbreviated"><title>Neuroprotection in MPTP models</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Neuroprotection in Parkinson models varies with toxin administration protocol</title></titleInfo><name type="personal"><namePart type="given">David W.</namePart><namePart type="family">Anderson</namePart><affiliation>Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia PA 19107, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kristin A.</namePart><namePart type="family">Bradbury</namePart><affiliation>Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia PA 19107, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jay S.</namePart><namePart type="family">Schneider</namePart><affiliation>Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia PA 19107, USA</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">2006-12</dateIssued><edition>Received 2 August 2006, revised 20 September 2006, accepted 21 September 2006</edition><copyrightDate encoding="w3cdtf">2006</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="tables">2</extent><extent unit="references">47</extent><extent unit="words">7620</extent></physicalDescription><abstract lang="en">Numerous factors contribute to substantia nigra pars compacta (SNc) dopamine (DA) neuron death in Parkinson's disease (PD), thus complicating the search for effective neuroprotective agents for this disease. Although the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated mouse has been widely used for assessing neuroprotective agents for PD, the pathological processes resulting from MPTP exposure can vary greatly depending upon the MPTP administration protocol. This study assessed the degree to which the neuroprotective efficacy of particular agents may depend upon the MPTP administration protocol (i.e. acute vs. subacute toxin administration). Endpoints analysed were changes in tyrosine hydroxylase (TH) and NeuN cell numbers in the SNc, striatal DA and metabolite levels, and striatal TH+ fiber density. The efficacy of putative neuroprotective agents [i.e. LIGA 20, nicotinamide and pramipexole (PPX)] varied depending upon the MPTP administration protocol. LIGA 20 spared striatal DA levels in both MPTP models, while nicotinamide was only effective in the acute toxin administration model and PPX was only effective in the subacute model. In both MPTP models, LIGA 20 and nicotinamide significantly spared DAergic neurons; PPX only spared DAergic neurons in the subacute model. Only acute MPTP‐treated mice that received nicotinamide had a significant sparing of striatal DAergic fibers. These results underscore the need to assess putative neuroprotective agents for PD in multiple animal models using multiple endpoints. This strategy may better identify compounds with broad neuroprotective/neurorestorative profiles that may be more likely to be clinically effective.</abstract><subject lang="en"><genre>Keywords</genre><topic>dopamine</topic><topic>mouse</topic><topic>MPTP</topic><topic>Parkinsonism</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>2006</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>3174</start><end>3182</end><total>9</total></extent></part></relatedItem><identifier type="istex">31CAFC3DA664FAA799C02076FACA71DBA2419D5D</identifier><identifier type="DOI">10.1111/j.1460-9568.2006.05192.x</identifier><identifier type="ArticleID">EJN5192</identifier><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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