Comparison of unilateral and bilateral intrastriatal 6‐hydroxydopamine‐induced axon terminal lesions: Evidence for interhemispheric functional coupling of the two nigrostriatal pathways
Identifieur interne : 002460 ( Main/Corpus ); précédent : 002459; suivant : 002461Comparison of unilateral and bilateral intrastriatal 6‐hydroxydopamine‐induced axon terminal lesions: Evidence for interhemispheric functional coupling of the two nigrostriatal pathways
Auteurs : Alexandra Roedter ; Christian Winkler ; Madjid Samii ; Gerhard F. Walter ; Almuth Brandis ; Guido NikkhahSource :
- Journal of Comparative Neurology [ 0021-9967 ] ; 2001-04-02.
English descriptors
- KwdEn :
Abstract
Partial lesions of the nigrostriatal dopamine system can be induced reliably by the intrastriatal injection of 6‐hydroxydopamine (6‐OHDA) and are considered to be analogous to the early stages of human Parkinson's disease. Previous studies have established a clear correlation between different doses and placements of the 6‐OHDA toxin and the degree of neurodegenerative changes and behavioral impairments. In the present study, the influence of the interdependence between the two nigrostriatal systems in both hemispheres on the effects on sensorimotor behavioral performances after terminal 6‐OHDA lesions was investigated. The behavioral effects were correlated to the extent of nigral dopamine neuron cell and striatal tyrosine‐hydroxylase (TH)‐positive fiber loss. Sprague‐Dawley rats receiving unilateral intrastriatal 6‐OHDA injections (4 × 5 μg) exhibited a 30–70% reduction in striatal TH‐positive fiber density along an anterior‐posterior gradient, an 80% loss of nigral dopamine neurons and a mild degree of behavioral impairments as revealed by amphetamine‐induced rotational asymmetry, and a reduced performance in the stepping and postural balance tests. When the same amount of toxin was injected twice into both hemispheres (2 × 4 × 5 μg), additional behavioral deficits were observed, consisting of a significant, but temporary, weight loss, a stable reduction in general locomotor activity and explorational behavior, and a long‐term deficit in skilled forelimb use. This is interesting in light of the morphological findings, in which uni‐ and bilaterally lesioned animals did not differ significantly in the extent of TH‐immunoreactive fiber and dopamine neuron loss within the nigrostriatal system in each lesioned hemisphere. These results indicate that the interdependent regulation of the two nigrostriatal systems may provide some compensatory support for the function and behavioral performance of the lesioned side via the normal unlesioned side, which is lost in animals with bilateral lesions of the nigrostriatal system. Therefore, this model of uni‐ and bilateral partial lesions of the nigrostriatal system, as characterized in the present study, may foster further exploration of compensatory functional mechanisms active in the early stages of Parkinson's disease and promote development of novel neuroprotective and restorative strategies. J. Comp. Neurol. 432:217–229, 2001. © 2001 Wiley‐Liss, Inc.
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DOI: 10.1002/cne.1098
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Previous studies have established a clear correlation between different doses and placements of the 6‐OHDA toxin and the degree of neurodegenerative changes and behavioral impairments. In the present study, the influence of the interdependence between the two nigrostriatal systems in both hemispheres on the effects on sensorimotor behavioral performances after terminal 6‐OHDA lesions was investigated. The behavioral effects were correlated to the extent of nigral dopamine neuron cell and striatal tyrosine‐hydroxylase (TH)‐positive fiber loss. Sprague‐Dawley rats receiving unilateral intrastriatal 6‐OHDA injections (4 × 5 μg) exhibited a 30–70% reduction in striatal TH‐positive fiber density along an anterior‐posterior gradient, an 80% loss of nigral dopamine neurons and a mild degree of behavioral impairments as revealed by amphetamine‐induced rotational asymmetry, and a reduced performance in the stepping and postural balance tests. When the same amount of toxin was injected twice into both hemispheres (2 × 4 × 5 μg), additional behavioral deficits were observed, consisting of a significant, but temporary, weight loss, a stable reduction in general locomotor activity and explorational behavior, and a long‐term deficit in skilled forelimb use. This is interesting in light of the morphological findings, in which uni‐ and bilaterally lesioned animals did not differ significantly in the extent of TH‐immunoreactive fiber and dopamine neuron loss within the nigrostriatal system in each lesioned hemisphere. These results indicate that the interdependent regulation of the two nigrostriatal systems may provide some compensatory support for the function and behavioral performance of the lesioned side via the normal unlesioned side, which is lost in animals with bilateral lesions of the nigrostriatal system. Therefore, this model of uni‐ and bilateral partial lesions of the nigrostriatal system, as characterized in the present study, may foster further exploration of compensatory functional mechanisms active in the early stages of Parkinson's disease and promote development of novel neuroprotective and restorative strategies. J. Comp. Neurol. 432:217–229, 2001. © 2001 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Alexandra Roedter</name><affiliations><json:string>Neurosurgical Clinic, Nordstadt Hospital, D‐30167 Hannover, Germany</json:string></affiliations></json:item><json:item><name>Christian Winkler</name><affiliations><json:string>Neurosurgical Clinic, Nordstadt Hospital, D‐30167 Hannover, Germany</json:string><json:string>Neurological Clinic, Hannover Medical School, D‐30625 Hannover, Germany</json:string></affiliations></json:item><json:item><name>Madjid Samii</name><affiliations><json:string>Neurosurgical Clinic, Nordstadt Hospital, D‐30167 Hannover, Germany</json:string></affiliations></json:item><json:item><name>Gerhard F. 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Previous studies have established a clear correlation between different doses and placements of the 6‐OHDA toxin and the degree of neurodegenerative changes and behavioral impairments. In the present study, the influence of the interdependence between the two nigrostriatal systems in both hemispheres on the effects on sensorimotor behavioral performances after terminal 6‐OHDA lesions was investigated. The behavioral effects were correlated to the extent of nigral dopamine neuron cell and striatal tyrosine‐hydroxylase (TH)‐positive fiber loss. Sprague‐Dawley rats receiving unilateral intrastriatal 6‐OHDA injections (4 × 5 μg) exhibited a 30–70% reduction in striatal TH‐positive fiber density along an anterior‐posterior gradient, an 80% loss of nigral dopamine neurons and a mild degree of behavioral impairments as revealed by amphetamine‐induced rotational asymmetry, and a reduced performance in the stepping and postural balance tests. When the same amount of toxin was injected twice into both hemispheres (2 × 4 × 5 μg), additional behavioral deficits were observed, consisting of a significant, but temporary, weight loss, a stable reduction in general locomotor activity and explorational behavior, and a long‐term deficit in skilled forelimb use. This is interesting in light of the morphological findings, in which uni‐ and bilaterally lesioned animals did not differ significantly in the extent of TH‐immunoreactive fiber and dopamine neuron loss within the nigrostriatal system in each lesioned hemisphere. These results indicate that the interdependent regulation of the two nigrostriatal systems may provide some compensatory support for the function and behavioral performance of the lesioned side via the normal unlesioned side, which is lost in animals with bilateral lesions of the nigrostriatal system. Therefore, this model of uni‐ and bilateral partial lesions of the nigrostriatal system, as characterized in the present study, may foster further exploration of compensatory functional mechanisms active in the early stages of Parkinson's disease and promote development of novel neuroprotective and restorative strategies. J. Comp. 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Previous studies have established a clear correlation between different doses and placements of the 6‐OHDA toxin and the degree of neurodegenerative changes and behavioral impairments. In the present study, the influence of the interdependence between the two nigrostriatal systems in both hemispheres on the effects on sensorimotor behavioral performances after terminal 6‐OHDA lesions was investigated. The behavioral effects were correlated to the extent of nigral dopamine neuron cell and striatal tyrosine‐hydroxylase (TH)‐positive fiber loss. Sprague‐Dawley rats receiving unilateral intrastriatal 6‐OHDA injections (4 × 5 μg) exhibited a 30–70% reduction in striatal TH‐positive fiber density along an anterior‐posterior gradient, an 80% loss of nigral dopamine neurons and a mild degree of behavioral impairments as revealed by amphetamine‐induced rotational asymmetry, and a reduced performance in the stepping and postural balance tests. When the same amount of toxin was injected twice into both hemispheres (2 × 4 × 5 μg), additional behavioral deficits were observed, consisting of a significant, but temporary, weight loss, a stable reduction in general locomotor activity and explorational behavior, and a long‐term deficit in skilled forelimb use. This is interesting in light of the morphological findings, in which uni‐ and bilaterally lesioned animals did not differ significantly in the extent of TH‐immunoreactive fiber and dopamine neuron loss within the nigrostriatal system in each lesioned hemisphere. These results indicate that the interdependent regulation of the two nigrostriatal systems may provide some compensatory support for the function and behavioral performance of the lesioned side via the normal unlesioned side, which is lost in animals with bilateral lesions of the nigrostriatal system. Therefore, this model of uni‐ and bilateral partial lesions of the nigrostriatal system, as characterized in the present study, may foster further exploration of compensatory functional mechanisms active in the early stages of Parkinson's disease and promote development of novel neuroprotective and restorative strategies. J. Comp. 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Neurol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="20"><doi origin="wiley" registered="yes">10.1002/cne.v432:2</doi><numberingGroup><numbering type="journalVolume" number="432">432</numbering><numbering type="journalIssue">2</numbering></numberingGroup><coverDate startDate="2001-04-02">2 April 2001</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="1098" status="forIssue"><doi origin="wiley" registered="yes">10.1002/cne.1098</doi><idGroup><id type="unit" value="CNE1098"></id></idGroup><countGroup><count type="pageTotal" number="13"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">Articles</title></titleGroup><copyright ownership="publisher">Copyright © 2001 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2000-07-20"></event><event type="manuscriptRevised" date="2000-10-17"></event><event type="manuscriptAccepted" date="2000-12-28"></event><event type="firstOnline" date="2001-02-27"></event><event type="publishedOnlineFinalForm" date="2001-02-27"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-01"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-15"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-30"></event></eventGroup><numberingGroup><numbering type="pageFirst">217</numbering><numbering type="pageLast">229</numbering></numberingGroup><correspondenceTo>Neurosurgical Clinic, Nordstadt Hospital, Haltenhoffstrasse 41, D‐30167 Hannover, Germany</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:CNE.CNE1098.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="12"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="58"></count><count type="wordTotal" number="10330"></count></countGroup><titleGroup><title type="main" xml:lang="en">Comparison of unilateral and bilateral intrastriatal 6‐hydroxydopamine‐induced axon terminal lesions: Evidence for interhemispheric functional coupling of the two nigrostriatal pathways</title><title type="short" xml:lang="en">6‐OHDA‐Induced Axon Terminal Lesions</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Alexandra</givenNames><familyName>Roedter</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Christian</givenNames><familyName>Winkler</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Madjid</givenNames><familyName>Samii</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Gerhard F.</givenNames><familyName>Walter</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Almuth</givenNames><familyName>Brandis</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Guido</givenNames><familyName>Nikkhah</familyName></personName><contactDetails><email>GNikkhah@compuserve.com</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="DE" type="organization"><unparsedAffiliation>Neurosurgical Clinic, Nordstadt Hospital, D‐30167 Hannover, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Neurological Clinic, Hannover Medical School, D‐30625 Hannover, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="DE" type="organization"><unparsedAffiliation>Institute of Neuropathology, Hannover Medical School, D‐30625 Hannover, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">neurodegeneration</keyword><keyword xml:id="kwd3">basal ganglia</keyword><keyword xml:id="kwd4">dopamine</keyword><keyword xml:id="kwd5">skilled forelimb use</keyword><keyword xml:id="kwd6">stepping</keyword></keywordGroup><fundingInfo><fundingAgency>Deutsche Forschungsgemeinschaft</fundingAgency><fundingNumber>DFG Ni 330/4‐1</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Partial lesions of the nigrostriatal dopamine system can be induced reliably by the intrastriatal injection of 6‐hydroxydopamine (6‐OHDA) and are considered to be analogous to the early stages of human Parkinson's disease. Previous studies have established a clear correlation between different doses and placements of the 6‐OHDA toxin and the degree of neurodegenerative changes and behavioral impairments. In the present study, the influence of the interdependence between the two nigrostriatal systems in both hemispheres on the effects on sensorimotor behavioral performances after terminal 6‐OHDA lesions was investigated. The behavioral effects were correlated to the extent of nigral dopamine neuron cell and striatal tyrosine‐hydroxylase (TH)‐positive fiber loss. Sprague‐Dawley rats receiving unilateral intrastriatal 6‐OHDA injections (4 × 5 μg) exhibited a 30–70% reduction in striatal TH‐positive fiber density along an anterior‐posterior gradient, an 80% loss of nigral dopamine neurons and a mild degree of behavioral impairments as revealed by amphetamine‐induced rotational asymmetry, and a reduced performance in the stepping and postural balance tests. When the same amount of toxin was injected twice into both hemispheres (2 × 4 × 5 μg), additional behavioral deficits were observed, consisting of a significant, but temporary, weight loss, a stable reduction in general locomotor activity and explorational behavior, and a long‐term deficit in skilled forelimb use. This is interesting in light of the morphological findings, in which uni‐ and bilaterally lesioned animals did not differ significantly in the extent of TH‐immunoreactive fiber and dopamine neuron loss within the nigrostriatal system in each lesioned hemisphere. These results indicate that the interdependent regulation of the two nigrostriatal systems may provide some compensatory support for the function and behavioral performance of the lesioned side via the normal unlesioned side, which is lost in animals with bilateral lesions of the nigrostriatal system. Therefore, this model of uni‐ and bilateral partial lesions of the nigrostriatal system, as characterized in the present study, may foster further exploration of compensatory functional mechanisms active in the early stages of Parkinson's disease and promote development of novel neuroprotective and restorative strategies. J. Comp. Neurol. 432:217–229, 2001. © 2001 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Comparison of unilateral and bilateral intrastriatal 6‐hydroxydopamine‐induced axon terminal lesions: Evidence for interhemispheric functional coupling of the two nigrostriatal pathways</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>6‐OHDA‐Induced Axon Terminal Lesions</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Comparison of unilateral and bilateral intrastriatal 6‐hydroxydopamine‐induced axon terminal lesions: Evidence for interhemispheric functional coupling of the two nigrostriatal pathways</title></titleInfo><name type="personal"><namePart type="given">Alexandra</namePart><namePart type="family">Roedter</namePart><affiliation>Neurosurgical Clinic, Nordstadt Hospital, D‐30167 Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christian</namePart><namePart type="family">Winkler</namePart><affiliation>Neurosurgical Clinic, Nordstadt Hospital, D‐30167 Hannover, Germany</affiliation><affiliation>Neurological Clinic, Hannover Medical School, D‐30625 Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Madjid</namePart><namePart type="family">Samii</namePart><affiliation>Neurosurgical Clinic, Nordstadt Hospital, D‐30167 Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gerhard F.</namePart><namePart type="family">Walter</namePart><affiliation>Institute of Neuropathology, Hannover Medical School, D‐30625 Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Almuth</namePart><namePart type="family">Brandis</namePart><affiliation>Institute of Neuropathology, Hannover Medical School, D‐30625 Hannover, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Guido</namePart><namePart type="family">Nikkhah</namePart><affiliation>Neurosurgical Clinic, Nordstadt Hospital, D‐30167 Hannover, Germany</affiliation><description>Correspondence: Neurosurgical Clinic, Nordstadt Hospital, Haltenhoffstrasse 41, D‐30167 Hannover, Germany</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>John Wiley & Sons, Inc.</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2001-04-02</dateIssued><dateCaptured encoding="w3cdtf">2000-07-20</dateCaptured><dateValid encoding="w3cdtf">2000-12-28</dateValid><copyrightDate encoding="w3cdtf">2001</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">12</extent><extent unit="tables">2</extent><extent unit="references">58</extent><extent unit="words">10330</extent></physicalDescription><abstract lang="en">Partial lesions of the nigrostriatal dopamine system can be induced reliably by the intrastriatal injection of 6‐hydroxydopamine (6‐OHDA) and are considered to be analogous to the early stages of human Parkinson's disease. Previous studies have established a clear correlation between different doses and placements of the 6‐OHDA toxin and the degree of neurodegenerative changes and behavioral impairments. In the present study, the influence of the interdependence between the two nigrostriatal systems in both hemispheres on the effects on sensorimotor behavioral performances after terminal 6‐OHDA lesions was investigated. The behavioral effects were correlated to the extent of nigral dopamine neuron cell and striatal tyrosine‐hydroxylase (TH)‐positive fiber loss. Sprague‐Dawley rats receiving unilateral intrastriatal 6‐OHDA injections (4 × 5 μg) exhibited a 30–70% reduction in striatal TH‐positive fiber density along an anterior‐posterior gradient, an 80% loss of nigral dopamine neurons and a mild degree of behavioral impairments as revealed by amphetamine‐induced rotational asymmetry, and a reduced performance in the stepping and postural balance tests. When the same amount of toxin was injected twice into both hemispheres (2 × 4 × 5 μg), additional behavioral deficits were observed, consisting of a significant, but temporary, weight loss, a stable reduction in general locomotor activity and explorational behavior, and a long‐term deficit in skilled forelimb use. This is interesting in light of the morphological findings, in which uni‐ and bilaterally lesioned animals did not differ significantly in the extent of TH‐immunoreactive fiber and dopamine neuron loss within the nigrostriatal system in each lesioned hemisphere. These results indicate that the interdependent regulation of the two nigrostriatal systems may provide some compensatory support for the function and behavioral performance of the lesioned side via the normal unlesioned side, which is lost in animals with bilateral lesions of the nigrostriatal system. Therefore, this model of uni‐ and bilateral partial lesions of the nigrostriatal system, as characterized in the present study, may foster further exploration of compensatory functional mechanisms active in the early stages of Parkinson's disease and promote development of novel neuroprotective and restorative strategies. J. Comp. Neurol. 432:217–229, 2001. © 2001 Wiley‐Liss, Inc.</abstract><note type="funding">Deutsche Forschungsgemeinschaft - No. DFG Ni 330/4‐1; </note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>neurodegeneration</topic><topic>basal ganglia</topic><topic>dopamine</topic><topic>skilled forelimb use</topic><topic>stepping</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Comparative Neurology</title></titleInfo><titleInfo type="abbreviated"><title>J. Comp. Neurol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Article</topic></subject><identifier type="ISSN">0021-9967</identifier><identifier type="eISSN">1096-9861</identifier><identifier type="DOI">10.1002/(ISSN)1096-9861</identifier><identifier type="PublisherID">CNE</identifier><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>432</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>217</start><end>229</end><total>13</total></extent></part></relatedItem><identifier type="istex">A877EE715125493EA10CE04D1C132576A7CAAA04</identifier><identifier type="DOI">10.1002/cne.1098</identifier><identifier type="ArticleID">CNE1098</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2001 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>John Wiley & Sons, Inc.</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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