Unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the subthalamic nucleus and substantia nigra in the rat
Identifieur interne : 002130 ( Istex/Corpus ); précédent : 002129; suivant : 002131Unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the subthalamic nucleus and substantia nigra in the rat
Auteurs : S. Breit ; L. Lessmann ; A. Benazzouz ; J. B. SchulzSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2005-11.
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Abstract
Recent data suggest a role for the pedunculopontine nucleus (PPN) in the pathophysiology of Parkinson's disease. Although there is anatomical evidence that the PPN and the basal ganglia are reciprocally connected, the functional importance of these connections is poorly understood. Lesioning of the PPN was shown to induce akinesia in primates, whereas in the 6‐hydroxydopamine rat model the PPN was found to be hyperactive. As both nigrostriatal dopamine depletion and lesioning of the PPN were shown to induce akinesia and parkinsonism, the present study was performed in order to investigate the changes in neuronal activity of the subthalamic nucleus (STN) and the substantia nigra pars reticulata (SNr) after unilateral ibotenic acid lesioning of the PPN and after unilateral 6‐hydroxydopamine lesioning of the substantia nigra pars compacta (SNc). The firing rate of STN neurones significantly increased from 10.2 ± 6.2 (mean ± SD) to 14.6 ± 11.7 spikes/s after lesion of the PPN and to 18.6 ± 14.5 spikes/s after lesion of the SNc. The activity of the SNr significantly increased from 19.6 ± 10.5 to 28.7 ± 13.4 spikes/s after PPN lesioning and to 23.5 ± 10.8 spikes/s after SNc lesioning. Furthermore, PPN lesion decreased the number of spontaneously firing dopaminergic SNc cells, while having no effect on their firing rate. The results of our study show that lesion of the PPN leads to hyperactivity of the STN and SNr, similar to the changes induced by lesion of the SNc. Moreover, the decreased activity of SNc cells observed after PPN lesion might be at the origin of activity changes in the STN and SNr.
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DOI: 10.1111/j.1460-9568.2005.04402.x
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ISTEX:00E15A4979A2F6AA59D6167776ECA03A9FAE5467Le document en format XML
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Lessmann</name><affiliation><mods:affiliation>Neurodegeneration Department, Center of Neurology and Hertie Institute for Clinical Brain Research, University of Tübingen, Hoppe‐Seyler‐Strasse 3, 72076 Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Benazzouz, A" sort="Benazzouz, A" uniqKey="Benazzouz A" first="A." last="Benazzouz">A. Benazzouz</name><affiliation><mods:affiliation>Laboratoire de Neurophysiologie, Basal Gang, CNRS UMR5543, Université Victor Segalen, Bordeaux, France</mods:affiliation></affiliation></author><author><name sortKey="Schulz, J B" sort="Schulz, J B" uniqKey="Schulz J" first="J. B." last="Schulz">J. B. 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Breit</name><affiliation><mods:affiliation>Neurodegeneration Department, Center of Neurology and Hertie Institute for Clinical Brain Research, University of Tübingen, Hoppe‐Seyler‐Strasse 3, 72076 Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Lessmann, L" sort="Lessmann, L" uniqKey="Lessmann L" first="L." last="Lessmann">L. Lessmann</name><affiliation><mods:affiliation>Neurodegeneration Department, Center of Neurology and Hertie Institute for Clinical Brain Research, University of Tübingen, Hoppe‐Seyler‐Strasse 3, 72076 Tübingen, Germany</mods:affiliation></affiliation></author><author><name sortKey="Benazzouz, A" sort="Benazzouz, A" uniqKey="Benazzouz A" first="A." last="Benazzouz">A. Benazzouz</name><affiliation><mods:affiliation>Laboratoire de Neurophysiologie, Basal Gang, CNRS UMR5543, Université Victor Segalen, Bordeaux, France</mods:affiliation></affiliation></author><author><name sortKey="Schulz, J B" sort="Schulz, J B" uniqKey="Schulz J" first="J. B." last="Schulz">J. B. Schulz</name><affiliation><mods:affiliation>Department of Neurodegeneration and Restorative Research, Centers of Neurological Medicine and Molecular Physiology of the Brain (CMPB), University of Göttingen, Germany</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 Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2005-11">2005-11</date><biblScope unit="volume">22</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="2283">2283</biblScope><biblScope unit="page" to="2294">2294</biblScope></imprint><idno type="ISSN">0953-816X</idno></series><idno type="istex">00E15A4979A2F6AA59D6167776ECA03A9FAE5467</idno><idno type="DOI">10.1111/j.1460-9568.2005.04402.x</idno><idno type="ArticleID">EJN4402</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0953-816X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>6‐hydroxydopamine</term><term>akinesia</term><term>extracellular recordings</term><term>pedunculopontine nucleus</term><term>substantia nigra</term><term>subthalamic nucleus</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Recent data suggest a role for the pedunculopontine nucleus (PPN) in the pathophysiology of Parkinson's disease. Although there is anatomical evidence that the PPN and the basal ganglia are reciprocally connected, the functional importance of these connections is poorly understood. Lesioning of the PPN was shown to induce akinesia in primates, whereas in the 6‐hydroxydopamine rat model the PPN was found to be hyperactive. As both nigrostriatal dopamine depletion and lesioning of the PPN were shown to induce akinesia and parkinsonism, the present study was performed in order to investigate the changes in neuronal activity of the subthalamic nucleus (STN) and the substantia nigra pars reticulata (SNr) after unilateral ibotenic acid lesioning of the PPN and after unilateral 6‐hydroxydopamine lesioning of the substantia nigra pars compacta (SNc). The firing rate of STN neurones significantly increased from 10.2 ± 6.2 (mean ± SD) to 14.6 ± 11.7 spikes/s after lesion of the PPN and to 18.6 ± 14.5 spikes/s after lesion of the SNc. The activity of the SNr significantly increased from 19.6 ± 10.5 to 28.7 ± 13.4 spikes/s after PPN lesioning and to 23.5 ± 10.8 spikes/s after SNc lesioning. Furthermore, PPN lesion decreased the number of spontaneously firing dopaminergic SNc cells, while having no effect on their firing rate. The results of our study show that lesion of the PPN leads to hyperactivity of the STN and SNr, similar to the changes induced by lesion of the SNc. Moreover, the decreased activity of SNc cells observed after PPN lesion might be at the origin of activity changes in the STN and SNr.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>S. Breit</name><affiliations><json:string>Neurodegeneration Department, Center of Neurology and Hertie Institute for Clinical Brain Research, University of Tübingen, Hoppe‐Seyler‐Strasse 3, 72076 Tübingen, Germany</json:string></affiliations></json:item><json:item><name>L. Lessmann</name><affiliations><json:string>Neurodegeneration Department, Center of Neurology and Hertie Institute for Clinical Brain Research, University of Tübingen, Hoppe‐Seyler‐Strasse 3, 72076 Tübingen, Germany</json:string></affiliations></json:item><json:item><name>A. Benazzouz</name><affiliations><json:string>Laboratoire de Neurophysiologie, Basal Gang, CNRS UMR5543, Université Victor Segalen, Bordeaux, France</json:string></affiliations></json:item><json:item><name>J. B. Schulz</name><affiliations><json:string>Department of Neurodegeneration and Restorative Research, Centers of Neurological Medicine and Molecular Physiology of the Brain (CMPB), University of Göttingen, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>akinesia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>extracellular recordings</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>6‐hydroxydopamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>pedunculopontine nucleus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>substantia nigra</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>subthalamic nucleus</value></json:item></subject><articleId><json:string>EJN4402</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Recent data suggest a role for the pedunculopontine nucleus (PPN) in the pathophysiology of Parkinson's disease. Although there is anatomical evidence that the PPN and the basal ganglia are reciprocally connected, the functional importance of these connections is poorly understood. Lesioning of the PPN was shown to induce akinesia in primates, whereas in the 6‐hydroxydopamine rat model the PPN was found to be hyperactive. As both nigrostriatal dopamine depletion and lesioning of the PPN were shown to induce akinesia and parkinsonism, the present study was performed in order to investigate the changes in neuronal activity of the subthalamic nucleus (STN) and the substantia nigra pars reticulata (SNr) after unilateral ibotenic acid lesioning of the PPN and after unilateral 6‐hydroxydopamine lesioning of the substantia nigra pars compacta (SNc). The firing rate of STN neurones significantly increased from 10.2 ± 6.2 (mean ± SD) to 14.6 ± 11.7 spikes/s after lesion of the PPN and to 18.6 ± 14.5 spikes/s after lesion of the SNc. The activity of the SNr significantly increased from 19.6 ± 10.5 to 28.7 ± 13.4 spikes/s after PPN lesioning and to 23.5 ± 10.8 spikes/s after SNc lesioning. Furthermore, PPN lesion decreased the number of spontaneously firing dopaminergic SNc cells, while having no effect on their firing rate. The results of our study show that lesion of the PPN leads to hyperactivity of the STN and SNr, similar to the changes induced by lesion of the SNc. Moreover, the decreased activity of SNc cells observed after PPN lesion might be at the origin of activity changes in the STN and SNr.</abstract><qualityIndicators><score>8.464</score><pdfVersion>1.4</pdfVersion><pdfPageSize>595 x 782 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1619</abstractCharCount><pdfWordCount>7429</pdfWordCount><pdfCharCount>45621</pdfCharCount><pdfPageCount>12</pdfPageCount><abstractWordCount>247</abstractWordCount></qualityIndicators><title>Unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the subthalamic nucleus and substantia nigra in the rat</title><refBibs><json:item><author><json:item><name>E.E. Benarroch</name></json:item><json:item><name>A.M. Schmeichel</name></json:item><json:item><name>J.E. 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Neurol.</title></host><title>The pedunculopontine nucleus in Parkinson's disease</title></json:item></refBibs><genre><json:string>article</json:string></genre><host><volume>22</volume><publisherId><json:string>EJN</json:string></publisherId><pages><total>12</total><last>2294</last><first>2283</first></pages><issn><json:string>0953-816X</json:string></issn><issue>9</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-9568</json:string></eissn><title>European Journal of Neuroscience</title><doi><json:string>10.1111/(ISSN)1460-9568</json:string></doi></host><categories><wos><json:string>science</json:string><json:string>neurosciences</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & neurosurgery</json:string></scienceMetrix></categories><publicationDate>2005</publicationDate><copyrightDate>2005</copyrightDate><doi><json:string>10.1111/j.1460-9568.2005.04402.x</json:string></doi><id>00E15A4979A2F6AA59D6167776ECA03A9FAE5467</id><score>0.090836</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/00E15A4979A2F6AA59D6167776ECA03A9FAE5467/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/00E15A4979A2F6AA59D6167776ECA03A9FAE5467/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/00E15A4979A2F6AA59D6167776ECA03A9FAE5467/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the subthalamic nucleus and substantia nigra in the rat</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2005</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the subthalamic nucleus and substantia nigra in the rat</title><author xml:id="author-1"><persName><forename type="first">S.</forename><surname>Breit</surname></persName><note type="biography">S.B. and L.L. contributed equally to this work.</note><affiliation>S.B. and L.L. contributed equally to this work.</affiliation><affiliation>Neurodegeneration Department, Center of Neurology and Hertie Institute for Clinical Brain Research, University of Tübingen, Hoppe‐Seyler‐Strasse 3, 72076 Tübingen, Germany</affiliation></author><author xml:id="author-2"><persName><forename type="first">L.</forename><surname>Lessmann</surname></persName><note type="biography">S.B. and L.L. contributed equally to this work.</note><affiliation>S.B. and L.L. contributed equally to this work.</affiliation><affiliation>Neurodegeneration Department, Center of Neurology and Hertie Institute for Clinical Brain Research, University of Tübingen, Hoppe‐Seyler‐Strasse 3, 72076 Tübingen, Germany</affiliation></author><author xml:id="author-3"><persName><forename type="first">A.</forename><surname>Benazzouz</surname></persName><affiliation>Laboratoire de Neurophysiologie, Basal Gang, CNRS UMR5543, Université Victor Segalen, Bordeaux, France</affiliation></author><author xml:id="author-4"><persName><forename type="first">J. B.</forename><surname>Schulz</surname></persName><affiliation>Department of Neurodegeneration and Restorative Research, Centers of Neurological Medicine and Molecular Physiology of the Brain (CMPB), University of Göttingen, Germany</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 Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2005-11"></date><biblScope unit="volume">22</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="2283">2283</biblScope><biblScope unit="page" to="2294">2294</biblScope></imprint></monogr><idno type="istex">00E15A4979A2F6AA59D6167776ECA03A9FAE5467</idno><idno type="DOI">10.1111/j.1460-9568.2005.04402.x</idno><idno type="ArticleID">EJN4402</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2005</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Recent data suggest a role for the pedunculopontine nucleus (PPN) in the pathophysiology of Parkinson's disease. Although there is anatomical evidence that the PPN and the basal ganglia are reciprocally connected, the functional importance of these connections is poorly understood. Lesioning of the PPN was shown to induce akinesia in primates, whereas in the 6‐hydroxydopamine rat model the PPN was found to be hyperactive. As both nigrostriatal dopamine depletion and lesioning of the PPN were shown to induce akinesia and parkinsonism, the present study was performed in order to investigate the changes in neuronal activity of the subthalamic nucleus (STN) and the substantia nigra pars reticulata (SNr) after unilateral ibotenic acid lesioning of the PPN and after unilateral 6‐hydroxydopamine lesioning of the substantia nigra pars compacta (SNc). The firing rate of STN neurones significantly increased from 10.2 ± 6.2 (mean ± SD) to 14.6 ± 11.7 spikes/s after lesion of the PPN and to 18.6 ± 14.5 spikes/s after lesion of the SNc. The activity of the SNr significantly increased from 19.6 ± 10.5 to 28.7 ± 13.4 spikes/s after PPN lesioning and to 23.5 ± 10.8 spikes/s after SNc lesioning. Furthermore, PPN lesion decreased the number of spontaneously firing dopaminergic SNc cells, while having no effect on their firing rate. The results of our study show that lesion of the PPN leads to hyperactivity of the STN and SNr, similar to the changes induced by lesion of the SNc. Moreover, the decreased activity of SNc cells observed after PPN lesion might be at the origin of activity changes in the STN and SNr.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>akinesia</term></item><item><term>extracellular recordings</term></item><item><term>6‐hydroxydopamine</term></item><item><term>pedunculopontine nucleus</term></item><item><term>substantia nigra</term></item><item><term>subthalamic nucleus</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/00E15A4979A2F6AA59D6167776ECA03A9FAE5467/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 Science 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="11009"><doi origin="wiley">10.1111/ejn.2005.22.issue-9</doi><numberingGroup><numbering type="journalVolume" number="22">22</numbering><numbering type="journalIssue" number="9">9</numbering></numberingGroup><coverDate startDate="2005-11">November 2005</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="16" status="forIssue"><doi origin="wiley">10.1111/j.1460-9568.2005.04402.x</doi><idGroup><id type="unit" value="EJN4402"></id></idGroup><countGroup><count type="pageTotal" number="12"></count></countGroup><titleGroup><title type="tocHeading1">Research Reports</title></titleGroup><eventGroup><event type="firstOnline" date="2005-11-01"></event><event type="publishedOnlineFinalForm" date="2005-11-01"></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="2283">2283</numbering><numbering type="pageLast" number="2294">2294</numbering></numberingGroup><correspondenceTo>Dr Sorin Breit, as above.
E‐mail: <email normalForm="sorin.breit@uni-tuebingen.de">sorin.breit@uni‐tuebingen.de</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EJN.EJN4402.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 8 March 2005, revised 9 July 2005, accepted 9 August 2005</unparsedEditorialHistory><countGroup><count type="figureTotal" number="8"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="76"></count><count type="wordTotal" number="5725"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the subthalamic nucleus and substantia nigra in the rat</title><title type="shortAuthors">S. Breit <i>et al.</i></title><title type="short">Unilateral lesion of the pedunculopontine nucleus</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" noteRef="#fn1"><personName><givenNames>S.</givenNames><familyName>Breit</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1" noteRef="#fn1"><personName><givenNames>L.</givenNames><familyName>Lessmann</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>A.</givenNames><familyName>Benazzouz</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a3"><personName><givenNames>J. B.</givenNames><familyName>Schulz</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="DE"><unparsedAffiliation>Neurodegeneration Department, Center of Neurology and Hertie Institute for Clinical Brain Research, University of Tübingen, Hoppe‐Seyler‐Strasse 3, 72076 Tübingen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="FR"><unparsedAffiliation>Laboratoire de Neurophysiologie, Basal Gang, CNRS UMR5543, Université Victor Segalen, Bordeaux, France</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="DE"><unparsedAffiliation>Department of Neurodegeneration and Restorative Research, Centers of Neurological Medicine and Molecular Physiology of the Brain (CMPB), University of Göttingen, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">akinesia</keyword><keyword xml:id="k2">extracellular recordings</keyword><keyword xml:id="k3">6‐hydroxydopamine</keyword><keyword xml:id="k4">pedunculopontine nucleus</keyword><keyword xml:id="k5">substantia nigra</keyword><keyword xml:id="k6">subthalamic nucleus</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Recent data suggest a role for the pedunculopontine nucleus (PPN) in the pathophysiology of Parkinson's disease. Although there is anatomical evidence that the PPN and the basal ganglia are reciprocally connected, the functional importance of these connections is poorly understood. Lesioning of the PPN was shown to induce akinesia in primates, whereas in the 6‐hydroxydopamine rat model the PPN was found to be hyperactive. As both nigrostriatal dopamine depletion and lesioning of the PPN were shown to induce akinesia and parkinsonism, the present study was performed in order to investigate the changes in neuronal activity of the subthalamic nucleus (STN) and the substantia nigra pars reticulata (SNr) after unilateral ibotenic acid lesioning of the PPN and after unilateral 6‐hydroxydopamine lesioning of the substantia nigra pars compacta (SNc). The firing rate of STN neurones significantly increased from 10.2 ± 6.2 (mean ± SD) to 14.6 ± 11.7 spikes/s after lesion of the PPN and to 18.6 ± 14.5 spikes/s after lesion of the SNc. The activity of the SNr significantly increased from 19.6 ± 10.5 to 28.7 ± 13.4 spikes/s after PPN lesioning and to 23.5 ± 10.8 spikes/s after SNc lesioning. Furthermore, PPN lesion decreased the number of spontaneously firing dopaminergic SNc cells, while having no effect on their firing rate. The results of our study show that lesion of the PPN leads to hyperactivity of the STN and SNr, similar to the changes induced by lesion of the SNc. Moreover, the decreased activity of SNc cells observed after PPN lesion might be at the origin of activity changes in the STN and SNr.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><label>*</label><p> S.B. and L.L. contributed equally to this work.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the subthalamic nucleus and substantia nigra in the rat</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Unilateral lesion of the pedunculopontine nucleus</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the subthalamic nucleus and substantia nigra in the rat</title></titleInfo><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Breit</namePart><affiliation>Neurodegeneration Department, Center of Neurology and Hertie Institute for Clinical Brain Research, University of Tübingen, Hoppe‐Seyler‐Strasse 3, 72076 Tübingen, Germany</affiliation><description>S.B. and L.L. contributed equally to this work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L.</namePart><namePart type="family">Lessmann</namePart><affiliation>Neurodegeneration Department, Center of Neurology and Hertie Institute for Clinical Brain Research, University of Tübingen, Hoppe‐Seyler‐Strasse 3, 72076 Tübingen, Germany</affiliation><description>S.B. and L.L. contributed equally to this work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Benazzouz</namePart><affiliation>Laboratoire de Neurophysiologie, Basal Gang, CNRS UMR5543, Université Victor Segalen, Bordeaux, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. B.</namePart><namePart type="family">Schulz</namePart><affiliation>Department of Neurodegeneration and Restorative Research, Centers of Neurological Medicine and Molecular Physiology of the Brain (CMPB), University of Göttingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Science Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2005-11</dateIssued><edition>Received 8 March 2005, revised 9 July 2005, accepted 9 August 2005</edition><copyrightDate encoding="w3cdtf">2005</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">8</extent><extent unit="references">76</extent><extent unit="words">5725</extent></physicalDescription><abstract lang="en">Recent data suggest a role for the pedunculopontine nucleus (PPN) in the pathophysiology of Parkinson's disease. Although there is anatomical evidence that the PPN and the basal ganglia are reciprocally connected, the functional importance of these connections is poorly understood. Lesioning of the PPN was shown to induce akinesia in primates, whereas in the 6‐hydroxydopamine rat model the PPN was found to be hyperactive. As both nigrostriatal dopamine depletion and lesioning of the PPN were shown to induce akinesia and parkinsonism, the present study was performed in order to investigate the changes in neuronal activity of the subthalamic nucleus (STN) and the substantia nigra pars reticulata (SNr) after unilateral ibotenic acid lesioning of the PPN and after unilateral 6‐hydroxydopamine lesioning of the substantia nigra pars compacta (SNc). The firing rate of STN neurones significantly increased from 10.2 ± 6.2 (mean ± SD) to 14.6 ± 11.7 spikes/s after lesion of the PPN and to 18.6 ± 14.5 spikes/s after lesion of the SNc. The activity of the SNr significantly increased from 19.6 ± 10.5 to 28.7 ± 13.4 spikes/s after PPN lesioning and to 23.5 ± 10.8 spikes/s after SNc lesioning. Furthermore, PPN lesion decreased the number of spontaneously firing dopaminergic SNc cells, while having no effect on their firing rate. The results of our study show that lesion of the PPN leads to hyperactivity of the STN and SNr, similar to the changes induced by lesion of the SNc. Moreover, the decreased activity of SNc cells observed after PPN lesion might be at the origin of activity changes in the STN and SNr.</abstract><subject lang="en"><genre>keywords</genre><topic>akinesia</topic><topic>extracellular recordings</topic><topic>6‐hydroxydopamine</topic><topic>pedunculopontine nucleus</topic><topic>substantia nigra</topic><topic>subthalamic nucleus</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>2005</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>2283</start><end>2294</end><total>12</total></extent></part></relatedItem><identifier type="istex">00E15A4979A2F6AA59D6167776ECA03A9FAE5467</identifier><identifier type="DOI">10.1111/j.1460-9568.2005.04402.x</identifier><identifier type="ArticleID">EJN4402</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Science Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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