Effect of MPTP‐induced denervation on basal ganglia GABAB receptors: Correlation with dopamine concentrations and dopamine transporter
Identifieur interne : 000C10 ( Istex/Corpus ); précédent : 000C09; suivant : 000C11Effect of MPTP‐induced denervation on basal ganglia GABAB receptors: Correlation with dopamine concentrations and dopamine transporter
Auteurs : Frédéric Calon ; Nadia Lavertu ; Anne-Marie Lemieux ; Marc Morissette ; Martin Goulet ; Richard Grondin ; Pierre J. Blanchet ; Paul J. Bédard ; Thérèse Di PaoloSource :
- Synapse [ 0887-4476 ] ; 2001-06-01.
English descriptors
Abstract
We investigated the effect of MPTP‐induced lesion of the substantia nigra pars compacta (SNpc) dopaminergic neurons on GABAB receptors in the basal ganglia of mice and monkeys using receptor autoradiography and in situ hybridization. The extent of the lesion was measured with striatal catecholamine content, striatal binding of 125I‐RTI‐121 to dopamine transporter (DAT), and DAT expression in the SNpc. GABAB receptors in mice brain were evaluated using 3H‐CGP54626 and its expression was measured with oligonucleotides probes targeting the mRNAs of GABAB(1a+b), GABAB(1a), GABAB(1b), GABAB(2) subunits. In monkeys, 125I‐CGP64213 and selective probes for GABAB(1a+b) and GABAB(2) mRNAs were used. In mice, dopamine content, 125I‐RTI‐121 binding, and DAT expression were reduced by 44%, 40%, and 39% after a dose of 40 mg/kg of MPTP and 74%, 70%, and 34% after 120 mg/kg of MPTP, respectively. In monkeys, dopamine content and DAT expression were decreased by more than 90% and 80%, respectively. In the striatum and the subthalamic nucleus, GABAB receptors were unchanged following MPTP in both species. In the SNpc of mice, MPTP (120 mg/kg) induced a significant decrease of 3H‐CGP54626 binding (−10%) and of the expression of GABAB(1a+b) mRNA (−13%). The decrease of the expression of GABAB(1a+b) mRNA was correlated with dopamine content, 125I‐RTI‐121 binding and DAT expression. In MPTP‐treated monkeys, 125I‐CGP64213 binding (−40%), GABAB(1a+b) mRNA (−69%) and GABAB(2) mRNA (−66%) were also significantly decreased in the SNpc. Our results suggest that MPTP‐induced denervation is associated with a decrease of GABAB receptors restricted to the SNpc. These observations may be relevant to the pathophysiology of motor disorders involving dysfunction of the basal ganglia such as Parkinson disease. Synapse 40:225–234, 2001. © 2001 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/syn.1045
Links to Exploration step
ISTEX:8DD5BCF1B10708AE3857882704F6FE29F9090748Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Effect of MPTP‐induced denervation on basal ganglia GABAB receptors: Correlation with dopamine concentrations and dopamine transporter</title><author><name sortKey="Calon, Frederic" sort="Calon, Frederic" uniqKey="Calon F" first="Frédéric" last="Calon">Frédéric Calon</name><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Lavertu, Nadia" sort="Lavertu, Nadia" uniqKey="Lavertu N" first="Nadia" last="Lavertu">Nadia Lavertu</name><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Lemieux, Anne Arie" sort="Lemieux, Anne Arie" uniqKey="Lemieux A" first="Anne-Marie" last="Lemieux">Anne-Marie Lemieux</name><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Morissette, Marc" sort="Morissette, Marc" uniqKey="Morissette M" first="Marc" last="Morissette">Marc Morissette</name><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Goulet, Martin" sort="Goulet, Martin" uniqKey="Goulet M" first="Martin" last="Goulet">Martin Goulet</name><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Grondin, Richard" sort="Grondin, Richard" uniqKey="Grondin R" first="Richard" last="Grondin">Richard Grondin</name><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Blanchet, Pierre J" sort="Blanchet, Pierre J" uniqKey="Blanchet P" first="Pierre J." last="Blanchet">Pierre J. Blanchet</name><affiliation><mods:affiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Bedard, Paul J" sort="Bedard, Paul J" uniqKey="Bedard P" first="Paul J." last="Bédard">Paul J. Bédard</name><affiliation><mods:affiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), 2705 Laurier Boulevard, Sainte‐Foy, Qc, Canada G1V 4G2</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:8DD5BCF1B10708AE3857882704F6FE29F9090748</idno><date when="2001" year="2001">2001</date><idno type="doi">10.1002/syn.1045</idno><idno type="url">https://api-v5.istex.fr/document/8DD5BCF1B10708AE3857882704F6FE29F9090748/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000C10</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000C10</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Effect of MPTP‐induced denervation on basal ganglia GABAB receptors: Correlation with dopamine concentrations and dopamine transporter</title><author><name sortKey="Calon, Frederic" sort="Calon, Frederic" uniqKey="Calon F" first="Frédéric" last="Calon">Frédéric Calon</name><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Lavertu, Nadia" sort="Lavertu, Nadia" uniqKey="Lavertu N" first="Nadia" last="Lavertu">Nadia Lavertu</name><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Lemieux, Anne Arie" sort="Lemieux, Anne Arie" uniqKey="Lemieux A" first="Anne-Marie" last="Lemieux">Anne-Marie Lemieux</name><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Morissette, Marc" sort="Morissette, Marc" uniqKey="Morissette M" first="Marc" last="Morissette">Marc Morissette</name><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Goulet, Martin" sort="Goulet, Martin" uniqKey="Goulet M" first="Martin" last="Goulet">Martin Goulet</name><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Grondin, Richard" sort="Grondin, Richard" uniqKey="Grondin R" first="Richard" last="Grondin">Richard Grondin</name><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Blanchet, Pierre J" sort="Blanchet, Pierre J" uniqKey="Blanchet P" first="Pierre J." last="Blanchet">Pierre J. Blanchet</name><affiliation><mods:affiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Bedard, Paul J" sort="Bedard, Paul J" uniqKey="Bedard P" first="Paul J." last="Bédard">Paul J. Bédard</name><affiliation><mods:affiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</mods:affiliation></affiliation></author><author><name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), 2705 Laurier Boulevard, Sainte‐Foy, Qc, Canada G1V 4G2</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Synapse</title><title level="j" type="abbrev">Synapse</title><idno type="ISSN">0887-4476</idno><idno type="eISSN">1098-2396</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2001-06-01">2001-06-01</date><biblScope unit="volume">40</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="225">225</biblScope><biblScope unit="page" to="234">234</biblScope></imprint><idno type="ISSN">0887-4476</idno></series><idno type="istex">8DD5BCF1B10708AE3857882704F6FE29F9090748</idno><idno type="DOI">10.1002/syn.1045</idno><idno type="ArticleID">SYN1045</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0887-4476</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>GABA</term><term>Parkinson</term><term>autoradiography</term><term>dopamine</term><term>in situ hybridization</term><term>substantia nigra</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We investigated the effect of MPTP‐induced lesion of the substantia nigra pars compacta (SNpc) dopaminergic neurons on GABAB receptors in the basal ganglia of mice and monkeys using receptor autoradiography and in situ hybridization. The extent of the lesion was measured with striatal catecholamine content, striatal binding of 125I‐RTI‐121 to dopamine transporter (DAT), and DAT expression in the SNpc. GABAB receptors in mice brain were evaluated using 3H‐CGP54626 and its expression was measured with oligonucleotides probes targeting the mRNAs of GABAB(1a+b), GABAB(1a), GABAB(1b), GABAB(2) subunits. In monkeys, 125I‐CGP64213 and selective probes for GABAB(1a+b) and GABAB(2) mRNAs were used. In mice, dopamine content, 125I‐RTI‐121 binding, and DAT expression were reduced by 44%, 40%, and 39% after a dose of 40 mg/kg of MPTP and 74%, 70%, and 34% after 120 mg/kg of MPTP, respectively. In monkeys, dopamine content and DAT expression were decreased by more than 90% and 80%, respectively. In the striatum and the subthalamic nucleus, GABAB receptors were unchanged following MPTP in both species. In the SNpc of mice, MPTP (120 mg/kg) induced a significant decrease of 3H‐CGP54626 binding (−10%) and of the expression of GABAB(1a+b) mRNA (−13%). The decrease of the expression of GABAB(1a+b) mRNA was correlated with dopamine content, 125I‐RTI‐121 binding and DAT expression. In MPTP‐treated monkeys, 125I‐CGP64213 binding (−40%), GABAB(1a+b) mRNA (−69%) and GABAB(2) mRNA (−66%) were also significantly decreased in the SNpc. Our results suggest that MPTP‐induced denervation is associated with a decrease of GABAB receptors restricted to the SNpc. These observations may be relevant to the pathophysiology of motor disorders involving dysfunction of the basal ganglia such as Parkinson disease. Synapse 40:225–234, 2001. © 2001 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Frédéric Calon</name><affiliations><json:string>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</json:string></affiliations></json:item><json:item><name>Nadia Lavertu</name><affiliations><json:string>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</json:string></affiliations></json:item><json:item><name>Anne‐Marie Lemieux</name><affiliations><json:string>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</json:string></affiliations></json:item><json:item><name>Marc Morissette</name><affiliations><json:string>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</json:string></affiliations></json:item><json:item><name>Martin Goulet</name><affiliations><json:string>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</json:string></affiliations></json:item><json:item><name>Richard Grondin</name><affiliations><json:string>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</json:string><json:string>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</json:string></affiliations></json:item><json:item><name>Pierre J. Blanchet</name><affiliations><json:string>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</json:string></affiliations></json:item><json:item><name>Paul J. Bédard</name><affiliations><json:string>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</json:string></affiliations></json:item><json:item><name>Thérèse Di Paolo</name><affiliations><json:string>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</json:string><json:string>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), 2705 Laurier Boulevard, Sainte‐Foy, Qc, Canada G1V 4G2</json:string></affiliations></json:item></author><subject><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>Parkinson</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dopamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>GABA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>autoradiography</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>in situ hybridization</value></json:item></subject><articleId><json:string>SYN1045</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>We investigated the effect of MPTP‐induced lesion of the substantia nigra pars compacta (SNpc) dopaminergic neurons on GABAB receptors in the basal ganglia of mice and monkeys using receptor autoradiography and in situ hybridization. The extent of the lesion was measured with striatal catecholamine content, striatal binding of 125I‐RTI‐121 to dopamine transporter (DAT), and DAT expression in the SNpc. GABAB receptors in mice brain were evaluated using 3H‐CGP54626 and its expression was measured with oligonucleotides probes targeting the mRNAs of GABAB(1a+b), GABAB(1a), GABAB(1b), GABAB(2) subunits. In monkeys, 125I‐CGP64213 and selective probes for GABAB(1a+b) and GABAB(2) mRNAs were used. In mice, dopamine content, 125I‐RTI‐121 binding, and DAT expression were reduced by 44%, 40%, and 39% after a dose of 40 mg/kg of MPTP and 74%, 70%, and 34% after 120 mg/kg of MPTP, respectively. In monkeys, dopamine content and DAT expression were decreased by more than 90% and 80%, respectively. In the striatum and the subthalamic nucleus, GABAB receptors were unchanged following MPTP in both species. In the SNpc of mice, MPTP (120 mg/kg) induced a significant decrease of 3H‐CGP54626 binding (−10%) and of the expression of GABAB(1a+b) mRNA (−13%). The decrease of the expression of GABAB(1a+b) mRNA was correlated with dopamine content, 125I‐RTI‐121 binding and DAT expression. In MPTP‐treated monkeys, 125I‐CGP64213 binding (−40%), GABAB(1a+b) mRNA (−69%) and GABAB(2) mRNA (−66%) were also significantly decreased in the SNpc. Our results suggest that MPTP‐induced denervation is associated with a decrease of GABAB receptors restricted to the SNpc. These observations may be relevant to the pathophysiology of motor disorders involving dysfunction of the basal ganglia such as Parkinson disease. Synapse 40:225–234, 2001. © 2001 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>8</score><pdfVersion>1.2</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1855</abstractCharCount><pdfWordCount>6217</pdfWordCount><pdfCharCount>39723</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>273</abstractWordCount></qualityIndicators><title>Effect of MPTP‐induced denervation on basal ganglia GABAB receptors: Correlation with dopamine concentrations and dopamine transporter</title><genre><json:string>article</json:string></genre><host><title>Synapse</title><language><json:string>unknown</json:string></language><doi><json:string>10.1002/(ISSN)1098-2396</json:string></doi><issn><json:string>0887-4476</json:string></issn><eissn><json:string>1098-2396</json:string></eissn><publisherId><json:string>SYN</json:string></publisherId><volume>40</volume><issue>3</issue><pages><first>225</first><last>234</last><total>10</total></pages><genre><json:string>journal</json:string></genre></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><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences medicales</json:string><json:string>neurologie</json:string></inist></categories><publicationDate>2001</publicationDate><copyrightDate>2001</copyrightDate><doi><json:string>10.1002/syn.1045</json:string></doi><id>8DD5BCF1B10708AE3857882704F6FE29F9090748</id><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api-v5.istex.fr/document/8DD5BCF1B10708AE3857882704F6FE29F9090748/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api-v5.istex.fr/document/8DD5BCF1B10708AE3857882704F6FE29F9090748/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api-v5.istex.fr/document/8DD5BCF1B10708AE3857882704F6FE29F9090748/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Effect of MPTP‐induced denervation on basal ganglia GABAB receptors: Correlation with dopamine concentrations and dopamine transporter</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><availability><p>Copyright © 2001 Wiley‐Liss, Inc.</p></availability><date>2001</date></publicationStmt><notesStmt><note>Medical Research Council of Canada</note><note>Novartis</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Effect of MPTP‐induced denervation on basal ganglia GABAB receptors: Correlation with dopamine concentrations and dopamine transporter</title><author xml:id="author-1"><persName><forename type="first">Frédéric</forename><surname>Calon</surname></persName><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</affiliation></author><author xml:id="author-2"><persName><forename type="first">Nadia</forename><surname>Lavertu</surname></persName><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</affiliation></author><author xml:id="author-3"><persName><forename type="first">Anne‐Marie</forename><surname>Lemieux</surname></persName><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</affiliation></author><author xml:id="author-4"><persName><forename type="first">Marc</forename><surname>Morissette</surname></persName><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</affiliation></author><author xml:id="author-5"><persName><forename type="first">Martin</forename><surname>Goulet</surname></persName><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</affiliation></author><author xml:id="author-6"><persName><forename type="first">Richard</forename><surname>Grondin</surname></persName><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</affiliation><affiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</affiliation></author><author xml:id="author-7"><persName><forename type="first">Pierre J.</forename><surname>Blanchet</surname></persName><affiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</affiliation></author><author xml:id="author-8"><persName><forename type="first">Paul J.</forename><surname>Bédard</surname></persName><affiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</affiliation></author><author xml:id="author-9"><persName><forename type="first">Thérèse</forename><surname>Di Paolo</surname></persName><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</affiliation><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), 2705 Laurier Boulevard, Sainte‐Foy, Qc, Canada G1V 4G2</affiliation></author></analytic><monogr><title level="j">Synapse</title><title level="j" type="abbrev">Synapse</title><idno type="pISSN">0887-4476</idno><idno type="eISSN">1098-2396</idno><idno type="DOI">10.1002/(ISSN)1098-2396</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2001-06-01"></date><biblScope unit="volume">40</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="225">225</biblScope><biblScope unit="page" to="234">234</biblScope></imprint></monogr><idno type="istex">8DD5BCF1B10708AE3857882704F6FE29F9090748</idno><idno type="DOI">10.1002/syn.1045</idno><idno type="ArticleID">SYN1045</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We investigated the effect of MPTP‐induced lesion of the substantia nigra pars compacta (SNpc) dopaminergic neurons on GABAB receptors in the basal ganglia of mice and monkeys using receptor autoradiography and in situ hybridization. The extent of the lesion was measured with striatal catecholamine content, striatal binding of 125I‐RTI‐121 to dopamine transporter (DAT), and DAT expression in the SNpc. GABAB receptors in mice brain were evaluated using 3H‐CGP54626 and its expression was measured with oligonucleotides probes targeting the mRNAs of GABAB(1a+b), GABAB(1a), GABAB(1b), GABAB(2) subunits. In monkeys, 125I‐CGP64213 and selective probes for GABAB(1a+b) and GABAB(2) mRNAs were used. In mice, dopamine content, 125I‐RTI‐121 binding, and DAT expression were reduced by 44%, 40%, and 39% after a dose of 40 mg/kg of MPTP and 74%, 70%, and 34% after 120 mg/kg of MPTP, respectively. In monkeys, dopamine content and DAT expression were decreased by more than 90% and 80%, respectively. In the striatum and the subthalamic nucleus, GABAB receptors were unchanged following MPTP in both species. In the SNpc of mice, MPTP (120 mg/kg) induced a significant decrease of 3H‐CGP54626 binding (−10%) and of the expression of GABAB(1a+b) mRNA (−13%). The decrease of the expression of GABAB(1a+b) mRNA was correlated with dopamine content, 125I‐RTI‐121 binding and DAT expression. In MPTP‐treated monkeys, 125I‐CGP64213 binding (−40%), GABAB(1a+b) mRNA (−69%) and GABAB(2) mRNA (−66%) were also significantly decreased in the SNpc. Our results suggest that MPTP‐induced denervation is associated with a decrease of GABAB receptors restricted to the SNpc. These observations may be relevant to the pathophysiology of motor disorders involving dysfunction of the basal ganglia such as Parkinson disease. Synapse 40:225–234, 2001. © 2001 Wiley‐Liss, Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>substantia nigra</term></item><item><term>Parkinson</term></item><item><term>dopamine</term></item><item><term>GABA</term></item><item><term>autoradiography</term></item><item><term>in situ hybridization</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2000-08-13">Received</change><change when="2000-12-02">Registration</change><change when="2001-06-01">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/8DD5BCF1B10708AE3857882704F6FE29F9090748/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>John Wiley & Sons, Inc.</publisherName><publisherLoc>New York</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1098-2396</doi><issn type="print">0887-4476</issn><issn type="electronic">1098-2396</issn><idGroup><id type="product" value="SYN"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="SYNAPSE">Synapse</title><title type="short">Synapse</title></titleGroup></publicationMeta><publicationMeta level="part" position="30"><doi origin="wiley" registered="yes">10.1002/syn.v40:3</doi><numberingGroup><numbering type="journalVolume" number="40">40</numbering><numbering type="journalIssue">3</numbering></numberingGroup><coverDate startDate="2001-06-01">1 June 2001</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="80" status="forIssue"><doi origin="wiley" registered="yes">10.1002/syn.1045</doi><idGroup><id type="unit" value="SYN1045"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><copyright ownership="publisher">Copyright © 2001 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2000-08-13"></event><event type="manuscriptAccepted" date="2000-12-02"></event><event type="firstOnline" date="2001-04-09"></event><event type="publishedOnlineFinalForm" date="2001-04-09"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-04"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-10"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-03"></event></eventGroup><numberingGroup><numbering type="pageFirst">225</numbering><numbering type="pageLast">234</numbering></numberingGroup><correspondenceTo>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), 2705 Laurier Boulevard, Sainte‐Foy, Qc, Canada G1V 4G2</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:SYN.SYN1045.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="48"></count><count type="wordTotal" number="7569"></count></countGroup><titleGroup><title type="main" xml:lang="en">Effect of MPTP‐induced denervation on basal ganglia GABA<sub>B</sub> receptors: Correlation with dopamine concentrations and dopamine transporter</title><title type="short" xml:lang="en">GABA<sub>B</sub> Receptors in MPTP‐Treated Animals</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Frédéric</givenNames><familyName>Calon</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Nadia</givenNames><familyName>Lavertu</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Anne‐Marie</givenNames><familyName>Lemieux</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Marc</givenNames><familyName>Morissette</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Martin</givenNames><familyName>Goulet</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Richard</givenNames><familyName>Grondin</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Pierre J.</givenNames><familyName>Blanchet</familyName></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Paul J.</givenNames><familyName>Bédard</familyName></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Thérèse</givenNames><familyName>Di Paolo</familyName></personName><contactDetails><email>therese.dipaolo@crchul.ulaval.ca</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CA" type="organization"><unparsedAffiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="CA" type="organization"><unparsedAffiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">substantia nigra</keyword><keyword xml:id="kwd2">Parkinson</keyword><keyword xml:id="kwd3">dopamine</keyword><keyword xml:id="kwd4">GABA</keyword><keyword xml:id="kwd5">autoradiography</keyword><keyword xml:id="kwd6">in situ hybridization</keyword></keywordGroup><fundingInfo><fundingAgency>Medical Research Council of Canada</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Novartis</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We investigated the effect of MPTP‐induced lesion of the substantia nigra pars compacta (SNpc) dopaminergic neurons on GABA<sub>B</sub> receptors in the basal ganglia of mice and monkeys using receptor autoradiography and in situ hybridization. The extent of the lesion was measured with striatal catecholamine content, striatal binding of <sup>125</sup>I‐RTI‐121 to dopamine transporter (DAT), and DAT expression in the SNpc. GABA<sub>B</sub> receptors in mice brain were evaluated using <sup>3</sup>H‐CGP54626 and its expression was measured with oligonucleotides probes targeting the mRNAs of GABA<sub>B(1a+b)</sub>, GABA<sub>B(1a)</sub>, GABA<sub>B(1b)</sub>, GABA<sub>B(2)</sub> subunits. In monkeys, <sup>125</sup>I‐CGP64213 and selective probes for GABA<sub>B(1a+b)</sub> and GABA<sub>B(2)</sub> mRNAs were used. In mice, dopamine content, <sup>125</sup>I‐RTI‐121 binding, and DAT expression were reduced by 44%, 40%, and 39% after a dose of 40 mg/kg of MPTP and 74%, 70%, and 34% after 120 mg/kg of MPTP, respectively. In monkeys, dopamine content and DAT expression were decreased by more than 90% and 80%, respectively. In the striatum and the subthalamic nucleus, GABA<sub>B</sub> receptors were unchanged following MPTP in both species. In the SNpc of mice, MPTP (120 mg/kg) induced a significant decrease of <sup>3</sup>H‐CGP54626 binding (−10%) and of the expression of GABA<sub>B(1a+b)</sub> mRNA (−13%). The decrease of the expression of GABA<sub>B(1a+b)</sub> mRNA was correlated with dopamine content, <sup>125</sup>I‐RTI‐121 binding and DAT expression. In MPTP‐treated monkeys, <sup>125</sup>I‐CGP64213 binding (−40%), GABA<sub>B(1a+b)</sub> mRNA (−69%) and GABA<sub>B(2)</sub> mRNA (−66%) were also significantly decreased in the SNpc. Our results suggest that MPTP‐induced denervation is associated with a decrease of GABA<sub>B</sub> receptors restricted to the SNpc. These observations may be relevant to the pathophysiology of motor disorders involving dysfunction of the basal ganglia such as Parkinson disease. Synapse 40:225–234, 2001. © 2001 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Effect of MPTP‐induced denervation on basal ganglia GABAB receptors: Correlation with dopamine concentrations and dopamine transporter</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>GABAB Receptors in MPTP‐Treated Animals</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Effect of MPTP‐induced denervation on basal ganglia GABAB receptors: Correlation with dopamine concentrations and dopamine transporter</title></titleInfo><name type="personal"><namePart type="given">Frédéric</namePart><namePart type="family">Calon</namePart><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nadia</namePart><namePart type="family">Lavertu</namePart><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anne‐Marie</namePart><namePart type="family">Lemieux</namePart><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marc</namePart><namePart type="family">Morissette</namePart><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Martin</namePart><namePart type="family">Goulet</namePart><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Richard</namePart><namePart type="family">Grondin</namePart><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</affiliation><affiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pierre J.</namePart><namePart type="family">Blanchet</namePart><affiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paul J.</namePart><namePart type="family">Bédard</namePart><affiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, and Department of Medicine, Faculty of Medicine, Laval University, Québec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thérèse</namePart><namePart type="family">Di Paolo</namePart><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), Québec, and Faculty of Pharmacy, Laval University, Québec, Canada</affiliation><affiliation>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center (CHUL), 2705 Laurier Boulevard, Sainte‐Foy, Qc, Canada G1V 4G2</affiliation><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">2001-06-01</dateIssued><dateCaptured encoding="w3cdtf">2000-08-13</dateCaptured><dateValid encoding="w3cdtf">2000-12-02</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">4</extent><extent unit="tables">3</extent><extent unit="references">48</extent><extent unit="words">7569</extent></physicalDescription><abstract lang="en">We investigated the effect of MPTP‐induced lesion of the substantia nigra pars compacta (SNpc) dopaminergic neurons on GABAB receptors in the basal ganglia of mice and monkeys using receptor autoradiography and in situ hybridization. The extent of the lesion was measured with striatal catecholamine content, striatal binding of 125I‐RTI‐121 to dopamine transporter (DAT), and DAT expression in the SNpc. GABAB receptors in mice brain were evaluated using 3H‐CGP54626 and its expression was measured with oligonucleotides probes targeting the mRNAs of GABAB(1a+b), GABAB(1a), GABAB(1b), GABAB(2) subunits. In monkeys, 125I‐CGP64213 and selective probes for GABAB(1a+b) and GABAB(2) mRNAs were used. In mice, dopamine content, 125I‐RTI‐121 binding, and DAT expression were reduced by 44%, 40%, and 39% after a dose of 40 mg/kg of MPTP and 74%, 70%, and 34% after 120 mg/kg of MPTP, respectively. In monkeys, dopamine content and DAT expression were decreased by more than 90% and 80%, respectively. In the striatum and the subthalamic nucleus, GABAB receptors were unchanged following MPTP in both species. In the SNpc of mice, MPTP (120 mg/kg) induced a significant decrease of 3H‐CGP54626 binding (−10%) and of the expression of GABAB(1a+b) mRNA (−13%). The decrease of the expression of GABAB(1a+b) mRNA was correlated with dopamine content, 125I‐RTI‐121 binding and DAT expression. In MPTP‐treated monkeys, 125I‐CGP64213 binding (−40%), GABAB(1a+b) mRNA (−69%) and GABAB(2) mRNA (−66%) were also significantly decreased in the SNpc. Our results suggest that MPTP‐induced denervation is associated with a decrease of GABAB receptors restricted to the SNpc. These observations may be relevant to the pathophysiology of motor disorders involving dysfunction of the basal ganglia such as Parkinson disease. Synapse 40:225–234, 2001. © 2001 Wiley‐Liss, Inc.</abstract><note type="funding">Medical Research Council of Canada</note><note type="funding">Novartis</note><subject lang="en"><genre>keywords</genre><topic>substantia nigra</topic><topic>Parkinson</topic><topic>dopamine</topic><topic>GABA</topic><topic>autoradiography</topic><topic>in situ hybridization</topic></subject><relatedItem type="host"><titleInfo><title>Synapse</title></titleInfo><titleInfo type="abbreviated"><title>Synapse</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0887-4476</identifier><identifier type="eISSN">1098-2396</identifier><identifier type="DOI">10.1002/(ISSN)1098-2396</identifier><identifier type="PublisherID">SYN</identifier><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>40</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>225</start><end>234</end><total>10</total></extent></part></relatedItem><identifier type="istex">8DD5BCF1B10708AE3857882704F6FE29F9090748</identifier><identifier type="DOI">10.1002/syn.1045</identifier><identifier type="ArticleID">SYN1045</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)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000C10 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 000C10 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Canada
|area= ParkinsonCanadaV1
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:8DD5BCF1B10708AE3857882704F6FE29F9090748
|texte= Effect of MPTP‐induced denervation on basal ganglia GABAB receptors: Correlation with dopamine concentrations and dopamine transporter
}}
| This area was generated with Dilib version V0.6.29. |  |