Riluzole reduces hyperactivity of subthalamic neurons induced by unilateral 6‐OHDA lesion in the rat brain
Identifieur interne : 000668 ( Istex/Corpus ); précédent : 000667; suivant : 000669Riluzole reduces hyperactivity of subthalamic neurons induced by unilateral 6‐OHDA lesion in the rat brain
Auteurs : Oum-Kaltoum Hassani ; Mireille Mouroux ; Georg Andrees Bohme ; Jean-Marie Stutzmann ; Jean FégerSource :
- Movement Disorders [ 0885-3185 ] ; 2001-11.
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Abstract
An abnormal increase in the activity of neurons of the subthalamic nucleus is a key pathophysiological feature of Parkinson's disease. We sought to determine whether riluzole, a sodium channel inhibitor that interferes with glutamatergic neurotransmission, affects neuronal activity in this brain region. Intravenous administration of riluzole reduced the discharge rate of subthalamic neurons in rats with 6‐OHDA‐induced lesions of the midbrain. By contrast, no effect was observed in nonlesioned control animals. This property may contribute to the neuroprotective effects of riluzole in animal models of PD through the modulation of the glutamatergic inputs these neurons feedback to nigral dopaminergic neurons. © 2001 Movement Disorder Society.
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DOI: 10.1002/mds.1219
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ISTEX:316494D7CE943C7950A59D8A9E335C733DD1C046Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Riluzole reduces hyperactivity of subthalamic neurons induced by unilateral 6‐OHDA lesion in the rat brain</title><author><name sortKey="Hassani, Oum Altoum" sort="Hassani, Oum Altoum" uniqKey="Hassani O" first="Oum-Kaltoum" last="Hassani">Oum-Kaltoum Hassani</name><affiliation><mods:affiliation>Laboratoire de Pharmacologie, Faculté de Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Mouroux, Mireille" sort="Mouroux, Mireille" uniqKey="Mouroux M" first="Mireille" last="Mouroux">Mireille Mouroux</name><affiliation><mods:affiliation>Laboratoire de Pharmacologie, Faculté de Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Bohme, Georg Andrees" sort="Bohme, Georg Andrees" uniqKey="Bohme G" first="Georg Andrees" last="Bohme">Georg Andrees Bohme</name><affiliation><mods:affiliation>Aventis Pharma France S.A., Neurodegenerative Disease Group, Centre de Recherches de Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Stutzmann, Jean Arie" sort="Stutzmann, Jean Arie" uniqKey="Stutzmann J" first="Jean-Marie" last="Stutzmann">Jean-Marie Stutzmann</name><affiliation><mods:affiliation>Aventis Pharma France S.A., Neurodegenerative Disease Group, Centre de Recherches de Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Feger, Jean" sort="Feger, Jean" uniqKey="Feger J" first="Jean" last="Féger">Jean Féger</name><affiliation><mods:affiliation>Laboratoire de Pharmacologie, Faculté de Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM U‐289, Hopital de la Salpêtrière, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM U‐289, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75651 Paris Cedex 13, France</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:316494D7CE943C7950A59D8A9E335C733DD1C046</idno><date when="2001" year="2001">2001</date><idno type="doi">10.1002/mds.1219</idno><idno type="url">https://api.istex.fr/document/316494D7CE943C7950A59D8A9E335C733DD1C046/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000668</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000668</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Riluzole reduces hyperactivity of subthalamic neurons induced by unilateral 6‐OHDA lesion in the rat brain</title><author><name sortKey="Hassani, Oum Altoum" sort="Hassani, Oum Altoum" uniqKey="Hassani O" first="Oum-Kaltoum" last="Hassani">Oum-Kaltoum Hassani</name><affiliation><mods:affiliation>Laboratoire de Pharmacologie, Faculté de Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Mouroux, Mireille" sort="Mouroux, Mireille" uniqKey="Mouroux M" first="Mireille" last="Mouroux">Mireille Mouroux</name><affiliation><mods:affiliation>Laboratoire de Pharmacologie, Faculté de Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Bohme, Georg Andrees" sort="Bohme, Georg Andrees" uniqKey="Bohme G" first="Georg Andrees" last="Bohme">Georg Andrees Bohme</name><affiliation><mods:affiliation>Aventis Pharma France S.A., Neurodegenerative Disease Group, Centre de Recherches de Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Stutzmann, Jean Arie" sort="Stutzmann, Jean Arie" uniqKey="Stutzmann J" first="Jean-Marie" last="Stutzmann">Jean-Marie Stutzmann</name><affiliation><mods:affiliation>Aventis Pharma France S.A., Neurodegenerative Disease Group, Centre de Recherches de Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Feger, Jean" sort="Feger, Jean" uniqKey="Feger J" first="Jean" last="Féger">Jean Féger</name><affiliation><mods:affiliation>Laboratoire de Pharmacologie, Faculté de Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM U‐289, Hopital de la Salpêtrière, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>INSERM U‐289, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75651 Paris Cedex 13, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2001-11">2001-11</date><biblScope unit="volume">16</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1110">1110</biblScope><biblScope unit="page" to="1114">1114</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">316494D7CE943C7950A59D8A9E335C733DD1C046</idno><idno type="DOI">10.1002/mds.1219</idno><idno type="ArticleID">MDS1219</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>basal ganglia</term><term>excitotoxicity</term><term>glutamate release</term><term>neurodegenerative diseases</term><term>neuroprotection</term><term>sodium channels blockers</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">An abnormal increase in the activity of neurons of the subthalamic nucleus is a key pathophysiological feature of Parkinson's disease. We sought to determine whether riluzole, a sodium channel inhibitor that interferes with glutamatergic neurotransmission, affects neuronal activity in this brain region. Intravenous administration of riluzole reduced the discharge rate of subthalamic neurons in rats with 6‐OHDA‐induced lesions of the midbrain. By contrast, no effect was observed in nonlesioned control animals. This property may contribute to the neuroprotective effects of riluzole in animal models of PD through the modulation of the glutamatergic inputs these neurons feedback to nigral dopaminergic neurons. © 2001 Movement Disorder Society.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Oum‐Kaltoum Hassani PhD</name><affiliations><json:string>Laboratoire de Pharmacologie, Faculté de Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France</json:string></affiliations></json:item><json:item><name>Mireille Mouroux PhD</name><affiliations><json:string>Laboratoire de Pharmacologie, Faculté de Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France</json:string></affiliations></json:item><json:item><name>Georg Andrees Bohme PharmD, PhD</name><affiliations><json:string>Aventis Pharma France S.A., Neurodegenerative Disease Group, Centre de Recherches de Paris, France</json:string></affiliations></json:item><json:item><name>Jean‐Marie Stutzmann PhD</name><affiliations><json:string>Aventis Pharma France S.A., Neurodegenerative Disease Group, Centre de Recherches de Paris, France</json:string></affiliations></json:item><json:item><name>Jean Féger PhD</name><affiliations><json:string>Laboratoire de Pharmacologie, Faculté de Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France</json:string><json:string>INSERM U‐289, Hopital de la Salpêtrière, Paris, France</json:string><json:string>INSERM U‐289, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75651 Paris Cedex 13, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>basal ganglia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neuroprotection</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>glutamate release</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>sodium channels blockers</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neurodegenerative diseases</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>excitotoxicity</value></json:item></subject><articleId><json:string>MDS1219</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>shortCommunication</json:string></originalGenre><abstract>An abnormal increase in the activity of neurons of the subthalamic nucleus is a key pathophysiological feature of Parkinson's disease. We sought to determine whether riluzole, a sodium channel inhibitor that interferes with glutamatergic neurotransmission, affects neuronal activity in this brain region. Intravenous administration of riluzole reduced the discharge rate of subthalamic neurons in rats with 6‐OHDA‐induced lesions of the midbrain. By contrast, no effect was observed in nonlesioned control animals. 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antagonists</title></json:item></refBibs><genre><json:string>brief-communication</json:string></genre><host><volume>16</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>5</total><last>1114</last><first>1110</first></pages><issn><json:string>0885-3185</json:string></issn><issue>6</issue><subject><json:item><value>Brief Report</value></json:item></subject><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><categories><wos><json:string>science</json:string><json:string>clinical neurology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & 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brain</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><availability><p>Copyright © 2001 Movement Disorder Society</p></availability><date>2001</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Riluzole reduces hyperactivity of subthalamic neurons induced by unilateral 6‐OHDA lesion in the rat brain</title><author xml:id="author-1"><persName><forename type="first">Oum‐Kaltoum</forename><surname>Hassani</surname></persName><roleName type="degree">PhD</roleName><affiliation>Laboratoire de Pharmacologie, Faculté de Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France</affiliation></author><author xml:id="author-2"><persName><forename type="first">Mireille</forename><surname>Mouroux</surname></persName><roleName type="degree">PhD</roleName><affiliation>Laboratoire de Pharmacologie, Faculté de Sciences 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We sought to determine whether riluzole, a sodium channel inhibitor that interferes with glutamatergic neurotransmission, affects neuronal activity in this brain region. Intravenous administration of riluzole reduced the discharge rate of subthalamic neurons in rats with 6‐OHDA‐induced lesions of the midbrain. By contrast, no effect was observed in nonlesioned control animals. This property may contribute to the neuroprotective effects of riluzole in animal models of PD through the modulation of the glutamatergic inputs these neurons feedback to nigral dopaminergic neurons. © 2001 Movement Disorder Society.</abstract><subject lang="en"><genre>keywords</genre><topic>basal ganglia</topic><topic>neuroprotection</topic><topic>Parkinson's disease</topic><topic>glutamate release</topic><topic>sodium channels blockers</topic><topic>neurodegenerative diseases</topic><topic>excitotoxicity</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. 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