Riluzole reduces hyperactivity of subthalamic neurons induced by unilateral 6‐OHDA lesion in the rat brain
Identifieur interne : 002E01 ( Istex/Corpus ); précédent : 002E00; suivant : 002E02Riluzole 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
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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. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Brief Report</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>1110</start><end>1114</end><total>5</total></extent></part></relatedItem><identifier type="istex">316494D7CE943C7950A59D8A9E335C733DD1C046</identifier><identifier type="DOI">10.1002/mds.1219</identifier><identifier type="ArticleID">MDS1219</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2001 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>John Wiley & Sons, Inc.</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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