Forelimb dyskinesia mediated by high‐frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of N‐methyl‐d‐aspartate receptors
Identifieur interne : 001419 ( Istex/Corpus ); précédent : 001418; suivant : 001420Forelimb dyskinesia mediated by high‐frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of N‐methyl‐d‐aspartate receptors
Auteurs : Adrien Quintana ; Christophe Melon ; Lydia Kerkerian-Le Goff ; Pascal Salin ; Marc Savasta ; Véronique Sgambato-FaureSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2010-08.
English descriptors
- KwdEn :
Abstract
Dyskinesia is a major side‐effect of chronic l‐DOPA administration, the reference treatment for Parkinson’s disease. High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the l‐DOPA requirement. However, inappropriate stimulation can also trigger dyskinetic movements, in both human and rodents. We investigated whether STN‐HFS‐evoked forelimb dyskinesia involved changes in glutamatergic neurotransmission as previously reported for l‐DOPA‐induced dyskinesias, focusing on the role of NR2B‐containing N‐methyl‐d‐aspartate receptors (NR2B/NMDARs). We applied STN‐HFS in normal rats at intensities above and below the threshold for triggering forelimb dyskinesia. Dyskinesiogenic STN‐HFS induced the activation of NR2B (as assessed by immunodetection of the phosphorylated residue Tyr1472) in neurons of the subthalamic nucleus, entopeduncular nucleus, motor thalamus and forelimb motor cortex. The severity of STN‐HFS‐induced forelimb dyskinesia was decreased in a dose‐dependent manner by systemic injections of CP‐101,606, a selective blocker of NR2B/NMDARs, but was either unaffected or increased by the non‐selective N‐methyl‐d‐aspartate receptor antagonist, MK‐801.
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DOI: 10.1111/j.1460-9568.2010.07290.x
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<front><div type="abstract" xml:lang="en">Dyskinesia is a major side‐effect of chronic l‐DOPA administration, the reference treatment for Parkinson’s disease. High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the l‐DOPA requirement. However, inappropriate stimulation can also trigger dyskinetic movements, in both human and rodents. We investigated whether STN‐HFS‐evoked forelimb dyskinesia involved changes in glutamatergic neurotransmission as previously reported for l‐DOPA‐induced dyskinesias, focusing on the role of NR2B‐containing N‐methyl‐d‐aspartate receptors (NR2B/NMDARs). We applied STN‐HFS in normal rats at intensities above and below the threshold for triggering forelimb dyskinesia. Dyskinesiogenic STN‐HFS induced the activation of NR2B (as assessed by immunodetection of the phosphorylated residue Tyr1472) in neurons of the subthalamic nucleus, entopeduncular nucleus, motor thalamus and forelimb motor cortex. The severity of STN‐HFS‐induced forelimb dyskinesia was decreased in a dose‐dependent manner by systemic injections of CP‐101,606, a selective blocker of NR2B/NMDARs, but was either unaffected or increased by the non‐selective N‐methyl‐d‐aspartate receptor antagonist, MK‐801.</div>
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<abstract>Dyskinesia is a major side‐effect of chronic l‐DOPA administration, the reference treatment for Parkinson’s disease. High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the l‐DOPA requirement. However, inappropriate stimulation can also trigger dyskinetic movements, in both human and rodents. We investigated whether STN‐HFS‐evoked forelimb dyskinesia involved changes in glutamatergic neurotransmission as previously reported for l‐DOPA‐induced dyskinesias, focusing on the role of NR2B‐containing N‐methyl‐d‐aspartate receptors (NR2B/NMDARs). We applied STN‐HFS in normal rats at intensities above and below the threshold for triggering forelimb dyskinesia. Dyskinesiogenic STN‐HFS induced the activation of NR2B (as assessed by immunodetection of the phosphorylated residue Tyr1472) in neurons of the subthalamic nucleus, entopeduncular nucleus, motor thalamus and forelimb motor cortex. The severity of STN‐HFS‐induced forelimb dyskinesia was decreased in a dose‐dependent manner by systemic injections of CP‐101,606, a selective blocker of NR2B/NMDARs, but was either unaffected or increased by the non‐selective N‐methyl‐d‐aspartate receptor antagonist, MK‐801.</abstract>
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<affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</affiliation>
<affiliation>Université Joseph Fourier, Grenoble, France</affiliation>
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<author xml:id="author-2"><persName><forename type="first">Christophe</forename>
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<affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</affiliation>
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<author xml:id="author-3"><persName><forename type="first">Lydia Kerkerian‐Le</forename>
<surname>Goff</surname>
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<affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</affiliation>
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<author xml:id="author-4"><persName><forename type="first">Pascal</forename>
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<affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</affiliation>
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<affiliation>Université Joseph Fourier, Grenoble, France</affiliation>
<affiliation>Centre Hospitalier Universitaire, BP217, Grenoble, France</affiliation>
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<author xml:id="author-6"><persName><forename type="first">Véronique</forename>
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<affiliation>Université Joseph Fourier, Grenoble, France</affiliation>
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<abstract xml:lang="en"><p>Dyskinesia is a major side‐effect of chronic l‐DOPA administration, the reference treatment for Parkinson’s disease. High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the l‐DOPA requirement. However, inappropriate stimulation can also trigger dyskinetic movements, in both human and rodents. We investigated whether STN‐HFS‐evoked forelimb dyskinesia involved changes in glutamatergic neurotransmission as previously reported for l‐DOPA‐induced dyskinesias, focusing on the role of NR2B‐containing N‐methyl‐d‐aspartate receptors (NR2B/NMDARs). We applied STN‐HFS in normal rats at intensities above and below the threshold for triggering forelimb dyskinesia. Dyskinesiogenic STN‐HFS induced the activation of NR2B (as assessed by immunodetection of the phosphorylated residue Tyr1472) in neurons of the subthalamic nucleus, entopeduncular nucleus, motor thalamus and forelimb motor cortex. The severity of STN‐HFS‐induced forelimb dyskinesia was decreased in a dose‐dependent manner by systemic injections of CP‐101,606, a selective blocker of NR2B/NMDARs, but was either unaffected or increased by the non‐selective N‐methyl‐d‐aspartate receptor antagonist, MK‐801.</p>
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<correspondenceTo>Dr Marc Savasta, <sup>1</sup>
Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), as above.
E‐mail: <email normalForm="marc.savasta@ujf-grenoble.fr">marc.savasta@ujf‐grenoble.fr</email>
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<contentMeta><unparsedEditorialHistory>Received 22 February 2010, revised 14 April 2010, accepted 20 April 2010</unparsedEditorialHistory>
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<titleGroup><title type="main">Forelimb dyskinesia mediated by high‐frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of <i>N</i>
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<title type="shortAuthors">A. Quintana <i>et al.</i>
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<title type="short">STN‐HFS‐induced forelimb dyskinesia</title>
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<affiliation xml:id="a5" countryCode="FR"><unparsedAffiliation>Centre de Neuroscience Cognitive, Centre National de la Recherche Scientifique, UMR 5229, Université de Lyon I, Bron, France</unparsedAffiliation>
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<keywordGroup xml:lang="en"><keyword xml:id="k1">106</keyword>
<keyword xml:id="k2">CP‐101</keyword>
<keyword xml:id="k3">glutamate</keyword>
<keyword xml:id="k4">high frequency stimulation</keyword>
<keyword xml:id="k5">rat</keyword>
<keyword xml:id="k6">subthalamic nucleus</keyword>
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<p>Dyskinesia is a major side‐effect of chronic <sc>l</sc>
‐DOPA administration, the reference treatment for Parkinson’s disease. High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the <sc>l</sc>
‐DOPA requirement. However, inappropriate stimulation can also trigger dyskinetic movements, in both human and rodents. We investigated whether STN‐HFS‐evoked forelimb dyskinesia involved changes in glutamatergic neurotransmission as previously reported for <sc>l</sc>
‐DOPA‐induced dyskinesias, focusing on the role of NR2B‐containing <i>N</i>
‐methyl‐<sc>d</sc>
‐aspartate receptors (NR2B/NMDARs). We applied STN‐HFS in normal rats at intensities above and below the threshold for triggering forelimb dyskinesia. Dyskinesiogenic STN‐HFS induced the activation of NR2B (as assessed by immunodetection of the phosphorylated residue Tyr<sup>1472</sup>
) in neurons of the subthalamic nucleus, entopeduncular nucleus, motor thalamus and forelimb motor cortex. The severity of STN‐HFS‐induced forelimb dyskinesia was decreased in a dose‐dependent manner by systemic injections of CP‐101,606, a selective blocker of NR2B/NMDARs, but was either unaffected or increased by the non‐selective <i>N</i>
‐methyl‐<sc>d</sc>
‐aspartate receptor antagonist, MK‐801.</p>
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<mods version="3.6"><titleInfo lang="en"><title>Forelimb dyskinesia mediated by high‐frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of N‐methyl‐d‐aspartate receptors</title>
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<titleInfo type="abbreviated" lang="en"><title>STN‐HFS‐induced forelimb dyskinesia</title>
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<titleInfo type="alternative" contentType="CDATA" lang="en"><title>Forelimb dyskinesia mediated by high‐frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of N‐methyl‐d‐aspartate receptors</title>
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<name type="personal"><namePart type="given">Adrien</namePart>
<namePart type="family">Quintana</namePart>
<affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</affiliation>
<affiliation>Université Joseph Fourier, Grenoble, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Christophe</namePart>
<namePart type="family">Melon</namePart>
<affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Lydia Kerkerian‐Le</namePart>
<namePart type="family">Goff</namePart>
<affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Pascal</namePart>
<namePart type="family">Salin</namePart>
<affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Marc</namePart>
<namePart type="family">Savasta</namePart>
<affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</affiliation>
<affiliation>Université Joseph Fourier, Grenoble, France</affiliation>
<affiliation>Centre Hospitalier Universitaire, BP217, Grenoble, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Véronique</namePart>
<namePart type="family">Sgambato‐Faure</namePart>
<affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</affiliation>
<affiliation>Université Joseph Fourier, Grenoble, France</affiliation>
<affiliation>Centre de Neuroscience Cognitive, Centre National de la Recherche Scientifique, UMR 5229, Université de Lyon I, Bron, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
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<originInfo><publisher>Blackwell Publishing Ltd</publisher>
<place><placeTerm type="text">Oxford, UK</placeTerm>
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<dateIssued encoding="w3cdtf">2010-08</dateIssued>
<edition>Received 22 February 2010, revised 14 April 2010, accepted 20 April 2010</edition>
<copyrightDate encoding="w3cdtf">2010</copyrightDate>
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<abstract lang="en">Dyskinesia is a major side‐effect of chronic l‐DOPA administration, the reference treatment for Parkinson’s disease. High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the l‐DOPA requirement. However, inappropriate stimulation can also trigger dyskinetic movements, in both human and rodents. We investigated whether STN‐HFS‐evoked forelimb dyskinesia involved changes in glutamatergic neurotransmission as previously reported for l‐DOPA‐induced dyskinesias, focusing on the role of NR2B‐containing N‐methyl‐d‐aspartate receptors (NR2B/NMDARs). We applied STN‐HFS in normal rats at intensities above and below the threshold for triggering forelimb dyskinesia. Dyskinesiogenic STN‐HFS induced the activation of NR2B (as assessed by immunodetection of the phosphorylated residue Tyr1472) in neurons of the subthalamic nucleus, entopeduncular nucleus, motor thalamus and forelimb motor cortex. The severity of STN‐HFS‐induced forelimb dyskinesia was decreased in a dose‐dependent manner by systemic injections of CP‐101,606, a selective blocker of NR2B/NMDARs, but was either unaffected or increased by the non‐selective N‐methyl‐d‐aspartate receptor antagonist, MK‐801.</abstract>
<subject lang="en"><genre>keywords</genre>
<topic>106</topic>
<topic>CP‐101</topic>
<topic>glutamate</topic>
<topic>high frequency stimulation</topic>
<topic>rat</topic>
<topic>subthalamic nucleus</topic>
</subject>
<relatedItem type="host"><titleInfo><title>European Journal of Neuroscience</title>
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<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>2010</date>
<detail type="volume"><caption>vol.</caption>
<number>32</number>
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<detail type="issue"><caption>no.</caption>
<number>3</number>
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<extent unit="pages"><start>423</start>
<end>434</end>
<total>12</total>
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