La maladie de Parkinson en France (serveur d'exploration)

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Neurochemical mechanisms induced by high frequency stimulation of the subthalamic nucleus: Increase of extracellular striatal glutamate and GABA in normal and hemiparkinsonian rats

Identifieur interne : 000637 ( PascalFrancis/Curation ); précédent : 000636; suivant : 000638

Neurochemical mechanisms induced by high frequency stimulation of the subthalamic nucleus: Increase of extracellular striatal glutamate and GABA in normal and hemiparkinsonian rats

Auteurs : Nicolas Bruet [France] ; Francois Windels [France] ; Carole Carcenac [France] ; Claude Feuerstein [France] ; Anne Bertrand [France] ; Annie Poupard [France] ; Marc Savasta [France]

Source :

RBID : Pascal:04-0365262

Descripteurs français

English descriptors

Abstract

High frequency stimulation (HFS) (130 Hz) of the subthalamic nucleus (STN) provides beneficial effects in patients suffering from severe parkinsonism, but the mechanisms underlying these clinical results remain to be clarified. To date, very little is known concerning the effects of STN-HFS on neurochemical transmission in the different basal ganglia nuclei and in particular the striatum. This study examines the effects of STN-HFS in intact and hemiparkinsonian rats on extracellular striatal glutamate (Glu) and GABA levels by means of intracerebral microdialysis. Unilateral STN-HFS was found to induce a significant bilateral increase of striatal Glu and GABA both in intact and in dopamine-lesioned animals. In intact rats, these increases were reversed by local administration of the Dl antagonist SCH 23390, but were potentiated by the D2 antagonist sulpiride. Potentiation was also observed after local administration of both D1 and D2 antagonists whose amplitude was similar to that measured in hemiparkinsonian rats. These data furnish the first evidence that STN-HFS influences striatal amino-acid transmission and that this influence is modulated by dopamine. They provide evidence that the effects of STN-HFS are not only restricted to the direct STN targets, but also involve adaptive changes within other structures of the basal ganglia circuitry.
pA  
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A08 01  1  ENG  @1 Neurochemical mechanisms induced by high frequency stimulation of the subthalamic nucleus: Increase of extracellular striatal glutamate and GABA in normal and hemiparkinsonian rats
A11 01  1    @1 BRUET (Nicolas)
A11 02  1    @1 WINDELS (Francois)
A11 03  1    @1 CARCENAC (Carole)
A11 04  1    @1 FEUERSTEIN (Claude)
A11 05  1    @1 BERTRAND (Anne)
A11 06  1    @1 POUPARD (Annie)
A11 07  1    @1 SAVASTA (Marc)
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C01 01    ENG  @0 High frequency stimulation (HFS) (130 Hz) of the subthalamic nucleus (STN) provides beneficial effects in patients suffering from severe parkinsonism, but the mechanisms underlying these clinical results remain to be clarified. To date, very little is known concerning the effects of STN-HFS on neurochemical transmission in the different basal ganglia nuclei and in particular the striatum. This study examines the effects of STN-HFS in intact and hemiparkinsonian rats on extracellular striatal glutamate (Glu) and GABA levels by means of intracerebral microdialysis. Unilateral STN-HFS was found to induce a significant bilateral increase of striatal Glu and GABA both in intact and in dopamine-lesioned animals. In intact rats, these increases were reversed by local administration of the Dl antagonist SCH 23390, but were potentiated by the D2 antagonist sulpiride. Potentiation was also observed after local administration of both D1 and D2 antagonists whose amplitude was similar to that measured in hemiparkinsonian rats. These data furnish the first evidence that STN-HFS influences striatal amino-acid transmission and that this influence is modulated by dopamine. They provide evidence that the effects of STN-HFS are not only restricted to the direct STN targets, but also involve adaptive changes within other structures of the basal ganglia circuitry.
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C07 08  X  FRE  @0 Extrapyramidal syndrome @5 41
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C07 08  X  SPA  @0 Extrapiramidal síndrome @5 41
C07 09  X  FRE  @0 Maladie dégénérative @5 42
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N21       @1 208
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<s1>CARCENAC (Carole)</s1>
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<fA11 i1="04" i2="1">
<s1>FEUERSTEIN (Claude)</s1>
</fA11>
<fA11 i1="05" i2="1">
<s1>BERTRAND (Anne)</s1>
</fA11>
<fA11 i1="06" i2="1">
<s1>POUPARD (Annie)</s1>
</fA11>
<fA11 i1="07" i2="1">
<s1>SAVASTA (Marc)</s1>
</fA11>
<fA14 i1="01">
<s1>Equipe Neurochimie et Neuroplasticité Fonctionnelles, INSERM U.318-Neurosciences Précliniques, Université Joseph Fourier, Pavillon de Neurologie</s1>
<s2>Grenoble</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA20>
<s1>1228-1240</s1>
</fA20>
<fA21>
<s1>2003</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>3036</s2>
<s5>354000118888160040</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2004 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>69 ref.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>04-0365262</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Journal of neuropathology and experimental neurology</s0>
</fA64>
<fA66 i1="01">
<s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>High frequency stimulation (HFS) (130 Hz) of the subthalamic nucleus (STN) provides beneficial effects in patients suffering from severe parkinsonism, but the mechanisms underlying these clinical results remain to be clarified. To date, very little is known concerning the effects of STN-HFS on neurochemical transmission in the different basal ganglia nuclei and in particular the striatum. This study examines the effects of STN-HFS in intact and hemiparkinsonian rats on extracellular striatal glutamate (Glu) and GABA levels by means of intracerebral microdialysis. Unilateral STN-HFS was found to induce a significant bilateral increase of striatal Glu and GABA both in intact and in dopamine-lesioned animals. In intact rats, these increases were reversed by local administration of the Dl antagonist SCH 23390, but were potentiated by the D2 antagonist sulpiride. Potentiation was also observed after local administration of both D1 and D2 antagonists whose amplitude was similar to that measured in hemiparkinsonian rats. These data furnish the first evidence that STN-HFS influences striatal amino-acid transmission and that this influence is modulated by dopamine. They provide evidence that the effects of STN-HFS are not only restricted to the direct STN targets, but also involve adaptive changes within other structures of the basal ganglia circuitry.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002B17</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Parkinson maladie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Parkinson disease</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Parkinson enfermedad</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Haute fréquence</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>High frequency</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Alta frecuencia</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Noyau sousthalamique</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Subthalamic nucleus</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Núcleo subtalámico</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Système nerveux pathologie</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Glutamate</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Glutamate</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Glutamato</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>GABA</s0>
<s2>NK</s2>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>GABA</s0>
<s2>NK</s2>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>GABA</s0>
<s2>NK</s2>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Animal</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Animal</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Animal</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Rat</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Rat</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Rata</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Chromatographie phase liquide</s0>
<s5>11</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Liquid chromatography</s0>
<s5>11</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Cromatografía fase líquida</s0>
<s5>11</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Microdialyse</s0>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Microdialysis</s0>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Microdiálisis</s0>
<s5>12</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Encéphale pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Système nerveux central</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Central nervous system</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Sistema nervioso central</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Aminoacide excitateur</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Excitatory aminoacid</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Aminoácido excitador</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Neurotransmetteur</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Neurotransmitter</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Neurotransmisor</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE">
<s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>42</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>42</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE">
<s0>Système nerveux central pathologie</s0>
<s5>43</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>43</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>43</s5>
</fC07>
<fN21>
<s1>208</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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