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 : 000D97 ( PascalFrancis/Corpus ); précédent : 000D96; suivant : 000D98Neurochemical 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 ; Francois Windels ; Carole Carcenac ; Claude Feuerstein ; Anne Bertrand ; Annie Poupard ; Marc SavastaSource :
- Journal of neuropathology and experimental neurology [ 0022-3069 ] ; 2003.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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.
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Format Inist (serveur)
NO : | PASCAL 04-0365262 INIST |
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ET : | Neurochemical mechanisms induced by high frequency stimulation of the subthalamic nucleus: Increase of extracellular striatal glutamate and GABA in normal and hemiparkinsonian rats |
AU : | BRUET (Nicolas); WINDELS (Francois); CARCENAC (Carole); FEUERSTEIN (Claude); BERTRAND (Anne); POUPARD (Annie); SAVASTA (Marc) |
AF : | Equipe Neurochimie et Neuroplasticité Fonctionnelles, INSERM U.318-Neurosciences Précliniques, Université Joseph Fourier, Pavillon de Neurologie/Grenoble/France (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Journal of neuropathology and experimental neurology; ISSN 0022-3069; Coden JNENAD; Etats-Unis; Da. 2003; Vol. 62; No. 12; Pp. 1228-1240; Bibl. 69 ref. |
LA : | Anglais |
EA : | 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. |
CC : | 002B17 |
FD : | Parkinson maladie; Haute fréquence; Noyau sousthalamique; Système nerveux pathologie; Glutamate; GABA; Animal; Rat; Chromatographie phase liquide; Microdialyse |
FG : | Rodentia; Mammalia; Vertebrata; Encéphale pathologie; Système nerveux central; Aminoacide excitateur; Neurotransmetteur; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie |
ED : | Parkinson disease; High frequency; Subthalamic nucleus; Nervous system diseases; Glutamate; GABA; Animal; Rat; Liquid chromatography; Microdialysis |
EG : | Rodentia; Mammalia; Vertebrata; Cerebral disorder; Central nervous system; Excitatory aminoacid; Neurotransmitter; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease |
SD : | Parkinson enfermedad; Alta frecuencia; Núcleo subtalámico; Sistema nervioso patología; Glutamato; GABA; Animal; Rata; Cromatografía fase líquida; Microdiálisis |
LO : | INIST-3036.354000118888160040 |
ID : | 04-0365262 |
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<front><div type="abstract" xml:lang="en">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.</div>
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<s5>06</s5>
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<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>
<server><NO>PASCAL 04-0365262 INIST</NO>
<ET>Neurochemical mechanisms induced by high frequency stimulation of the subthalamic nucleus: Increase of extracellular striatal glutamate and GABA in normal and hemiparkinsonian rats</ET>
<AU>BRUET (Nicolas); WINDELS (Francois); CARCENAC (Carole); FEUERSTEIN (Claude); BERTRAND (Anne); POUPARD (Annie); SAVASTA (Marc)</AU>
<AF>Equipe Neurochimie et Neuroplasticité Fonctionnelles, INSERM U.318-Neurosciences Précliniques, Université Joseph Fourier, Pavillon de Neurologie/Grenoble/France (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of neuropathology and experimental neurology; ISSN 0022-3069; Coden JNENAD; Etats-Unis; Da. 2003; Vol. 62; No. 12; Pp. 1228-1240; Bibl. 69 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002B17</CC>
<FD>Parkinson maladie; Haute fréquence; Noyau sousthalamique; Système nerveux pathologie; Glutamate; GABA; Animal; Rat; Chromatographie phase liquide; Microdialyse</FD>
<FG>Rodentia; Mammalia; Vertebrata; Encéphale pathologie; Système nerveux central; Aminoacide excitateur; Neurotransmetteur; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie</FG>
<ED>Parkinson disease; High frequency; Subthalamic nucleus; Nervous system diseases; Glutamate; GABA; Animal; Rat; Liquid chromatography; Microdialysis</ED>
<EG>Rodentia; Mammalia; Vertebrata; Cerebral disorder; Central nervous system; Excitatory aminoacid; Neurotransmitter; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease</EG>
<SD>Parkinson enfermedad; Alta frecuencia; Núcleo subtalámico; Sistema nervioso patología; Glutamato; GABA; Animal; Rata; Cromatografía fase líquida; Microdiálisis</SD>
<LO>INIST-3036.354000118888160040</LO>
<ID>04-0365262</ID>
</server>
</inist>
</record>
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