ParkinsonCanadaV1, PascalFrancis, Curation, bibRecord, 000132

Alteration of glutamate receptors in the striatum of dyskinetic 1 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated monkeys following dopamine agonist treatment

Identifieur interne : 000132 ( PascalFrancis/Curation ); précédent : 000131; suivant : 000133

Alteration of glutamate receptors in the striatum of dyskinetic 1 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated monkeys following dopamine agonist treatment

Auteurs : Frédéric Calon [Canada] ; Marc Morissette [Canada] ; Othman Ghribi [Canada] ; Martin Goulet [Canada] ; Richard Grondin [Canada] ; Pierre J. Blanchet [Canada] ; Paul J. Bedard [Canada] ; Thérèse Di Paolo [Canada]

Source :

Progress in neuro-psychopharmacology & biological psychiatry [ 0278-5846 ] ; 2002.

RBID : Pascal:02-0226511

Descripteurs français

Pascal (Inist)
- Corps strié, Modèle animal, Dyskinésie, Animal, Singe, Encéphale, Système nerveux central, Récepteur glutamate, Récepteur dopaminergique D2, Récepteur dopaminergique D1, Agoniste, Antagoniste, Récepteur AMPA, Récepteur NMDA, Interaction moléculaire, Pathogénie, Transmission glutamatergique, Glycine, Pyridine(1-méthyl-4-phényl-1,2,3,6-tétrahydro), Toxicité, Glutamate, Glutamine.
Wicri :
- topic : Singe.

English descriptors

KwdEn :
- AMPA receptor, Agonist, Animal, Animal model, Antagonist, Brain (vertebrata), Central nervous system, Corpus striatum, D1 Dopamine receptor, D2 Dopamine receptor, Dyskinesia, Glutamate, Glutamate receptor, Glutamatergic transmission, Glutamine, Glycine, Molecular interaction, Monkey, NMDA receptor, Pathogenesis, Toxicity.

Abstract

The effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced nigrostriatal lesion and dopaminomimetic treatment on parameters of glutamatergic activity within the basal ganglia of monkeys were studied in relation with the development of dyskinesias. Drug-naive controls, saline-treated MPTP monkeys, as well as MPTP monkeys treated with either a long-acting D₂ agonist (cabergoline) or a D₁ agonist (SKF-82958) given by intermittent injections or continuous infusion, were included in this study. ³H-L-glutamate, ³H-α-amino-3-hydroxy-5-methylisoxasole-4-propionate (AMPA), ³H-glycine, ³H-CGP39653 (an N-methyl-D-aspartate, NMDA, antagonist selective for NR1/NR2A assembly) and ³H-Ro 25-6981 (an NMDA antagonist selective for NR1/NR2B assembly), specific binding to glutamate receptors, the expression of the NR1 subunit of NMDA receptors and glutamate, glutamine and glycine concentrations were studied by autoradiography, in situ hybridization and high-performance liquid chromatography (HPLC), respectively. Pulsatile SKF-82958 and cabergoline treatment relieved parkinsonian symptoms, whereas animals continuously treated with SKF-82958 remained akinetic. Pulsatile SKF-82958 induced dyskinesias in two of the three animals tested, whereas cabergoline did not. MPTP induced no significant changes of striatal specific binding of the radioligands used, NR1 mRNA expression and amino acid concentrations. In the putamen, pulsatile SKF-82958 treatment was associated with decreased content of glycine and glutamate, whereas only glycine was decreased in cabergoline-treated monkeys. Cabergoline and continuous administration of SKF-82958 led to lower levels of NR1 mRNA in the caudate in comparison to pulsatile SKF-82958 administration. The development of dyskinesias following a D₁ agonist treatment was associated with an upregulation of ³H-glutamate [+49%], ³H-AMPA [+38%], ³H-CGP39653 [+111%], ³H-glycine [+26%, nonsignificant] and ³H-Ro 25-6981 [+33%] specific binding in the striatum in comparison to nondyskinetic MPTP monkeys. Our data suggest that supersensitivity to glutamatergic input in the striatum might play a role in the pathogenesis of dopaminomimetic-induced dyskinesias and further support the therapeutic potential of glutamate antagonists in Parkinson's disease.

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A14	`04`			`@1 Department of Medicine, Faculty of Medicine, Laval University @2 Quebec, Quebec @3 CAN @Z 3 aut. @Z 5 aut. @Z 6 aut. @Z 7 aut.`
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C01	`01`		`ENG`	@0 The effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced nigrostriatal lesion and dopaminomimetic treatment on parameters of glutamatergic activity within the basal ganglia of monkeys were studied in relation with the development of dyskinesias. Drug-naive controls, saline-treated MPTP monkeys, as well as MPTP monkeys treated with either a long-acting D₂ agonist (cabergoline) or a D₁ agonist (SKF-82958) given by intermittent injections or continuous infusion, were included in this study. ³H-L-glutamate, ³H-α-amino-3-hydroxy-5-methylisoxasole-4-propionate (AMPA), ³H-glycine, ³H-CGP39653 (an N-methyl-D-aspartate, NMDA, antagonist selective for NR1/NR2A assembly) and ³H-Ro 25-6981 (an NMDA antagonist selective for NR1/NR2B assembly), specific binding to glutamate receptors, the expression of the NR1 subunit of NMDA receptors and glutamate, glutamine and glycine concentrations were studied by autoradiography, in situ hybridization and high-performance liquid chromatography (HPLC), respectively. Pulsatile SKF-82958 and cabergoline treatment relieved parkinsonian symptoms, whereas animals continuously treated with SKF-82958 remained akinetic. Pulsatile SKF-82958 induced dyskinesias in two of the three animals tested, whereas cabergoline did not. MPTP induced no significant changes of striatal specific binding of the radioligands used, NR1 mRNA expression and amino acid concentrations. In the putamen, pulsatile SKF-82958 treatment was associated with decreased content of glycine and glutamate, whereas only glycine was decreased in cabergoline-treated monkeys. Cabergoline and continuous administration of SKF-82958 led to lower levels of NR1 mRNA in the caudate in comparison to pulsatile SKF-82958 administration. The development of dyskinesias following a D₁ agonist treatment was associated with an upregulation of ³H-glutamate [+49%], ³H-AMPA [+38%], ³H-CGP39653 [+111%], ³H-glycine [+26%, nonsignificant] and ³H-Ro 25-6981 [+33%] specific binding in the striatum in comparison to nondyskinetic MPTP monkeys. Our data suggest that supersensitivity to glutamatergic input in the striatum might play a role in the pathogenesis of dopaminomimetic-induced dyskinesias and further support the therapeutic potential of glutamate antagonists in Parkinson's disease.
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C03	`01`	`X`	`ENG`	`@0 Corpus striatum @5 01`
C03	`01`	`X`	`SPA`	`@0 Cuerpo estriado @5 01`
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C03	`02`	`X`	`ENG`	`@0 Animal model @5 02`
C03	`02`	`X`	`SPA`	`@0 Modelo animal @5 02`
C03	`03`	`X`	`FRE`	`@0 Dyskinésie @5 04`
C03	`03`	`X`	`ENG`	`@0 Dyskinesia @5 04`
C03	`03`	`X`	`SPA`	`@0 Disquinesia @5 04`
C03	`04`	`X`	`FRE`	`@0 Animal @5 07`
C03	`04`	`X`	`ENG`	`@0 Animal @5 07`
C03	`04`	`X`	`SPA`	`@0 Animal @5 07`
C03	`05`	`X`	`FRE`	`@0 Singe @5 10`
C03	`05`	`X`	`ENG`	`@0 Monkey @5 10`
C03	`05`	`X`	`SPA`	`@0 Mono @5 10`
C03	`06`	`X`	`FRE`	`@0 Encéphale @5 11`
C03	`06`	`X`	`ENG`	`@0 Brain (vertebrata) @5 11`
C03	`06`	`X`	`SPA`	`@0 Encéfalo @5 11`
C03	`07`	`X`	`FRE`	`@0 Système nerveux central @5 12`
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C03	`08`	`X`	`FRE`	`@0 Récepteur glutamate @5 13`
C03	`08`	`X`	`ENG`	`@0 Glutamate receptor @5 13`
C03	`08`	`X`	`SPA`	`@0 Receptor glutámato @5 13`
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C03	`10`	`X`	`FRE`	`@0 Récepteur dopaminergique D1 @5 15`
C03	`10`	`X`	`ENG`	`@0 D1 Dopamine receptor @5 15 @6 «D1» Dopamine receptor`
C03	`10`	`X`	`SPA`	`@0 Receptor dopaminérgico D1 @5 15`
C03	`11`	`X`	`FRE`	`@0 Agoniste @5 16`
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C03	`11`	`X`	`SPA`	`@0 Agonista @5 16`
C03	`12`	`X`	`FRE`	`@0 Antagoniste @5 17`
C03	`12`	`X`	`ENG`	`@0 Antagonist @5 17`
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C03	`13`	`X`	`FRE`	`@0 Récepteur AMPA @5 18`
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C03	`14`	`X`	`ENG`	`@0 NMDA receptor @5 19`
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C03	`15`	`X`	`FRE`	`@0 Interaction moléculaire @5 20`
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C03	`18`	`X`	`FRE`	`@0 Glycine @2 NK @2 FR @5 23`
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C03	`21`	`X`	`FRE`	`@0 Glutamate @2 NK @2 FX @5 78`
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C03	`22`	`X`	`SPA`	`@0 Glutamina @2 NK @2 FR @5 79`
C07	`01`	`X`	`FRE`	`@0 Primates @2 NS`
C07	`01`	`X`	`ENG`	`@0 Primates @2 NS`
C07	`01`	`X`	`SPA`	`@0 Primates @2 NS`
C07	`02`	`X`	`FRE`	`@0 Mammalia @2 NS`
C07	`02`	`X`	`ENG`	`@0 Mammalia @2 NS`
C07	`02`	`X`	`SPA`	`@0 Mammalia @2 NS`
C07	`03`	`X`	`FRE`	`@0 Vertebrata @2 NS`
C07	`03`	`X`	`ENG`	`@0 Vertebrata @2 NS`
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C07	`06`	`X`	`FRE`	`@0 Mouvement involontaire @5 47`
C07	`06`	`X`	`ENG`	`@0 Involuntary movement @5 47`
C07	`06`	`X`	`SPA`	`@0 Movimiento involuntario @5 47`
C07	`07`	`X`	`FRE`	`@0 Extrapyramidal syndrome @5 48`
C07	`07`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 48`
C07	`07`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 48`
N21				`@1 133`
N82				`@1 PSI`

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Le document en format XML

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<series><title level="j" type="main">Progress in neuro-psychopharmacology & biological psychiatry</title>
<title level="j" type="abbreviated">Prog. neuro-psychopharmacol. biol. psychiatr.</title>
<idno type="ISSN">0278-5846</idno>
<imprint><date when="2002">2002</date>
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<seriesStmt><title level="j" type="main">Progress in neuro-psychopharmacology & biological psychiatry</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>AMPA receptor</term>
<term>Agonist</term>
<term>Animal</term>
<term>Animal model</term>
<term>Antagonist</term>
<term>Brain (vertebrata)</term>
<term>Central nervous system</term>
<term>Corpus striatum</term>
<term>D1 Dopamine receptor</term>
<term>D2 Dopamine receptor</term>
<term>Dyskinesia</term>
<term>Glutamate</term>
<term>Glutamate receptor</term>
<term>Glutamatergic transmission</term>
<term>Glutamine</term>
<term>Glycine</term>
<term>Molecular interaction</term>
<term>Monkey</term>
<term>NMDA receptor</term>
<term>Pathogenesis</term>
<term>Toxicity</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Corps strié</term>
<term>Modèle animal</term>
<term>Dyskinésie</term>
<term>Animal</term>
<term>Singe</term>
<term>Encéphale</term>
<term>Système nerveux central</term>
<term>Récepteur glutamate</term>
<term>Récepteur dopaminergique D2</term>
<term>Récepteur dopaminergique D1</term>
<term>Agoniste</term>
<term>Antagoniste</term>
<term>Récepteur AMPA</term>
<term>Récepteur NMDA</term>
<term>Interaction moléculaire</term>
<term>Pathogénie</term>
<term>Transmission glutamatergique</term>
<term>Glycine</term>
<term>Pyridine(1-méthyl-4-phényl-1,2,3,6-tétrahydro)</term>
<term>Toxicité</term>
<term>Glutamate</term>
<term>Glutamine</term>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Singe</term>
</keywords>
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<front><div type="abstract" xml:lang="en">The effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced nigrostriatal lesion and dopaminomimetic treatment on parameters of glutamatergic activity within the basal ganglia of monkeys were studied in relation with the development of dyskinesias. Drug-naive controls, saline-treated MPTP monkeys, as well as MPTP monkeys treated with either a long-acting D<sub>2</sub>
 agonist (cabergoline) or a D<sub>1</sub>
 agonist (SKF-82958) given by intermittent injections or continuous infusion, were included in this study. <sup>3</sup>
H-L-glutamate, <sup>3</sup>
H-α-amino-3-hydroxy-5-methylisoxasole-4-propionate (AMPA), <sup>3</sup>
H-glycine, <sup>3</sup>
H-CGP39653 (an N-methyl-D-aspartate, NMDA, antagonist selective for NR1/NR2A assembly) and <sup>3</sup>
H-Ro 25-6981 (an NMDA antagonist selective for NR1/NR2B assembly), specific binding to glutamate receptors, the expression of the NR1 subunit of NMDA receptors and glutamate, glutamine and glycine concentrations were studied by autoradiography, in situ hybridization and high-performance liquid chromatography (HPLC), respectively. Pulsatile SKF-82958 and cabergoline treatment relieved parkinsonian symptoms, whereas animals continuously treated with SKF-82958 remained akinetic. Pulsatile SKF-82958 induced dyskinesias in two of the three animals tested, whereas cabergoline did not. MPTP induced no significant changes of striatal specific binding of the radioligands used, NR1 mRNA expression and amino acid concentrations. In the putamen, pulsatile SKF-82958 treatment was associated with decreased content of glycine and glutamate, whereas only glycine was decreased in cabergoline-treated monkeys. Cabergoline and continuous administration of SKF-82958 led to lower levels of NR1 mRNA in the caudate in comparison to pulsatile SKF-82958 administration. The development of dyskinesias following a D<sub>1</sub>
 agonist treatment was associated with an upregulation of <sup>3</sup>
H-glutamate [+49%], <sup>3</sup>
H-AMPA [+38%], <sup>3</sup>
H-CGP39653 [+111%], <sup>3</sup>
H-glycine [+26%, nonsignificant] and <sup>3</sup>
H-Ro 25-6981 [+33%] specific binding in the striatum in comparison to nondyskinetic MPTP monkeys. Our data suggest that supersensitivity to glutamatergic input in the striatum might play a role in the pathogenesis of dopaminomimetic-induced dyskinesias and further support the therapeutic potential of glutamate antagonists in Parkinson's disease.</div>
</front>
</TEI>
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<fA11 i1="01" i2="1"><s1>CALON (Frédéric)</s1>
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<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Medicine, Faculty of Medicine, Laval University</s1>
<s2>Quebec, Quebec</s2>
<s3>CAN</s3>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA20><s1>127-138</s1>
</fA20>
<fA21><s1>2002</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>17544</s2>
<s5>354000102750070190</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2002 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>2 p.1/4</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>02-0226511</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Progress in neuro-psychopharmacology & biological psychiatry</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>The effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced nigrostriatal lesion and dopaminomimetic treatment on parameters of glutamatergic activity within the basal ganglia of monkeys were studied in relation with the development of dyskinesias. Drug-naive controls, saline-treated MPTP monkeys, as well as MPTP monkeys treated with either a long-acting D<sub>2</sub>
 agonist (cabergoline) or a D<sub>1</sub>
 agonist (SKF-82958) given by intermittent injections or continuous infusion, were included in this study. <sup>3</sup>
H-L-glutamate, <sup>3</sup>
H-α-amino-3-hydroxy-5-methylisoxasole-4-propionate (AMPA), <sup>3</sup>
H-glycine, <sup>3</sup>
H-CGP39653 (an N-methyl-D-aspartate, NMDA, antagonist selective for NR1/NR2A assembly) and <sup>3</sup>
H-Ro 25-6981 (an NMDA antagonist selective for NR1/NR2B assembly), specific binding to glutamate receptors, the expression of the NR1 subunit of NMDA receptors and glutamate, glutamine and glycine concentrations were studied by autoradiography, in situ hybridization and high-performance liquid chromatography (HPLC), respectively. Pulsatile SKF-82958 and cabergoline treatment relieved parkinsonian symptoms, whereas animals continuously treated with SKF-82958 remained akinetic. Pulsatile SKF-82958 induced dyskinesias in two of the three animals tested, whereas cabergoline did not. MPTP induced no significant changes of striatal specific binding of the radioligands used, NR1 mRNA expression and amino acid concentrations. In the putamen, pulsatile SKF-82958 treatment was associated with decreased content of glycine and glutamate, whereas only glycine was decreased in cabergoline-treated monkeys. Cabergoline and continuous administration of SKF-82958 led to lower levels of NR1 mRNA in the caudate in comparison to pulsatile SKF-82958 administration. The development of dyskinesias following a D<sub>1</sub>
 agonist treatment was associated with an upregulation of <sup>3</sup>
H-glutamate [+49%], <sup>3</sup>
H-AMPA [+38%], <sup>3</sup>
H-CGP39653 [+111%], <sup>3</sup>
H-glycine [+26%, nonsignificant] and <sup>3</sup>
H-Ro 25-6981 [+33%] specific binding in the striatum in comparison to nondyskinetic MPTP monkeys. Our data suggest that supersensitivity to glutamatergic input in the striatum might play a role in the pathogenesis of dopaminomimetic-induced dyskinesias and further support the therapeutic potential of glutamate antagonists in Parkinson's disease.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17I</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Corps strié</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Corpus striatum</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Cuerpo estriado</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Modèle animal</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Animal model</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Modelo animal</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Dyskinésie</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Dyskinesia</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Disquinesia</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Animal</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Animal</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Animal</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Singe</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Monkey</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Mono</s0>
<s5>10</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Encéphale</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Brain (vertebrata)</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Encéfalo</s0>
<s5>11</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Récepteur glutamate</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Glutamate receptor</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Receptor glutámato</s0>
<s5>13</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Récepteur dopaminergique D2</s0>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>D2 Dopamine receptor</s0>
<s5>14</s5>
<s6>«D2» Dopamine receptor</s6>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Receptor dopaminérgico D2</s0>
<s5>14</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Récepteur dopaminergique D1</s0>
<s5>15</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>D1 Dopamine receptor</s0>
<s5>15</s5>
<s6>«D1» Dopamine receptor</s6>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Receptor dopaminérgico D1</s0>
<s5>15</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Agoniste</s0>
<s5>16</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Agonist</s0>
<s5>16</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Agonista</s0>
<s5>16</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Antagoniste</s0>
<s5>17</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Antagonist</s0>
<s5>17</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Antagonista</s0>
<s5>17</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Récepteur AMPA</s0>
<s5>18</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>AMPA receptor</s0>
<s5>18</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Receptor AMPA</s0>
<s5>18</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE"><s0>Récepteur NMDA</s0>
<s5>19</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG"><s0>NMDA receptor</s0>
<s5>19</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA"><s0>Receptor NMDA</s0>
<s5>19</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE"><s0>Interaction moléculaire</s0>
<s5>20</s5>
</fC03>
<fC03 i1="15" i2="X" l="ENG"><s0>Molecular interaction</s0>
<s5>20</s5>
</fC03>
<fC03 i1="15" i2="X" l="SPA"><s0>Interacción molecular</s0>
<s5>20</s5>
</fC03>
<fC03 i1="16" i2="X" l="FRE"><s0>Pathogénie</s0>
<s5>21</s5>
</fC03>
<fC03 i1="16" i2="X" l="ENG"><s0>Pathogenesis</s0>
<s5>21</s5>
</fC03>
<fC03 i1="16" i2="X" l="SPA"><s0>Patogenia</s0>
<s5>21</s5>
</fC03>
<fC03 i1="17" i2="X" l="FRE"><s0>Transmission glutamatergique</s0>
<s5>22</s5>
</fC03>
<fC03 i1="17" i2="X" l="ENG"><s0>Glutamatergic transmission</s0>
<s5>22</s5>
</fC03>
<fC03 i1="17" i2="X" l="SPA"><s0>Transmision glutamatérgica</s0>
<s5>22</s5>
</fC03>
<fC03 i1="18" i2="X" l="FRE"><s0>Glycine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>23</s5>
</fC03>
<fC03 i1="18" i2="X" l="ENG"><s0>Glycine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>23</s5>
</fC03>
<fC03 i1="18" i2="X" l="SPA"><s0>Glicina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>23</s5>
</fC03>
<fC03 i1="19" i2="X" l="FRE"><s0>Pyridine(1-méthyl-4-phényl-1,2,3,6-tétrahydro)</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>24</s5>
<s6>Pyridine(«1»-méthyl-«4»-phényl-«1,2,3,6»-tétrahydro)</s6>
</fC03>
<fC03 i1="20" i2="X" l="FRE"><s0>Toxicité</s0>
<s5>35</s5>
</fC03>
<fC03 i1="20" i2="X" l="ENG"><s0>Toxicity</s0>
<s5>35</s5>
</fC03>
<fC03 i1="20" i2="X" l="SPA"><s0>Toxicidad</s0>
<s5>35</s5>
</fC03>
<fC03 i1="21" i2="X" l="FRE"><s0>Glutamate</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>78</s5>
</fC03>
<fC03 i1="21" i2="X" l="ENG"><s0>Glutamate</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>78</s5>
</fC03>
<fC03 i1="21" i2="X" l="SPA"><s0>Glutamato</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>78</s5>
</fC03>
<fC03 i1="22" i2="X" l="FRE"><s0>Glutamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>79</s5>
</fC03>
<fC03 i1="22" i2="X" l="ENG"><s0>Glutamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>79</s5>
</fC03>
<fC03 i1="22" i2="X" l="SPA"><s0>Glutamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>79</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Primates</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Primates</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Primates</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>Système nerveux pathologie</s0>
<s5>45</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>45</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>45</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Trouble neurologique</s0>
<s5>46</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Neurological disorder</s0>
<s5>46</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Trastorno neurológico</s0>
<s5>46</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Mouvement involontaire</s0>
<s5>47</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Involuntary movement</s0>
<s5>47</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Movimiento involuntario</s0>
<s5>47</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>48</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>48</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>48</s5>
</fC07>
<fN21><s1>133</s1>
</fN21>
<fN82><s1>PSI</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

Alteration of glutamate receptors in the striatum of dyskinetic 1 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated monkeys following dopamine agonist treatment

Alteration of glutamate receptors in the striatum of dyskinetic 1 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated monkeys following dopamine agonist treatment

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