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

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Functional interaction between mGlu 5 and NMDA receptors in a rat model of Parkinson's disease

Identifieur interne : 000758 ( PascalFrancis/Curation ); précédent : 000757; suivant : 000759

Functional interaction between mGlu 5 and NMDA receptors in a rat model of Parkinson's disease

Auteurs : Nathalie Turle-Lorenzo [France] ; Nathalie Breysse [France] ; Christelle Baunez [France] ; Marianne Amalric [France]

Source :

RBID : Pascal:05-0297430

Descripteurs français

English descriptors

Abstract

Rationale: Electrophysiological evidence suggests a synergistic relationship between metabotropic (mGlu) and ionotropic (iGlu) glutamate receptors. The functional consequences of these interactions have not been investigated in neurodegenerative diseases such as in Parkinson's disease. Objective: The goals ofthis study are as follows: (1) to investigate the effects of 2-methyl-6-(phenylethynyl)-pyridine (MPEP) and dizocilpine (MK- 801), antagonists at metabotropic glutamate 5 (mGlu5) and NMDA receptors, respectively, on the akinetic syndrome observed in bilateral 6-OHDA-lesioned rats; (2) to investigate if the effects of MPEP were potentiated by co-treatment with a behaviorally inactive dose of MK-801; and (3) to investigate the effects of L-DOPA alone and in combination with MPEP on the akinetic syndrome observed in 6-OHDA-lesioned rats. Methods: The effects of the different treatments (single and co-treatment) administered for 3 weeks were measured in 6-OHDA-lesioned rats trained to release a lever rapidly after a visual stimulus onset in a simple reaction time task. Results: MPEP 0.75 mg/kg reversed the akinetic deficits produced by striatal dopamine depletion, while MPEP 0.375 mg/kg had no effect. Co-administration with MK-801 0.02 mg/kg, ineffective alone, failed to speed the recovery process of MPEP 0.75 mg/kg but revealed the anti-akinetic action of MPEP 0.375 mg/kg. L-DOPA 3 mg/kg alone had a potent anti-akinetic effect in 6-OHDA lesioned rats, and this effect was not potentiated by a subthreshold MPEP treatment. Conclusion: These results support a critical role for mGlu5 receptor blockade in improving parkinsonian symptomatology either as a single treatment or in combination with low concentrations of L-DOPA and demonstrate an interaction between NMDA and mGluR5 in regulating these effects.
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A11 02  1    @1 BREYSSE (Nathalie)
A11 03  1    @1 BAUNEZ (Christelle)
A11 04  1    @1 AMALRIC (Marianne)
A12 01  1    @1 HIGGINS (Guy A.) @9 ed.
A12 02  1    @1 MICZEK (Klaus A.) @9 ed.
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A15 01      @1 NPS Pharmaceuticals, 300 Interpace Parkway @2 Parsippany, NJ 07054 @3 USA @Z 1 aut.
A15 02      @1 Department of Psychology, Pharmacology and Neuroscience and Psychiatry, Tufts University, Bacon Hall, 530 Boston Ave. @2 Medford, MA 02155 @3 USA @Z 2 aut.
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C01 01    ENG  @0 Rationale: Electrophysiological evidence suggests a synergistic relationship between metabotropic (mGlu) and ionotropic (iGlu) glutamate receptors. The functional consequences of these interactions have not been investigated in neurodegenerative diseases such as in Parkinson's disease. Objective: The goals ofthis study are as follows: (1) to investigate the effects of 2-methyl-6-(phenylethynyl)-pyridine (MPEP) and dizocilpine (MK- 801), antagonists at metabotropic glutamate 5 (mGlu5) and NMDA receptors, respectively, on the akinetic syndrome observed in bilateral 6-OHDA-lesioned rats; (2) to investigate if the effects of MPEP were potentiated by co-treatment with a behaviorally inactive dose of MK-801; and (3) to investigate the effects of L-DOPA alone and in combination with MPEP on the akinetic syndrome observed in 6-OHDA-lesioned rats. Methods: The effects of the different treatments (single and co-treatment) administered for 3 weeks were measured in 6-OHDA-lesioned rats trained to release a lever rapidly after a visual stimulus onset in a simple reaction time task. Results: MPEP 0.75 mg/kg reversed the akinetic deficits produced by striatal dopamine depletion, while MPEP 0.375 mg/kg had no effect. Co-administration with MK-801 0.02 mg/kg, ineffective alone, failed to speed the recovery process of MPEP 0.75 mg/kg but revealed the anti-akinetic action of MPEP 0.375 mg/kg. L-DOPA 3 mg/kg alone had a potent anti-akinetic effect in 6-OHDA lesioned rats, and this effect was not potentiated by a subthreshold MPEP treatment. Conclusion: These results support a critical role for mGlu5 receptor blockade in improving parkinsonian symptomatology either as a single treatment or in combination with low concentrations of L-DOPA and demonstrate an interaction between NMDA and mGluR5 in regulating these effects.
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N21       @1 206

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Pascal:05-0297430

Le document en format XML

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<div type="abstract" xml:lang="en">Rationale: Electrophysiological evidence suggests a synergistic relationship between metabotropic (mGlu) and ionotropic (iGlu) glutamate receptors. The functional consequences of these interactions have not been investigated in neurodegenerative diseases such as in Parkinson's disease. Objective: The goals ofthis study are as follows: (1) to investigate the effects of 2-methyl-6-(phenylethynyl)-pyridine (MPEP) and dizocilpine (MK- 801), antagonists at metabotropic glutamate 5 (mGlu5) and NMDA receptors, respectively, on the akinetic syndrome observed in bilateral 6-OHDA-lesioned rats; (2) to investigate if the effects of MPEP were potentiated by co-treatment with a behaviorally inactive dose of MK-801; and (3) to investigate the effects of L-DOPA alone and in combination with MPEP on the akinetic syndrome observed in 6-OHDA-lesioned rats. Methods: The effects of the different treatments (single and co-treatment) administered for 3 weeks were measured in 6-OHDA-lesioned rats trained to release a lever rapidly after a visual stimulus onset in a simple reaction time task. Results: MPEP 0.75 mg/kg reversed the akinetic deficits produced by striatal dopamine depletion, while MPEP 0.375 mg/kg had no effect. Co-administration with MK-801 0.02 mg/kg, ineffective alone, failed to speed the recovery process of MPEP 0.75 mg/kg but revealed the anti-akinetic action of MPEP 0.375 mg/kg. L-DOPA 3 mg/kg alone had a potent anti-akinetic effect in 6-OHDA lesioned rats, and this effect was not potentiated by a subthreshold MPEP treatment. Conclusion: These results support a critical role for mGlu5 receptor blockade in improving parkinsonian symptomatology either as a single treatment or in combination with low concentrations of L-DOPA and demonstrate an interaction between NMDA and mGluR5 in regulating these effects.</div>
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<fA43 i1="01">
<s1>INIST</s1>
<s2>1761</s2>
<s5>354000125666190090</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2005 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>44 ref.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>05-0297430</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Psychopharmacologia</s0>
</fA64>
<fA66 i1="01">
<s0>DEU</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>Rationale: Electrophysiological evidence suggests a synergistic relationship between metabotropic (mGlu) and ionotropic (iGlu) glutamate receptors. The functional consequences of these interactions have not been investigated in neurodegenerative diseases such as in Parkinson's disease. Objective: The goals ofthis study are as follows: (1) to investigate the effects of 2-methyl-6-(phenylethynyl)-pyridine (MPEP) and dizocilpine (MK- 801), antagonists at metabotropic glutamate 5 (mGlu5) and NMDA receptors, respectively, on the akinetic syndrome observed in bilateral 6-OHDA-lesioned rats; (2) to investigate if the effects of MPEP were potentiated by co-treatment with a behaviorally inactive dose of MK-801; and (3) to investigate the effects of L-DOPA alone and in combination with MPEP on the akinetic syndrome observed in 6-OHDA-lesioned rats. Methods: The effects of the different treatments (single and co-treatment) administered for 3 weeks were measured in 6-OHDA-lesioned rats trained to release a lever rapidly after a visual stimulus onset in a simple reaction time task. Results: MPEP 0.75 mg/kg reversed the akinetic deficits produced by striatal dopamine depletion, while MPEP 0.375 mg/kg had no effect. Co-administration with MK-801 0.02 mg/kg, ineffective alone, failed to speed the recovery process of MPEP 0.75 mg/kg but revealed the anti-akinetic action of MPEP 0.375 mg/kg. L-DOPA 3 mg/kg alone had a potent anti-akinetic effect in 6-OHDA lesioned rats, and this effect was not potentiated by a subthreshold MPEP treatment. Conclusion: These results support a critical role for mGlu5 receptor blockade in improving parkinsonian symptomatology either as a single treatment or in combination with low concentrations of L-DOPA and demonstrate an interaction between NMDA and mGluR5 in regulating these effects.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002B17G</s0>
</fC02>
<fC02 i1="02" i2="X">
<s0>002B02B06</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Interaction</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Interaction</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Interacción</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Récepteur NMDA</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>NMDA receptor</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Receptor NMDA</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Modèle animal</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Animal model</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Modelo animal</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Rat</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Rat</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Rata</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Parkinson maladie</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Parkinson disease</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Parkinson enfermedad</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Noyau gris central</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Basal ganglion</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Núcleo basal</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Pyridine</s0>
<s2>NK</s2>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Pyridine</s0>
<s2>NK</s2>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Piridina</s0>
<s2>NK</s2>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Dizocilpine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Dizocilpine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Dizocilpina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Antagoniste</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Antagonist</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Antagonista</s0>
<s5>09</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Oxidopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Oxidopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Oxidopamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>10</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE">
<s0>Lésion</s0>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG">
<s0>Lesion</s0>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA">
<s0>Lesión</s0>
<s5>11</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE">
<s0>Temps réaction</s0>
<s5>12</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG">
<s0>Reaction time</s0>
<s5>12</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA">
<s0>Tiempo reacción</s0>
<s5>12</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE">
<s0>Akinésie</s0>
<s5>13</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG">
<s0>Akinesia</s0>
<s5>13</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA">
<s0>Aquinesia</s0>
<s5>13</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE">
<s0>Glutamate</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>14</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG">
<s0>Glutamate</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>14</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA">
<s0>Glutamato</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>14</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE">
<s0>Animal</s0>
<s5>15</s5>
</fC03>
<fC03 i1="15" i2="X" l="ENG">
<s0>Animal</s0>
<s5>15</s5>
</fC03>
<fC03 i1="15" i2="X" l="SPA">
<s0>Animal</s0>
<s5>15</s5>
</fC03>
<fC03 i1="16" i2="X" l="FRE">
<s0>Récepteur métabotropique</s0>
<s5>16</s5>
</fC03>
<fC03 i1="16" i2="X" l="ENG">
<s0>Metabotropic receptor</s0>
<s5>16</s5>
</fC03>
<fC03 i1="16" i2="X" l="SPA">
<s0>Receptor metabotropico</s0>
<s5>16</s5>
</fC03>
<fC03 i1="17" i2="X" l="FRE">
<s0>Neuroprotecteur</s0>
<s5>26</s5>
</fC03>
<fC03 i1="17" i2="X" l="ENG">
<s0>Neuroprotective agent</s0>
<s5>26</s5>
</fC03>
<fC03 i1="17" i2="X" l="SPA">
<s0>Neuroprotector</s0>
<s5>26</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>Récepteur glutamate</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Glutamate receptor</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Receptor glutámato</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Système nerveux pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Encéphale pathologie</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Encéfalo patología</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>Système nerveux central pathologie</s0>
<s5>42</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>42</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE">
<s0>Système nerveux central</s0>
<s5>43</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG">
<s0>Central nervous system</s0>
<s5>43</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA">
<s0>Sistema nervioso central</s0>
<s5>43</s5>
</fC07>
<fC07 i1="11" i2="X" l="FRE">
<s0>Agoniste</s0>
<s5>44</s5>
</fC07>
<fC07 i1="11" i2="X" l="ENG">
<s0>Agonist</s0>
<s5>44</s5>
</fC07>
<fC07 i1="11" i2="X" l="SPA">
<s0>Agonista</s0>
<s5>44</s5>
</fC07>
<fC07 i1="12" i2="X" l="FRE">
<s0>Récepteur adrénergique</s0>
<s5>45</s5>
</fC07>
<fC07 i1="12" i2="X" l="ENG">
<s0>Adrenergic receptor</s0>
<s5>45</s5>
</fC07>
<fC07 i1="12" i2="X" l="SPA">
<s0>Receptor adrenérgico</s0>
<s5>45</s5>
</fC07>
<fC07 i1="13" i2="X" l="FRE">
<s0>Sympathomimétique</s0>
<s5>46</s5>
</fC07>
<fC07 i1="13" i2="X" l="ENG">
<s0>Sympathomimetic</s0>
<s5>46</s5>
</fC07>
<fC07 i1="13" i2="X" l="SPA">
<s0>Simpaticomimético</s0>
<s5>46</s5>
</fC07>
<fC07 i1="14" i2="X" l="FRE">
<s0>Trouble moteur</s0>
<s5>47</s5>
</fC07>
<fC07 i1="14" i2="X" l="ENG">
<s0>Motor system disorder</s0>
<s5>47</s5>
</fC07>
<fC07 i1="14" i2="X" l="SPA">
<s0>Trastorno motor</s0>
<s5>47</s5>
</fC07>
<fC07 i1="15" i2="X" l="FRE">
<s0>Trouble neurologique</s0>
<s5>48</s5>
</fC07>
<fC07 i1="15" i2="X" l="ENG">
<s0>Neurological disorder</s0>
<s5>48</s5>
</fC07>
<fC07 i1="15" i2="X" l="SPA">
<s0>Trastorno neurológico</s0>
<s5>48</s5>
</fC07>
<fC07 i1="16" i2="X" l="FRE">
<s0>Aminoacide excitateur</s0>
<s5>49</s5>
</fC07>
<fC07 i1="16" i2="X" l="ENG">
<s0>Excitatory aminoacid</s0>
<s5>49</s5>
</fC07>
<fC07 i1="16" i2="X" l="SPA">
<s0>Aminoácido excitador</s0>
<s5>49</s5>
</fC07>
<fC07 i1="17" i2="X" l="FRE">
<s0>Neurotransmetteur</s0>
<s5>50</s5>
</fC07>
<fC07 i1="17" i2="X" l="ENG">
<s0>Neurotransmitter</s0>
<s5>50</s5>
</fC07>
<fC07 i1="17" i2="X" l="SPA">
<s0>Neurotransmisor</s0>
<s5>50</s5>
</fC07>
<fN21>
<s1>206</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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