Functional interaction between mGlu 5 and NMDA receptors in a rat model of Parkinson's disease
Identifieur interne : 000758 ( PascalFrancis/Curation ); précédent : 000757; suivant : 000759Functional 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 :
- Psychopharmacologia [ 0033-3158 ] ; 2005.
Descripteurs français
- Pascal (Inist)
English descriptors
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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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<front><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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</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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