Selective Activation of mGlu4 Metabotropic Glutamate Receptors Is Protective against Excitotoxic Neuronal Death
Activation of group III metabotropic glutamate receptors (mGluR4, mGluR6, mGluR7, and mGluR8) has been established to be neuroprotective in vitro and in vivo. To disclose the identity of the receptor subtype(s) that exert(s) the protective effect, we have used group III agonists in combination with...
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Published in | The Journal of neuroscience Vol. 20; no. 17; pp. 6413 - 6420 |
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Main Authors | , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
Soc Neuroscience
01.09.2000
Society for Neuroscience |
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Abstract | Activation of group III metabotropic glutamate receptors (mGluR4, mGluR6, mGluR7, and mGluR8) has been established to be neuroprotective in vitro and in vivo. To disclose the identity of the receptor subtype(s) that exert(s) the protective effect, we have used group III agonists in combination with mGluR4 subtype-deficient mice (-/-). In cortical cultures prepared from wild-type (+/+) mice and exposed to a toxic pulse of NMDA, the selective group III agonist (+)-4-phosphonophenylglycine [(+)-PPG] reversed excitotoxicity with an EC(50) value of 4.9 microm, whereas its enantiomer (-)-PPG was inactive. This correlated closely with the potency of (+)-PPG in activating recombinant mGluR4a. In cortical neurons from -/- mice, (+)-PPG showed no protection against the NMDA insult up to 300 microm, whereas group I/II mGluR ligands still retained their protective activity. Classical group III agonists (l-2-amino-4-phosphonobutyrate and l-serine-O-phosphate) were also substantially neuroprotective against NMDA toxicity in +/+ and heterozygous (+/-) cultures but were inactive in -/- cultures. Interestingly, -/- cultures were more vulnerable to low concentrations of NMDA and showed higher extracellular glutamate levels compared with +/+ cultures. We have also examined neurodegeneration induced by intrastriatal infusion of NMDA in wild-type or mGluR4-deficient mice. Low doses of (R,S)-PPG (10 nmol/0.5 microl) substantially reduced NMDA toxicity in +/+ mice but were ineffective in -/- mice. Higher doses of (R,S)-PPG were neuroprotective in both strains of animals. Finally, microdialysis studies showed that intrastriatal infusion of NMDA increased extracellular glutamate levels to a greater extent in -/- than in +/+ mice, supporting the hypothesis that the mGluR4 subtype is necessary for the maintenance of the homeostasis of extracellular glutamate levels. |
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AbstractList | Activation of group III metabotropic glutamate receptors (mGluR4, mGluR6, mGluR7, and mGluR8) has been established to be neuroprotective in vitro and in vivo. To disclose the identity of the receptor subtype(s) that exert(s) the protective effect, we have used group III agonists in combination with mGluR4 subtype-deficient mice (-/-). In cortical cultures prepared from wild-type (+/+) mice and exposed to a toxic pulse of NMDA, the selective group III agonist (+)-4-phosphonophenylglycine [(+)-PPG] reversed excitotoxicity with an EC(50) value of 4.9 microm, whereas its enantiomer (-)-PPG was inactive. This correlated closely with the potency of (+)-PPG in activating recombinant mGluR4a. In cortical neurons from -/- mice, (+)-PPG showed no protection against the NMDA insult up to 300 microm, whereas group I/II mGluR ligands still retained their protective activity. Classical group III agonists (l-2-amino-4-phosphonobutyrate and l-serine-O-phosphate) were also substantially neuroprotective against NMDA toxicity in +/+ and heterozygous (+/-) cultures but were inactive in -/- cultures. Interestingly, -/- cultures were more vulnerable to low concentrations of NMDA and showed higher extracellular glutamate levels compared with +/+ cultures. We have also examined neurodegeneration induced by intrastriatal infusion of NMDA in wild-type or mGluR4-deficient mice. Low doses of (R,S)-PPG (10 nmol/0.5 microl) substantially reduced NMDA toxicity in +/+ mice but were ineffective in -/- mice. Higher doses of (R,S)-PPG were neuroprotective in both strains of animals. Finally, microdialysis studies showed that intrastriatal infusion of NMDA increased extracellular glutamate levels to a greater extent in -/- than in +/+ mice, supporting the hypothesis that the mGluR4 subtype is necessary for the maintenance of the homeostasis of extracellular glutamate levels. Activation of group III metabotropic glutamate receptors (mGluR4, mGluR6, mGluR7, and mGluR8) has been established to be neuroprotective in vitro and in vivo. To disclose the identity of the receptor subtype(s) that exert(s) the protective effect, we have used group III agonists in combination with mGluR4 subtype-deficient mice (-/-). In cortical cultures prepared from wild-type (+/+) mice and exposed to a toxic pulse of NMDA, the selective group III agonist (+)-4-phosphonophenylglycine [(+)-PPG] reversed excitotoxicity with an EC sub(50) value of 4.9 mu M, whereas its enantiomer (-)-PPG was inactive. This correlated closely with the potency of (+)-PPG in activating recombinant mGluR4a. In cortical neurons from -/- mice, (+)-PPG showed no protection against the NMDA insult up to 300 mu M, whereas group I/II mGluR ligands still retained their protective activity. Classical group III agonists (L-2-amino-4-phosphonobutyrate and L-serine-O-phosphate) were also substantially neuroprotective against NMDA toxicity in +/+ and heterozygous (+/-) cultures but were inactive in -/- cultures. Interestingly, -/- cultures were more vulnerable to low concentrations of NMDA and showed higher extracellular glutamate levels compared with +/+ cultures. We have also examined neurodegeneration induced by intrastriatal infusion of NMDA in wild-type or mGluR4-deficient mice. Low doses of (R,S)-PPG (10 nmol/0.5 mu l) substantially reduced NMDA toxicity in +/+ mice but were ineffective in -/- mice. Higher doses of (R,S)-PPG were neuroprotective in both strains of animals. Finally, microdialysis studies showed that intrastriatal infusion of NMDA increased extracellular glutamate levels to a greater extent in -/- than in +/+ mice, supporting the hypothesis that the mGluR4 subtype is necessary for the maintenance of the homeostasis of extracellular glutamate levels. Activation of group III metabotropic glutamate receptors (mGluR4, mGluR6, mGluR7, and mGluR8) has been established to be neuroprotective in vitro and in vivo . To disclose the identity of the receptor subtype(s) that exert(s) the protective effect, we have used group III agonists in combination with mGluR4 subtype-deficient mice (−/−). In cortical cultures prepared from wild-type (+/+) mice and exposed to a toxic pulse of NMDA, the selective group III agonist (+)-4-phosphonophenylglycine [(+)-PPG] reversed excitotoxicity with an EC 50 value of 4.9 μ m , whereas its enantiomer (−)-PPG was inactive. This correlated closely with the potency of (+)-PPG in activating recombinant mGluR4a. In cortical neurons from −/− mice, (+)-PPG showed no protection against the NMDA insult up to 300 μ m , whereas group I/II mGluR ligands still retained their protective activity. Classical group III agonists ( l -2-amino-4-phosphonobutyrate and l -serine- O -phosphate) were also substantially neuroprotective against NMDA toxicity in +/+ and heterozygous (+/−) cultures but were inactive in −/− cultures. Interestingly, −/− cultures were more vulnerable to low concentrations of NMDA and showed higher extracellular glutamate levels compared with +/+ cultures. We have also examined neurodegeneration induced by intrastriatal infusion of NMDA in wild-type or mGluR4-deficient mice. Low doses of ( R , S )-PPG (10 nmol/0.5 μl) substantially reduced NMDA toxicity in +/+ mice but were ineffective in −/− mice. Higher doses of ( R , S )-PPG were neuroprotective in both strains of animals. Finally, microdialysis studies showed that intrastriatal infusion of NMDA increased extracellular glutamate levels to a greater extent in −/− than in +/+ mice, supporting the hypothesis that the mGluR4 subtype is necessary for the maintenance of the homeostasis of extracellular glutamate levels. |
Author | Bruno, V Leonhardt, T Battaglia, G Gasparini, F Kuhn, R Catania, M. V Inderbitzin, W Nicoletti, F van der Putten, H Hampson, D. R Giuffrida, R Ksiazek, I Flor, P. J Lukic, S |
AuthorAffiliation | 1 Istituto Neurologico Mediterraneo Neuromed, 86077 Pozzilli, Italy 2 Novartis Pharma AG, Nervous System Research, CH-4002 Basel, Switzerland 4 Faculty of Pharmacy, University of Toronto, Canada M5S 2S2, and 5 Department of Pharmaceutical Sciences, University of Catania, 95125 Catania, Italy 3 Istituto di Bioimmagini e Fisiopatologia del Sistema Nervoso Centrale, Consiglio Nazionale delle Ricerche, 95125 Catania, Italy |
AuthorAffiliation_xml | – name: 3 Istituto di Bioimmagini e Fisiopatologia del Sistema Nervoso Centrale, Consiglio Nazionale delle Ricerche, 95125 Catania, Italy – name: 5 Department of Pharmaceutical Sciences, University of Catania, 95125 Catania, Italy – name: 4 Faculty of Pharmacy, University of Toronto, Canada M5S 2S2, and – name: 1 Istituto Neurologico Mediterraneo Neuromed, 86077 Pozzilli, Italy – name: 2 Novartis Pharma AG, Nervous System Research, CH-4002 Basel, Switzerland |
Author_xml | – sequence: 1 fullname: Bruno, V – sequence: 2 fullname: Battaglia, G – sequence: 3 fullname: Ksiazek, I – sequence: 4 fullname: van der Putten, H – sequence: 5 fullname: Catania, M. V – sequence: 6 fullname: Giuffrida, R – sequence: 7 fullname: Lukic, S – sequence: 8 fullname: Leonhardt, T – sequence: 9 fullname: Inderbitzin, W – sequence: 10 fullname: Gasparini, F – sequence: 11 fullname: Kuhn, R – sequence: 12 fullname: Hampson, D. R – sequence: 13 fullname: Nicoletti, F – sequence: 14 fullname: Flor, P. J |
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Snippet | Activation of group III metabotropic glutamate receptors (mGluR4, mGluR6, mGluR7, and mGluR8) has been established to be neuroprotective in vitro and in vivo.... Activation of group III metabotropic glutamate receptors (mGluR4, mGluR6, mGluR7, and mGluR8) has been established to be neuroprotective in vitro and in vivo .... |
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SubjectTerms | Aminobutyrates - pharmacology Animals Cells, Cultured Cerebral Cortex - cytology Cerebral Cortex - physiology Excitatory Amino Acid Agonists - pharmacology Glutamic Acid - metabolism Glycine - analogs & derivatives Glycine - pharmacology Heterozygote Mice Mice, Knockout N-Methyl-D-aspartic acid N-Methylaspartate - toxicity Nerve Degeneration - chemically induced Nerve Degeneration - physiopathology Neurons - cytology Neurons - drug effects Neurons - physiology Neuroprotective Agents - pharmacology Neurotoxins - pharmacology Receptors, Metabotropic Glutamate - deficiency Receptors, Metabotropic Glutamate - genetics Receptors, Metabotropic Glutamate - physiology Stereoisomerism |
Title | Selective Activation of mGlu4 Metabotropic Glutamate Receptors Is Protective against Excitotoxic Neuronal Death |
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