ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Extracellular signal-regulated kinase 1/2 is required for the induction of group I metabotropic glutamate receptor-mediated epileptiform discharges.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 55 citations in OpenAlex.
- Female-specific dysfunction of sensory neocortical circuits in a mouse model of autism mediated by mGluR5 and estrogen receptor α.Cell reports · 2024Article
- Group 1 Metabotropic Glutamate Receptors in Neurological and Psychiatric Diseases: Mechanisms and Prospective.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022Review
- Insights on the Functional Interaction between Group 1 Metabotropic Glutamate Receptors (mGluRI) and ErbB Receptors.International journal of molecular sciences · 2020Review
- Lovastatin suppresses hyperexcitability and seizure in Angelman syndrome model.Neurobiology of disease · 2018Article
- miR-217-casein kinase-2 cross talk regulates ERK activation in ganglioglioma.Journal of molecular medicine (Berlin, Germany) · 2017Article
- Effects of pharmacological treatments on hippocampal NCAM1 and ERK2 expression in epileptic rats with cognitive dysfunction.Oncology letters · 2016Article
- APP Causes Hyperexcitability in Fragile X Mice.Frontiers in molecular neuroscience · 2016Article
- Extracellular glutamate exposure facilitates group I mGluR-mediated epileptogenesis in the hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Neuronal BC RNAs cooperate with eIF4B to mediate activity-dependent translational control.The Journal of cell biology · 2014Article
- Biotransformation of a novel positive allosteric modulator of metabotropic glutamate receptor subtype 5 contributes to seizure-like adverse events in rats involving a receptor agonism-dependent mechanism.Drug metabolism and disposition: the biological fate of chemicals · 2013Article
- Unique signaling profiles of positive allosteric modulators of metabotropic glutamate receptor subtype 5 determine differences in in vivo activity.Biological psychiatry · 2013Article
- Persistent receptor activity underlies group I mGluR-mediated cellular plasticity in CA3 neuron.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Lovastatin corrects excess protein synthesis and prevents epileptogenesis in a mouse model of fragile X syndrome.Neuron · 2013Article
- Pathological plasticity in fragile X syndrome.Neural plasticity · 2012Review
- Fragile X syndrome and targeted treatment trials.Results and problems in cell differentiation · 2012Review
- Dual regulation of fragile X mental retardation protein by group I metabotropic glutamate receptors controls translation-dependent epileptogenesis in the hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Regulatory RNAs in brain function and disorders.Brain research · 2010Review
- Cellular plasticity for group I mGluR-mediated epileptogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Dynamic seizure-related changes in extracellular signal-regulated kinase activation in a mouse model of temporal lobe epilepsy.Neuroscience · 2008Article
- mGluR1/5 subtype-specific calcium signalling and induction of long-term potentiation in rat hippocampal oriens/alveus interneurones.The Journal of physiology · 2006Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Transient stimulation of group I metabotropic glutamate receptors (mGluRs) induces persistent prolonged epileptiform discharges in hippocampal slices via a protein synthesis-dependent process. At present, the signaling process underlying the induction of these epileptiform discharges remains unknown. We examined the possible role of extracellular signal-regulated kinases (ERK1 and ERK2) because these kinases can be activated by group I mGluRs, and their activation may regulate gene expression and alter protein synthesis. The group I mGluR agonist (S)-3,5-dihydroxyphenylglycine (DHPG; 50 microm) induced activation of ERK1/2 in hippocampal slices. 2-(2-Diamino-3-methoxyphenyl-4H-1-benzopyran-4-one (PD98059) (50 microm) a specific inhibitor of mitogen-activated protein kinase kinase (MEK), suppressed ERK1/2 activation by DHPG. PD98059 or another MEK inhibitor, 1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio]butadiene (10 microm), also prevented the induction of the prolonged epileptiform discharges by DHPG. In the presence of ionotropic glutamate receptor inhibitors and tetrodotoxin (blockers), DHPG-induced epileptiform discharges were suppressed, whereas ERK1/2 activation persisted. Protein kinase C inhibitors (2-[1-(3-dimethylaminopropyl)-5-methoxyindol-3-yl]-3-(1H-indol-3-yl) maleimide, 1 microm; or chelerythrine, 10 microm) did not prevent the generation of DHPG-induced epileptiform discharges, nor did they suppress the activation of ERK1/2 by DHPG in slices pretreated with the blockers. Genistein (30 microm), a broad-spectrum tyrosine kinase inhibitor, suppressed the DHPG-induced epileptiform discharges and the ERK1/2 activation in the presence of blockers. Induction of DHPG-mediated epileptiform discharges was also suppressed by 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-D]pyrimidine (10 microm), an Src-family tyrosine kinase inhibitor. The study shows that group I mGluRs activate ERK1/2 through a tyrosine kinase-dependent process and that this activation of ERK1/2 is necessary for the induction of prolonged epileptiform discharges in the hippocampus.
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