ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Dual regulation of fragile X mental retardation protein by group I metabotropic glutamate receptors controls translation-dependent epileptogenesis in the hippocampus.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- DJ-1-mediated repression of the RNA-binding protein FMRP is predicted to impact known Alzheimer's disease-related protein networks.Journal of Alzheimer's disease : JAD · 2024Article
- FMRP phosphorylation and interactions with Cdh1 regulate association with dendritic RNA granules and MEF2-triggered synapse elimination.Neurobiology of disease · 2023Article
- Group 1 Metabotropic Glutamate Receptors in Neurological and Psychiatric Diseases: Mechanisms and Prospective.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022Review
- Hyperexcitability and Homeostasis in Fragile X Syndrome.Frontiers in molecular neuroscience · 2021Article
- mGluR5 Negative Modulators for Fragile X: Treatment Resistance and Persistence.Frontiers in psychiatry · 2021Article
- Physiology and Therapeutic Potential of SK, H, and M Medium AfterHyperPolarization Ion Channels.Frontiers in molecular neuroscience · 2021Review
- Post-translational modifications of the Fragile X Mental Retardation Protein in neuronal function and dysfunction.Molecular psychiatry · 2020Review
- Early-Onset Network Hyperexcitability in Presymptomatic Alzheimer's Disease Transgenic Mice Is Suppressed by Passive Immunization with Anti-Human APP/Aβ Antibody and by mGluR5 Blockade.Frontiers in aging neuroscience · 2017Article
- Article
- APP Causes Hyperexcitability in Fragile X Mice.Frontiers in molecular neuroscience · 2016Article
- A 3' untranslated region variant in FMR1 eliminates neuronal activity-dependent translation of FMRP by disrupting binding of the RNA-binding protein HuR.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Review
- The role of autophagy in epileptogenesis and in epilepsy-induced neuronal alterations.Journal of neural transmission (Vienna, Austria : 1996) · 2015Review
- Coordination between Translation and Degradation Regulates Inducibility of mGluR-LTD.Cell reports · 2015Article
- Homer protein-metabotropic glutamate receptor binding regulates endocannabinoid signaling and affects hyperexcitability in a mouse model of fragile X syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- 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
- Article
- 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
- Dephosphorylation-induced ubiquitination and degradation of FMRP in dendrites: a role in immediate early mGluR-stimulated translation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- The pathophysiology of fragile X (and what it teaches us about synapses).Annual review of neuroscience · 2012Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Group I metabotropic glutamate receptors (mGluRs) stimulation activates translation-dependent epileptogenesis in the hippocampus. This translation is regulated by repressors, including BC1 RNA and fragile X mental retardation protein (FMRP). Recent data indicate that group I mGluR stimulation exerts bidirectional control over FMRP level by activating translation and ubiquitin-proteasome system (UPS)-dependent proteolysis for the up- and downregulation of the protein, respectively. At present, the temporal relationship of translation and proteolysis on FMRP and their interplay for group I mGluR-mediated translation and epileptogenesis are unknown. We addressed these issues by using mouse hippocampal slices. Agonist [(S)-3,5-dihydroxyphenylglycine (DHPG)] stimulation of group I mGluRs caused a biphasic change in FMRP level. An initial decrease (within 10 min) was followed by an increase at 30 min. When slices were pretreated with translation inhibitor (anisomycin or cycloheximide), group I mGluRs elicited a sustained decrease in FMRP. This decrease was prevented by a proteasome inhibitor [Z-Leu-Leu-Leu-CHO (MG-132)]. When slices were pretreated with MG-132 alone, DHPG no longer elicited any change in FMRP. MG-132 also suppressed increase in other proteins, including postsynaptic density-95 and α-calcium/calmodulin-dependent protein kinase II, normally elicited by group I mGluR stimulation. Physiological experiments showed that proteasome inhibitor suppressed group I mGluR-induced prolonged synchronized discharges. However, proteasome inhibitor did not affect group I mGluR-induced prolonged synchronized discharges in Fmr1(-/-) preparations, where functional FMRP is absent. The results suggest that constitutive FMRP in hippocampal cells acts as a brake on group I mGluR-mediated translation and epileptogenesis. FMRP downregulation via UPS removes this brake enabling group I mGluR-mediated translation and epileptogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.