ArticleNature communications2015
MicroRNA miR124 is required for the expression of homeostatic synaptic plasticity.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed.
- Article
- Dynamic Changes in Serum Biochemical Indices and Alternative Splicing Events Revealed Molecular Regulatory Mechanisms in Rainbow Trout Under Copper Stress.Marine biotechnology (New York, N.Y.) · 2026Article
- Prolonged visual experience accelerates developmental synaptic downscaling via epigenetic regulation and Rab5c mediated AMPA receptor trafficking.Communications biology · 2026Article
- Molecular Interplay Between COVID-19 and Stroke: Experimental Insights Into MicroRNA-Regulated Neuroinflammation.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2026Article
- Combination of Cas9 and adeno-associated vectors enables efficient in vivo knockdown of precise miRNAs in the rodent and primate brain.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Repeated Clozapine Administration Causes Extensive Changes to the Expression of Coding and Non-coding RNAs, Including miR-124, in the Mouse Frontal Cortex.Molecular neurobiology · 2025Article
- MicroRNAs in the biology and hallmarks of neurodegenerative diseases.Trends in molecular medicine · 2025Review
- ADAR2-mediated Q/R editing of GluA2 in homeostatic synaptic plasticity.Science signaling · 2025Article
- microRNA-218-5p coordinates scaling of excitatory and inhibitory synapses during homeostatic synaptic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- ZNF787 and HDAC1 Mediate Blood-Brain Barrier Permeability in an In Vitro Model of Alzheimer's Disease Microenvironment.Neurotoxicity research · 2024Article
- Polyphenols Modulate the miRNAs Expression that Involved in Glioblastoma.Mini reviews in medicinal chemistry · 2024Review
- microRNA-124 directly suppresses Nodal and Notch to regulate mesodermal development.Developmental biology · 2023Article
- An insight into the sprawling microverse of microRNAs in depression pathophysiology and treatment response.Neuroscience and biobehavioral reviews · 2023Review
- Article
- Investigation of the Protective Effect of Extracellular Vesicle miR-124 on Retinal Ganglion Cells Using a Photolabile Paper-Based Chip.Investigative ophthalmology & visual science · 2023Article
- Optimized miR-124 reporters uncover differences in miR-124 expression among neuronal populationsFrontiers in neuroscience · 2023Article
- Review
- The Role of Dendritic Cells in the Host Response to Marek's Disease Virus (MDV) as Shown by Transcriptomic Analysis of Susceptible and Resistant Birds.Pathogens (Basel, Switzerland) · 2022Article
- Development of microglia-targeting adeno-associated viral vectors as tools to study microglial behavior in vivo.Communications biology · 2022Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors.
Funding
Abstract
Homeostatic synaptic plasticity is a compensatory response to alterations in neuronal activity. Chronic deprivation of neuronal activity results in an increase in synaptic AMPA receptors (AMPARs) and postsynaptic currents. The biogenesis of GluA2-lacking, calcium-permeable AMPARs (CP-AMPARs) plays a crucial role in the homeostatic response; however, the mechanisms leading to CP-AMPAR formation remain unclear. Here we show that the microRNA, miR124, is required for the generation of CP-AMPARs and homeostatic plasticity. miR124 suppresses GluA2 expression via targeting its 3'-UTR, leading to the formation of CP-AMPARs. Blockade of miR124 function abolishes the homeostatic response, whereas miR124 overexpression leads to earlier induction of homeostatic plasticity. miR124 transcription is controlled by an inhibitory transcription factor EVI1, acting by association with the deacetylase HDAC1. Our data support a cellular cascade in which inactivity relieves EVI1/HDAC-mediated inhibition of miR124 gene transcription, resulting in enhanced miR124 expression, formation of CP-AMPARs and subsequent induction of homeostatic synaptic plasticity.
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