ArticleProceedings of the National Academy of Sciences of the United States of America2015
Activity-dependent synaptic GRIP1 accumulation drives synaptic scaling up in response to action potential blockade.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
41 citing papers in PubMed, 59 citations in OpenAlex.
- Dysregulated GluA2-Y876 phosphorylation contributes to loss of synaptic upscaling in GRIP1 mutant mice with reduced sociability and increased repetitive behavior.Molecular psychiatry · 2026Article
- Prolonged visual experience accelerates developmental synaptic downscaling via epigenetic regulation and Rab5c mediated AMPA receptor trafficking.Communications biology · 2026Article
- Convergence and divergence of molecular mechanisms in Hebbian and homeostatic plasticity.Frontiers in synaptic neuroscience · 2026Review
- Activity Deprivation Modulates the Shank3/Homer1/mGluR5 Signaling Pathway to Enable Synaptic Upscaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Modular arrangement of synaptic and intrinsic homeostatic plasticity within visual cortical circuits.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Modular Arrangement of Synaptic and Intrinsic Homeostatic Plasticity within Visual Cortical Circuits.bioRxiv : the preprint server for biology · 2025Article
- Diverging from the Norm: Reevaluating What Miniature Excitatory Postsynaptic Currents Tell Us about Homeostatic Synaptic Plasticity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- Age-related dysregulation of homeostatic control in neuronal microcircuits.Nature neuroscience · 2023Article
- Inactivity and CaScientific reports · 2022Article
- A bidirectional switch in the Shank3 phosphorylation state biases synapses toward up- or downscaling.eLife · 2022Article
- Developmental Regulation of Homeostatic Plasticity in Mouse Primary Visual Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Homeostatic synaptic scaling establishes the specificity of an associative memory.Current biology : CB · 2021Article
- EphrinB2 and GRIP1 stabilize mushroom spines during denervation-induced homeostatic plasticity.Cell reports · 2021Article
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- Tight Regulation of Major Histocompatibility Complex I for the Spatial and Temporal Expression in the Hippocampal Neurons.Frontiers in cellular neuroscience · 2021Review
- GRIP1 regulates synaptic plasticity and learning and memory.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
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- Tyrosine phosphorylation of the AMPA receptor subunit GluA2 gates homeostatic synaptic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- AMPA receptors and their minions: auxiliary proteins in AMPA receptor trafficking.Cellular and molecular life sciences : CMLS · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Synaptic scaling is a form of homeostatic plasticity that stabilizes neuronal firing in response to changes in synapse number and strength. Scaling up in response to action-potential blockade is accomplished through increased synaptic accumulation of GluA2-containing AMPA receptors (AMPAR), but the receptor trafficking steps that drive this process remain largely obscure. Here, we show that the AMPAR-binding protein glutamate receptor-interacting protein-1 (GRIP1) is essential for regulated synaptic AMPAR accumulation during scaling up. Synaptic abundance of GRIP1 was enhanced by activity deprivation, directly increasing synaptic GRIP1 abundance through overexpression increased the amplitude of AMPA miniature excitatory postsynaptic currents (mEPSCs), and shRNA-mediated GRIP1 knockdown prevented scaling up of AMPA mEPSCs. Furthermore, knockdown and replace experiments targeting either GRIP1 or GluA2 revealed that scaling up requires the interaction between GRIP1 and GluA2. Finally, GRIP1 synaptic accumulation during scaling up did not require GluA2 binding. Taken together, our data support a model in which activity-dependent trafficking of GRIP1 to synaptic sites drives the forward trafficking and enhanced synaptic accumulation of GluA2-containing AMPAR during synaptic scaling up.
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Registered trials
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.