ArticleNeuron2020
Autism-Associated Shank3 Is Essential for Homeostatic Compensation in Rodent V1.
Article in Neuron, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 132 citations in OpenAlex.
- TNF-dependent regulation of synaptic plasticity and neuronal activity: implications for psychiatric disorders.Molecular psychiatry · 2026Review
- Dysregulated GluA2-Y876 phosphorylation contributes to loss of synaptic upscaling in GRIP1 mutant mice with reduced sociability and increased repetitive behavior.Molecular psychiatry · 2026Article
- Distinct synaptic mechanisms underlie NRXN1 variant and disorder background-dependent phenotypes in iPSC-derived neurons.Cell reports · 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
- A Frank Assessment of SHANK: Impacts of Pathogenic Variations in SHANK3 on Preclinical Models of Phelan McDermid Syndrome.Autism research : official journal of the International Society for Autism Research · 2025Review
- Learning-Associated Flexibility of Cortical Taste Coding Is Impaired in Shank3 Knockout Mice.bioRxiv : the preprint server for biology · 2025Article
- Distinct Synaptic Mechanisms DrivebioRxiv : the preprint server for biology · 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
- ADAR2-mediated Q/R editing of GluA2 in homeostatic synaptic plasticity.Science signaling · 2025Article
- DCC in the cerebral cortex is required for cognitive functions in mouse.Brain pathology (Zurich, Switzerland) · 2025Article
- Modular Arrangement of Synaptic and Intrinsic Homeostatic Plasticity within Visual Cortical Circuits.bioRxiv : the preprint server for biology · 2025Article
- Subjective sleep assessment in individuals withJournal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2024Article
- Therapeutic development approaches to treat haploinsufficiency diseases: restoring protein levels.Drug discovery today · 2024Review
- Degraded tactile coding in the Cntnap2 mouse model of autism.Cell reports · 2024Article
- Axo-axonic synaptic input drives homeostatic plasticity by tuning the axon initial segment structurally and functionally.Science advances · 2024Article
- Linking activity dyshomeostasis and sleep disturbances in Alzheimer disease.Nature reviews. Neuroscience · 2024Review
- Disrupted extracellular matrix and cell cycle genes in autism-associated Shank3 deficiency are targeted by lithium.Molecular psychiatry · 2024Article
- 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
- The Impact of Microglia on Neurodevelopment and Brain Function in Autism.Biomedicines · 2024Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in Shank3 are strongly associated with autism spectrum disorders and neural circuit changes in several brain areas, but the cellular mechanisms that underlie these defects are not understood. Homeostatic forms of plasticity allow central circuits to maintain stable function during experience-dependent development, leading us to ask whether loss of Shank3 might impair homeostatic plasticity and circuit-level compensation to perturbations. We found that Shank3 loss in vitro abolished synaptic scaling and intrinsic homeostatic plasticity, deficits that could be rescued by treatment with lithium. Further, Shank3 knockout severely compromised the in vivo ability of visual cortical circuits to recover from perturbations to sensory drive. Finally, lithium treatment ameliorated a repetitive self-grooming phenotype in Shank3 knockout mice. These findings demonstrate that Shank3 loss severely impairs the ability of central circuits to harness homeostatic mechanisms to compensate for perturbations in drive, which, in turn, may render them more vulnerable to such perturbations.
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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 Socratic graph.