ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Disruption of Arp2/3 results in asymmetric structural plasticity of dendritic spines and progressive synaptic and behavioral abnormalities.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
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Who cites it
101 citing papers in PubMed, 181 citations in OpenAlex.
- Alterations of actin in aging.Journal of cell science · 2026Review
- The Arp2/3 complex is required for in situ haptotactic response of microglia to iC3b.EMBO reports · 2026Article
- Novel epigenetic loci identified from an epigenome-wide association study underlying brain structural changes in bipolar disorder.Psychological medicine · 2026Article
- ARP2/3 complex mediates the neuropathology of PTEN-deficient human neural cells downstream of mTORC1 and mTORC2 hyperactivation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Rules of life at the interface of calcium signaling and mechanobiology.APL bioengineering · 2025Review
- S-ketamine exposure in early postnatal period induces social deficit mediated by excessive microglial synaptic pruning.Molecular psychiatry · 2025Article
- Cytoskeletal Proteins and Alzheimer's Disease Pathogenesis: Focusing on the Interplay with Tau Pathology.Biomolecules · 2025Review
- The Arp2/3 complex is required forbioRxiv : the preprint server for biology · 2025Article
- CellPHIE: Integrating Pathway Discovery With Pooled Profiling of Perturbations Uncovers Pathways of Huntington's Disease, Including Genetic Modifiers of Neuronal Development and Morphology.bioRxiv : the preprint server for biology · 2025Article
- Targeted Regulation of HSP70 by the ARP2/3 Complex in Mammary Epithelial Cells and Its Impact on Host Cell Apoptosis.Biomolecules · 2025Article
- BDNF-dependent nano-organization of Neogenin and the WAVE regulatory complex promotes actin remodeling in dendritic spines.iScience · 2024Article
- Pharmacological modulation of developmental and synaptic phenotypes in human SHANK3 deficient stem cell-derived neuronal models.Translational psychiatry · 2024Article
- Stem cell migration drives lung repair in living mice.Developmental cell · 2024Article
- Biophysical Modeling of Actin-Mediated Structural Plasticity Reveals Mechanical Adaptation in Dendritic Spines.eNeuro · 2024Article
- Overlap in synaptic neurological condition susceptibility pathways and the neural pannexin 1 interactome revealed by bioinformatics analyses.Channels (Austin, Tex.) · 2023Article
- Dual Regulation of Spine-Specific and Synapse-to-Nucleus Signaling by PKCδ during Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- EVL and MIM/MTSS1 regulate actin cytoskeletal remodeling to promote dendritic filopodia in neurons.The Journal of cell biology · 2023Article
- The WAVE complex drives the morphogenesis of the photoreceptor outer segment cilium.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- NCK1 Modulates Neuronal Actin Dynamics and Promotes Dendritic Spine, Synapse, and Memory Formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- c-Abl kinase at the crossroads of healthy synaptic remodeling and synaptic dysfunction in neurodegenerative diseases.Neural regeneration research · 2023Review
41 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
Abstract
Despite evidence for a strong genetic contribution to several major psychiatric disorders, individual candidate genes account for only a small fraction of these disorders, leading to the suggestion that multigenetic pathways may be involved. Several known genetic risk factors for psychiatric disease are related to the regulation of actin polymerization, which plays a key role in synaptic plasticity. To gain insight into and test the possible pathogenetic role of this pathway, we designed a conditional knock-out of the Arp2/3 complex, a conserved final output for actin signaling pathways that orchestrates de novo actin polymerization. Here we report that postnatal loss of the Arp2/3 subunit ArpC3 in forebrain excitatory neurons leads to an asymmetric structural plasticity of dendritic spines, followed by a progressive loss of spine synapses. This progression of synaptic deficits corresponds with an evolution of distinct cognitive, psychomotor, and social disturbances as the mice age. Together, these results point to the dysfunction of actin signaling, specifically that which converges to regulate Arp2/3, as an important cellular pathway that may contribute to the etiology of complex psychiatric disorders.
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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.