Disruption of Arp2/3 Results in Asymmetric Structural Plasticity of Dendritic Spines and Progressive Synaptic and Behavioral Abnormalities
Open accessAbstract
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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Actin cytoskeletal dynamics have a key role in the establishment and maintenance of dendritic arborizations and spines, and are critical for structural alterations in spine shape important for cellular forms of synaptic plasticity such as long-term potentiation and long-term depression.
“Actin cytoskeletal dynamics have a key role in the establishment and maintenance of both dendritic arborizations and spines, and are also critical for the structural alterations in spine shape important for cellular forms of synaptic plasticity, such as long-term potentiation and long-term depression.20, 21, 22, 23”
From The autism and schizophrenia associated gene CYFIP1 is critical for the maintenance of dendritic complexity and the stabilization of mature spines (2014) · cites this paper as [23]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredAlterations in the regulation of actin at dendritic spines by neurodevelopmental disease-associated proteins such as DISC1, DTNBP1, SHANK3, PAK3, Oligophrenin and SRGAP2 produce deficits in synaptic plasticity and in the formation and consolidation of long-term memories.
“Moreover, alterations in the regulation of actin at dendritic spines, by neurodevelopmental disease-associated proteins such as DISC1, DTNBP1, SHANK3, PAK3, Oligophrenin and SRGAP2, have been shown to produce deficits in both synaptic plasticity and the formation and consolidation of long-term memories.23, 24, 25, 26, 27, 28, 29”
From The autism and schizophrenia associated gene CYFIP1 is critical for the maintenance of dendritic complexity and the stabilization of mature spines (2014) · cites this paper as [23]
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- Authors
- Kim, I. H., Racz, B., Wang, H., Burianek, L., Weinberg, R., Yasuda, R., Wetsel, W. C., & Soderling, S. H.
- Affiliations
- Howard Hughes Medical Institute (US)
- University of North Carolina at Chapel Hill (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2013-04-03
- Volume
- 33
- Issue
- 14
- Pages
- 6081-6092
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3656411
- OpenAlex
- W2147602589
- Cited by
- 172
- References
- 16
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 10 · 2023: 8 · 2022: 11 · 2021: 11 · 2020: 8 · 2019: 19 · 2018: 11 · 2017: 15 · 2016: 25 · 2015: 17 · 2014: 16 · 2013: 5
- FWCI
- 10.29
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Repository of the Academy's Library (Library of the Hungarian Academy of Sciences) (acceptedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- UNC Libraries
- Funders
- Howard Hughes Medical Institute
- March of Dimes Foundation
- North Carolina Biotechnology Center
- Hungarian Scientific Research Fund (K83830)
- Magyar Tudományos Akadémia
- National Institutes of Health (NS059957)
- National Institute of Mental Health (U19MH082441, MH082441)
- National Institute on Drug Abuse (R01DA027807)
- National Institute of General Medical Sciences (T32GM007184)
- National Institute of Neurological Disorders and Stroke (R01NS059957, R01NS068410, R01NS035527)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- Arp2/3 complex, ARPC3, dendritic spines, actin polymerization, synaptic plasticity, conditional knockout, synaptic loss, mental illness, cognitive impairment, social behavior
- MeSH terms
- Potassium Channels, Sodium-Activated, Actins, Animals, Animals, Newborn, Bacterial Proteins, Mental Disorders, Disease Models, Animal, Embryo, Mammalian, Exploratory Behavior, Hippocampus, Luminescent Proteins, Memory, Mice, Transgenic, Neuronal Plasticity, Neurons, Proteins, Social Behavior, Reflex, Startle, Synapses, Time Factors, Potassium Channels, Signal Transduction, Receptors, Glutamate, Gene Expression Regulation, Developmental, Maze Learning, RNA, Untranslated, Photobleaching, Dendritic Spines, Green Fluorescent Proteins, Actin-Related Protein 2-3 Complex, Mice, Calcium-Calmodulin-Dependent Protein Kinase Kinase
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