ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
SynGAP regulates steady-state and activity-dependent phosphorylation of cofilin.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 130 citations in OpenAlex.
- The Synaptic Clock: SynGAP1 as a Molecular Timer of Postsynaptic Density Consolidation.Biomolecules · 2026Review
- Loss of Necdin causes social deficit and aberrant synaptic function through destabilization of SynGAP.Molecular psychiatry · 2026Article
- AAV delivery of full-length SYNGAP1 rescues epileptic and behavioral phenotypes in a mouse model of SYNGAP1-related disorders.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Developmental and Epileptic Encephalopathy: Pathogenesis of Intellectual Disability Beyond Channelopathies.Biomolecules · 2025Review
- Convergence of autism proteins at the cilium.bioRxiv : the preprint server for biology · 2025Article
- Metabotropic NMDAR Signaling Contributes to Sex Differences in Synaptic Plasticity and Episodic Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Synaptic neoteny of human cortical neurons requires species-specific balancing of SRGAP2-SYNGAP1 cross-inhibition.Neuron · 2024Article
- SYNGAP1 deficiency disrupts synaptic neoteny in xenotransplanted human cortical neurons in vivo.Neuron · 2024Article
- mRNA nuclear retention reduces AMPAR expression and promotes autistic behavior in UBE3A-overexpressing mice.EMBO reports · 2024Article
- Metabotropic NMDA Receptor Signaling Contributes to Sex Differences in Synaptic Plasticity and Episodic Memory.bioRxiv : the preprint server for biology · 2024Article
- Mapping proteomic composition of excitatory postsynaptic sites in the cerebellar cortex.Frontiers in molecular neuroscience · 2024Article
- Non-synaptic function of the autism spectrum disorder-associated gene SYNGAP1 in cortical neurogenesis.Nature neuroscience · 2023Article
- Mouse models ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Mouse models ofbioRxiv : the preprint server for biology · 2023Article
- A perspective on molecular signalling dysfunction, its clinical relevance and therapeutics in autism spectrum disorder.Experimental brain research · 2022Review
- Disrupted Timing of MET Signaling Derails the Developmental Maturation of Cortical Circuits and Leads to Altered Behavior in Mice.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Proteomics and weighted gene correlated network analysis reveal glutamatergic synapse signaling in diazepam treatment of alcohol withdrawal.Frontiers in pharmacology · 2022Article
- SynGAP splice variants display heterogeneous spatio-temporal expression and subcellular distribution in the developing mammalian brain.Journal of neurochemistry · 2020Article
- Interactions between calmodulin and neurogranin govern the dynamics of CaMKII as a leaky integrator.PLoS computational biology · 2020Article
- Article
19 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
SynGAP, a prominent Ras/Rap GTPase-activating protein in the postsynaptic density, regulates the timing of spine formation and trafficking of glutamate receptors in cultured neurons. However, the molecular mechanisms by which it does this are unknown. Here, we show that synGAP is a key regulator of spine morphology in adult mice. Heterozygous deletion of synGAP was sufficient to cause an excess of mushroom spines in adult brains, indicating that synGAP is involved in steady-state regulation of actin in mature spines. Both Ras- and Rac-GTP levels were elevated in forebrains from adult synGAP(+/-) mice. Rac is a well known regulator of actin polymerization and spine morphology. The steady-state level of phosphorylation of cofilin was also elevated in synGAP(+/-) mice. Cofilin, an F-actin severing protein that is inactivated by phosphorylation, is a downstream target of a pathway regulated by Rac. We show that transient regulation of cofilin by treatment with NMDA is also disrupted in synGAP mutant neurons. Treatment of wild-type neurons with 25 mum NMDA triggered transient dephosphorylation and activation of cofilin within 15 s. In contrast, neurons cultured from mice with a homozygous or heterozygous deletion of synGAP lacked the transient regulation by the NMDA receptor. Depression of EPSPs induced by a similar treatment of hippocampal slices with NMDA was disrupted in slices from synGAP(+/-) mice. Our data show that synGAP mediates a rate-limiting step in steady-state regulation of spine morphology and in transient NMDA-receptor-dependent regulation of the spine cytoskeleton.
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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.