Evidence map›Paper›PMID 25569349›Full record

ArticleNeuron2015

Rapid dispersion of SynGAP from synaptic spines triggers AMPA receptor insertion and spine enlargement during LTP.

Yoichi Araki, Menglong Zeng, Mingjie Zhang, Richard L Huganir

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 papers.

0numbers the graph read from it
0cells of the map it votes in
172citing papers in PubMed
10.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

172 citing papers in PubMed, 280 citations in OpenAlex.

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  10. CDKL5 modulates the plasticity of excitatory synapses via liquid-liquid phase separation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  11. Review
  12. Article
  13. Article
  14. Dynamic extracellular interactions with AMPA receptors.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  15. Review
  16. Article
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  18. Review
  19. Dissociation of SYNGAP1 enzymatic and structural roles: Intrinsic excitability and seizure susceptibility.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  20. Article

112 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Yoichi ArakiDepartment of Neuroscience and Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Menglong ZengDivision of Life Science, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong.
Mingjie ZhangDivision of Life Science, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong.
Richard L HuganirDepartment of Neuroscience and Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Electronic address: rhuganir@jhmi.edu.
Hong Kong University of Science and Technology · HKHoward Hughes Medical Institute · US

Funding

PDZ DOMAINS AND EXCITATORY SYNAPTIC FUNCTIONR01NS036715 · NINDS · JOHNS HOPKINS UNIVERSITY · PI HUGANIR, RICHARD L · 1997 to 2020
$8.6M
Regulation of the NMDA Receptor Signaling ComplexR01MH064856 · NIMH · JOHNS HOPKINS UNIVERSITY · PI HUGANIR, RICHARD L · 2002 to 2011
$3.6M
The Dynamic AMPA Receptor Interactome During Plasticity and LearningR37NS036715 · NINDS · JOHNS HOPKINS UNIVERSITY · PI Richard L Huganir · 2022 to 2026
$3.2M
Howard Hughes Medical InstituteNIMH NIH HHS MH64856NIMH NIH HHS R01 MH064856NINDS NIH HHS NS036715NINDS NIH HHS R01 NS036715NINDS NIH HHS R37 NS036715
6 · The paper itself

Abstract

SynGAP is a Ras-GTPase activating protein highly enriched at excitatory synapses in the brain. Previous studies have shown that CaMKII and the RAS-ERK pathway are critical for several forms of synaptic plasticity including LTP. NMDA receptor-dependent calcium influx has been shown to regulate the RAS-ERK pathway and downstream events that result in AMPA receptor synaptic accumulation, spine enlargement, and synaptic strengthening during LTP. However, the cellular mechanisms whereby calcium influx and CaMKII control Ras activity remain elusive. Using live-imaging techniques, we have found that SynGAP is rapidly dispersed from spines upon LTP induction in hippocampal neurons, and this dispersion depends on phosphorylation of SynGAP by CaMKII. Moreover, the degree of acute dispersion predicts the maintenance of spine enlargement. Thus, the synaptic dispersion of SynGAP by CaMKII phosphorylation during LTP represents a key signaling component that transduces CaMKII activity to small G protein-mediated spine enlargement, AMPA receptor synaptic incorporation, and synaptic potentiation.

Indexed as

AnimalsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Dendritic SpinesGTPase-Activating ProteinsHippocampusLong-Term PotentiationLong-Term Synaptic DepressionMAP Kinase Signaling SystemNeuronal PlasticityNeuronsPhosphorylationras ProteinsRatsReceptors, AMPAReceptors, N-Methyl-D-AspartateCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2GTPase-Activating Proteinsras ProteinsReceptors, AMPAReceptors, N-Methyl-D-AspartateSyngap1 protein, rat

Identifiers

PMID25569349
PMCPMC4428669
OpenAlexW1993505652

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.