Evidence map›Paper›PMID 24391850›Full record

ArticlePloS one2013

SynGAP regulates protein synthesis and homeostatic synaptic plasticity in developing cortical networks.

Chih-Chieh Wang, Richard G Held, Benjamin J Hall

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. SYNGAP-1 Mutation And Catatonia: A Case Series and Systematic Review.Journal of child and adolescent psychopharmacology · 2024
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. eNeuro · 2025
    Article
  9. Article
  10. Epigenetic regulation ofFrontiers in psychiatry · 2025
    Article
  11. Subjective sleep assessment in individuals withJournal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2024
    Article
  12. Review
  13. Article
  14. eNeuro · 2023
    Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. EndogenouseLife · 2022
    Article
  20. Article
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

3 authors at 1 institution in 1 country.

Chih-Chieh WangNeuroscience Program, School of Science and Engineering, Tulane University, New Orleans, Louisiana, United States of America.
Richard G HeldDepartment of Cell and Molecular Biology, School of Science and Engineering, Tulane University, New Orleans, Louisiana, United States of America.
Benjamin J HallNeuroscience Program, School of Science and Engineering, Tulane University, New Orleans, Louisiana, United States of America ; Department of Cell and Molecular Biology, School of Science and Engineering, Tulane University, New Orleans, Louisiana, United States of America.
Tulane University · US

Funding

Regulation of Protein Translation and Depression by Cortical NMDA Receptors.R01MH099378 · NIMH · TULANE UNIVERSITY OF LOUISIANA · PI TASKER, JEFFREY G · 2013 to 2014
$549k
Localized immobilization of ephrin-B2 for neurite guidance in 3D cultureR21NS065374 · NINDS · TULANE UNIVERSITY OF LOUISIANA · PI MOORE, MICHAEL J · 2009 to 2010
$328k
NIMH NIH HHS MH099378-01NIMH NIH HHS R01 MH099378NINDS NIH HHS NS065374NINDS NIH HHS R21 NS065374
6 · The paper itself

Abstract

Disrupting the balance between excitatory and inhibitory neurotransmission in the developing brain has been causally linked with intellectual disability (ID) and autism spectrum disorders (ASD). Excitatory synapse strength is regulated in the central nervous system by controlling the number of postsynaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs). De novo genetic mutations of the synaptic GTPase-activating protein (SynGAP) are associated with ID and ASD. SynGAP is enriched at excitatory synapses and genetic suppression of SynGAP increases excitatory synaptic strength. However, exactly how SynGAP acts to maintain synaptic AMPAR content is unclear. We show here that SynGAP limits excitatory synaptic strength, in part, by suppressing protein synthesis in cortical neurons. The data presented here from in vitro, rat and mouse cortical networks, demonstrate that regulation of translation by SynGAP involves ERK, mTOR, and the small GTP-binding protein Rheb. Furthermore, these data show that GluN2B-containing NMDARs and the cognitive kinase CaMKII act upstream of SynGAP and that this signaling cascade is required for proper translation-dependent homeostatic synaptic plasticity of excitatory synapses in developing cortical networks.

Indexed as

Protein BiosynthesisAnimalsCells, CulturedCerebral CortexElectrophysiologyEmbryo, MammalianFemaleGTPase-Activating ProteinsHomeostasisImmunoenzyme TechniquesMaleMiceNerve NetNeuronal PlasticityNeuronsras GTPase-Activating ProteinsGTPase-Activating Proteinsras GTPase-Activating ProteinsSyngap1 protein, mouseSyngap1 protein, ratTOR Serine-Threonine Kinases

Identifiers

PMID24391850
PMCPMC3877118
OpenAlexW2052008579

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.