Evidence map›Paper›PMID 23719165›Full record

ArticleNeuron2013

Homeostatic control of synaptic transmission by distinct glutamate receptors.

Dan Yan, Miwako Yamasaki, Christoph Straub, Masahiko Watanabe, Susumu Tomita

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  5. Translational medicine of the glutamate AMPA receptor.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2021
    Review
  6. Article
  7. Review
  8. Article
  9. UNC-18 and Tomosyn Antagonistically Control Synaptic Vesicle Priming Downstream of UNC-13 inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  10. Article
  11. Article
  12. Article
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  15. Relative contribution of TARPs γ-2 and γ-7 to cerebellar excitatory synaptic transmission and motor behavior.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  16. Article
  17. Article
  18. 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

5 authors at 2 institutions in 2 countries.

Dan YanProgram in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06520, USA.
Miwako Yamasaki
Christoph Straub
Masahiko Watanabe
Susumu Tomita
Yale University · USHokkaido University · JP

Funding

Regulation of glutamate receptors by calcium-dependent protein kinasesR01MH077939 · NIMH · YALE UNIVERSITY · PI TOMITA, SUSUMU · 2008 to 2023
$5.2M
Mechanism for Regulating Kainate-Type Glutamate Receptor ActivityR01MH085080 · NIMH · YALE UNIVERSITY · PI TOMITA, SUSUMU · 2010 to 2014
$2.0M
Regulation of glutamate receptors by calcium-dependent protein kinaseR56MH077939 · NIMH · YALE UNIVERSITY · PI TOMITA, SUSUMU · 2013 to 2014
$833k
NIMH NIH HHS MH077939NIMH NIH HHS MH085080NIMH NIH HHS R01 MH077939NIMH NIH HHS R01 MH085080NIMH NIH HHS R56 MH077939
6 · The paper itself

Abstract

Glutamate is the most abundant excitatory neurotransmitter in the brain, and distinct classes of glutamate receptors coordinate synaptic transmission and spike generation upon various levels of neuronal activity. However, the mechanisms remain unclear. Here, we found that loss of synaptic AMPA receptors increased kainate receptor activity in cerebellar granule cells without changing NMDA receptors. The augmentation of kainate receptor-mediated currents in the absence of AMPA receptor activity is required for spike generation and is mediated by the increased expression of the GluK5 high-affinity kainate receptor subunit. Increase in GluK5 expression is sufficient to enhance kainate receptor activity by modulating receptor channel properties, but not localization. Furthermore, we demonstrate that the combined loss of the AMPA receptor auxiliary TARPγ-2 subunit and the GluK5 subunit leads to early mouse lethality. Our findings reveal mechanisms mediated by distinct classes of postsynaptic glutamate receptors for the homeostatic maintenance of the neuronal activity.

Indexed as

Adaptation, PhysiologicalAnimalsCerebellumEvoked PotentialsFemaleIn Vitro TechniquesKainic Acid ReceptorsMaleMiceMice, Mutant StrainsReceptor Cross-TalkReceptors, AMPAReceptors, GlutamateReceptors, N-Methyl-D-AspartateSignal TransductionSynaptic PotentialsKainic Acid ReceptorsReceptors, AMPAReceptors, GlutamateReceptors, N-Methyl-D-Aspartate

Identifiers

PMID23719165
PMCPMC3668311
OpenAlexW1994279153

What OpenQuestion holds

Textmetadata
LicenceTDM
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.