Evidence map›Paper›PMID 28658618›Full record

ArticleCell reports2017

A Presynaptic Glutamate Receptor Subunit Confers Robustness to Neurotransmission and Homeostatic Potentiation.

Beril Kiragasi, Joyce Wondolowski, Yan Li, Dion K Dickman

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
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  5. Nonionic signaling rapidly remodels postsynaptic DLG to induce retrograde homeostatic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  15. Physiologic and Nanoscale Distinctions Define Glutamatergic Synapses in Tonic vs Phasic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
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  16. Article
  17. Article
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  19. Dlg Is Required for Short-Term Memory and Interacts with NMDAR in theInternational journal of molecular sciences · 2022
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  20. Review
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 1 country.

Beril KiragasiDepartment of Neurobiology, University of Southern California, Los Angeles, CA 90089, USA; USC Neuroscience Graduate Program, University of Southern California, Los Angeles, CA 90089, USA.
Joyce WondolowskiDepartment of Neurobiology, University of Southern California, Los Angeles, CA 90089, USA.
Yan LiSection on Neuronal Connectivity, Laboratory of Gene Regulation and Development, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.
Dion K DickmanDepartment of Neurobiology, University of Southern California, Los Angeles, CA 90089, USA. Electronic address: dickman@usc.edu.
University of Southern California · USEunice Kennedy Shriver National Institute of Child Health and Human Development · US

Funding

Molecular Mechanisms Governing the Homeostatic Control of Synaptic StrengthR01NS091546 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI DICKMAN, DION KAI · 2015 to 2024
$4.3M
NINDS NIH HHS R01 NS091546
6 · The paper itself

Abstract

Homeostatic signaling systems are thought to interface with other forms of plasticity to ensure flexible yet stable levels of neurotransmission. The role of neurotransmitter receptors in this process, beyond mediating neurotransmission itself, is not known. Through a forward genetic screen, we have identified the Drosophila kainate-type ionotropic glutamate receptor subunit DKaiR1D to be required for the retrograde, homeostatic potentiation of synaptic strength. DKaiR1D is necessary in presynaptic motor neurons, localized near active zones, and confers robustness to the calcium sensitivity of baseline synaptic transmission. Acute pharmacological blockade of DKaiR1D disrupts homeostatic plasticity, indicating that this receptor is required for the expression of this process, distinct from developmental roles. Finally, we demonstrate that calcium permeability through DKaiR1D is necessary for baseline synaptic transmission, but not for homeostatic signaling. We propose that DKaiR1D is a glutamate autoreceptor that promotes robustness to synaptic strength and plasticity with active zone specificity.

Indexed as

AnimalsGlutamic AcidHomeostasisHumansMiceReceptors, PresynapticSynaptic TransmissionGlutamic AcidReceptors, PresynapticautoreceptorDrosophilaglutamate receptorkainate receptorneuromuscular junctionsynaptic homeostasis

Identifiers

PMID28658618
PMCPMC5538789
OpenAlexW2729861849

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.