Evidence map›Paper›PMID 29742428›Full record

ArticleCell reports2018

A Glutamate Homeostat Controls the Presynaptic Inhibition of Neurotransmitter Release.

Xiling Li, Pragya Goel, Joyce Wondolowski, Jeremy Paluch, Dion Dickman

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Article
  3. CaeLife · 2024
    Article
  4. Article
  5. CabioRxiv : the preprint server for biology · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. 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
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Activity-Dependent Global Downscaling of Evoked Neurotransmitter Release across Glutamatergic Inputs inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  17. Developmental arrest ofDevelopment (Cambridge, England) · 2020
    Article
  18. Article
  19. Review
  20. Rapid and sustained homeostatic control of presynaptic exocytosis at a central synapse.Proceedings of the National Academy of Sciences of the United States of America · 2019
    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 1 institution in 1 country.

Xiling LiDepartment of Neurobiology, University of Southern California, Los Angeles, CA; USC Neuroscience Graduate Program, University of Southern California, Los Angeles, CA.
Pragya GoelDepartment of Neurobiology, University of Southern California, Los Angeles, CA; USC Graduate Program in Molecular and Computational Biology, University of Southern California, Los Angeles, CA.
Joyce WondolowskiDepartment of Neurobiology, University of Southern California, Los Angeles, CA.
Jeremy PaluchDepartment of Neurobiology, University of Southern California, Los Angeles, CA.
Dion DickmanDepartment of Neurobiology, University of Southern California, Los Angeles, CA. Electronic address: dickman@usc.edu.
University of Southern California · 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

We have interrogated the synaptic dialog that enables the bi-directional, homeostatic control of presynaptic efficacy at the glutamatergic Drosophila neuromuscular junction (NMJ). We find that homeostatic depression and potentiation use disparate genetic, induction, and expression mechanisms. Specifically, homeostatic potentiation is achieved through reduced CaMKII activity postsynaptically and increased abundance of active zone material presynaptically at one of the two neuronal subtypes innervating the NMJ, while homeostatic depression occurs without alterations in CaMKII activity and is expressed at both neuronal subtypes. Furthermore, homeostatic depression is only induced through excess presynaptic glutamate release and operates with disregard to the postsynaptic response. We propose that two independent homeostats modulate presynaptic efficacy at the Drosophila NMJ: one is an intercellular signaling system that potentiates synaptic strength following diminished postsynaptic excitability, while the other adaptively modulates presynaptic glutamate release through an autocrine mechanism without feedback from the postsynaptic compartment.

Indexed as

HomeostasisAnimalsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium ChannelsDrosophila melanogasterDrosophila ProteinsGlutamic AcidLong-Term PotentiationMutationNeural InhibitionNeuromuscular JunctionNeurotransmitter AgentsPresynaptic TerminalsReceptors, GlutamateSynaptic VesiclesBRP protein, DrosophilaCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium ChannelsDrosophila ProteinsGlutamic AcidNeurotransmitter AgentsReceptors, GlutamateDrosophila neuromuscular junctionglutamate homeostasishomeostatic synaptic plasticitysynaptic depression

Identifiers

PMID29742428
PMCPMC5973541
OpenAlexW2802878745

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.