Evidence map›Paper›PMID 29748610›Full record

ArticleNature communications2018

Distinct homeostatic modulations stabilize reduced postsynaptic receptivity in response to presynaptic DLK signaling.

Pragya Goel, Dion Dickman

Abstract read
In one paragraph

Article in Nature communications, 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
–field-weighted citation impact
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.

  1. Glutamate receptor composition atbioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. 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
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Muscle-fiber specific genetic manipulation ofFrontiers in physiology · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Developmental arrest ofDevelopment (Cambridge, England) · 2020
    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

2 authors.

Pragya GoelDepartment of Neurobiology, University of Southern California, Los Angeles, CA, 90089, USA.ORCID http://orcid.org/0000-0002-6348-4909
Dion DickmanDepartment of Neurobiology, University of Southern California, Los Angeles, CA, 90089, USA. dickman@usc.edu.ORCID http://orcid.org/0000-0003-1884-284X

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Molecular Mechanisms Governing the Homeostatic Control of Synaptic StrengthR01NS091546 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI DICKMAN, DION KAI · 2015 to 2024
$4.3M
NIH HHS P40 OD018537NINDS NIH HHS R01 NS091546
6 · The paper itself

Abstract

Synapses are constructed with the stability to last a lifetime, yet sufficiently flexible to adapt during injury. Although fundamental pathways that mediate intrinsic responses to neuronal injury have been defined, less is known about how synaptic partners adapt. We have investigated responses in the postsynaptic cell to presynaptic activation of the injury-related Dual Leucine Zipper Kinase pathway at the Drosophila neuromuscular junction. We find that the postsynaptic compartment reduces neurotransmitter receptor levels, thus depressing synaptic strength. Interestingly, this diminished state is stabilized through distinct modulations to two postsynaptic homeostatic signaling systems. First, a retrograde response normally triggered by reduced receptor levels is silenced, preventing a compensatory enhancement in presynaptic neurotransmitter release. However, when global presynaptic release is attenuated, a postsynaptic receptor scaling mechanism persists to adaptively stabilize this diminished neurotransmission state. Thus, the homeostatic set point of synaptic strength is recalibrated to a reduced state as synapses acclimate to injury.

Indexed as

AnimalsAnimals, Genetically ModifiedDrosophilaDrosophila ProteinsMAP Kinase Kinase KinasesNeuromuscular JunctionNeuronal PlasticityNeuronsNeurotransmitter AgentsPresynaptic TerminalsReceptors, GlutamateSignal TransductionSynaptic PotentialsDrosophila ProteinsMAP Kinase Kinase Kinasesmitogen-activated protein kinase kinase kinase 12Neurotransmitter AgentsReceptors, Glutamatewnd protein, Drosophila

Identifiers

PMID29748610
PMCPMC5945772

What OpenQuestion holds

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Registered trials

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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.