Evidence map›Paper›PMID 28539418›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017

Loss of Doc2-Dependent Spontaneous Neurotransmission Augments Glutamatergic Synaptic Strength.

Denise M O Ramirez, Devon C Crawford, Natali L Chanaday, Brent Trauterman, Lisa M Monteggia, Ege T Kavalali

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 29 citations in OpenAlex.

  1. Increased CA3 burst activity inbioRxiv : the preprint server for biology · 2026
    Article
  2. Review
  3. Integrative multi-omics identifiesPsychological medicine · 2026
    Article
  4. Review
  5. Review
  6. Review
  7. Synaptic basis of rapid antidepressant action.European archives of psychiatry and clinical neuroscience · 2025
    Review
  8. Article
  9. Article
  10. Rapid homeostatic plasticity and neuropsychiatric therapeutics.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. VAMP4 Maintains a CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. The Synaptic Vesicle Cycle Revisited: New Insights into the Modes and Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    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

6 authors at 2 institutions in 2 countries.

Denise M O RamirezDepartment of Neurology and Neurotherapeutics.ORCID 0000-0003-4090-033X
Devon C CrawfordDepartment of Neuroscience, and.ORCID 0000-0002-9354-4976
Natali L ChanadayDepartment of Neuroscience, and.ORCID 0000-0002-3376-5187
Brent TrautermanDepartment of Neuroscience, and.
Lisa M MonteggiaDepartment of Neuroscience, and.
Ege T KavalaliDepartment of Neuroscience, and Ege.Kavalali@UTSouthwestern.edu.ORCID 0000-0003-1777-227X
Nanotherapeutics (United States) · USTechnological Educational Institute of Eastern Macedonia and Thrace · GR

Funding

ANTIDEPRESSANTS & INTRACELLULAR SIGNALING LINKED TO BDNFR01MH070727 · NIMH · VANDERBILT UNIVERSITY · PI LISA M MONTEGGIA · 2005 to 2026
$8.9M
Role of SNARE Interactions in Central Synapse FunctionR01MH066198 · NIMH · VANDERBILT UNIVERSITY · PI KAVALALI, EGE T · 2004 to 2023
$7.9M
The role of spontaneous neurotransmission in synaptic plasticity and behaviorF32MH102915 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI CRAWFORD, DEVON C · 2013 to 2016
$161k
NIMH NIH HHS F32 MH102915NIMH NIH HHS R01 MH066198NIMH NIH HHS R01 MH070727
6 · The paper itself

Abstract

Action potential-evoked vesicle fusion comprises the majority of neurotransmission within chemical synapses, but action potential-independent spontaneous neurotransmission also contributes to the collection of signals sent to the postsynaptic cell. Previous work has implicated spontaneous neurotransmission in homeostatic synaptic scaling, but few studies have selectively manipulated spontaneous neurotransmission without substantial changes in evoked neurotransmission to study this function in detail. Here we used a quadruple knockdown strategy to reduce levels of proteins within the soluble calcium-binding double C2 domain (Doc2)-like protein family to selectively reduce spontaneous neurotransmission in cultured mouse and rat neurons. Activity-evoked responses appear normal while both excitatory and inhibitory spontaneous events exhibit reduced frequency. Excitatory miniature postsynaptic currents (mEPSCs), but not miniature inhibitory postsynaptic currents (mIPSCs), increase in amplitude after quadruple knockdown. This increase in synaptic efficacy correlates with reduced phosphorylation levels of eukaryotic elongation factor 2 and also requires the presence of elongation factor 2 kinase. Together, these data suggest that spontaneous neurotransmission independently contributes to the regulation of synaptic efficacy, and action potential-evoked and spontaneous neurotransmission can be segregated at least partially on a molecular level.

Indexed as

Action PotentialsAnimalsCalcium-Binding ProteinsCells, CulturedExcitatory Postsynaptic PotentialsFemaleGlutamic AcidMaleNerve Tissue ProteinsNeurotransmitter AgentsRatsRats, Sprague-DawleySynapsesSynaptic TransmissionCalcium-Binding ProteinsDOC2A protein, humanGlutamic AcidNerve Tissue ProteinsNeurotransmitter AgentsDoc2spontaneous neurotransmitter releasesynaptic scaling

Identifiers

PMID28539418
PMCPMC5490061
OpenAlexW2620051238

What OpenQuestion holds

Textmetadata
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.