Evidence map›Paper›PMID 28186166›Full record

ArticleNature communications2017

Selective molecular impairment of spontaneous neurotransmission modulates synaptic efficacy.

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

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.0field-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

37 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. The hippocampus as a central hub in ketamine's antidepressant action: from molecules to circuit rewiring.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Review
  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. Ketamine induced synaptic plasticity operates independently of long-term potentiation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Rapid homeostatic plasticity and neuropsychiatric therapeutics.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Review
  16. Article
  17. Spontaneously Recycling Synaptic Vesicles Constitute Readily Releasable Vesicles in Intact Neuromuscular Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  18. Review
  19. Review
  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

5 authors at 1 institution in 1 country.

Devon C CrawfordDepartment of Neuroscience, UT Southwestern Medical Center, Dallas, Texas 75390, USA.ORCID 0000-0002-9354-4976
Denise M O RamirezWhole Brain Microscopy Facility, Department of Neurology and Neurotherapeutics, UT Southwestern Medical Center, Dallas, Texas 75390, USA.
Brent TrautermanDepartment of Neuroscience, UT Southwestern Medical Center, Dallas, Texas 75390, USA.
Lisa M MonteggiaDepartment of Neuroscience, UT Southwestern Medical Center, Dallas, Texas 75390, USA.
Ege T KavalaliDepartment of Neuroscience, UT Southwestern Medical Center, Dallas, Texas 75390, USA.
Southwestern Medical Center · US

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

Recent studies suggest that stimulus-evoked and spontaneous neurotransmitter release processes are mechanistically distinct. Here we targeted the non-canonical synaptic vesicle SNAREs Vps10p-tail-interactor-1a (vti1a) and vesicle-associated membrane protein 7 (VAMP7) to specifically inhibit spontaneous release events and probe whether these events signal independently of evoked release to the postsynaptic neuron. We found that loss of vti1a and VAMP7 impairs spontaneous high-frequency glutamate release and augments unitary event amplitudes by reducing postsynaptic eukaryotic elongation factor 2 kinase (eEF2K) activity subsequent to the reduction in N-methyl-D-aspartate receptor (NMDAR) activity. Presynaptic, but not postsynaptic, loss of vti1a and VAMP7 occludes NMDAR antagonist-induced synaptic potentiation in an intact circuit, confirming the role of these vesicular SNAREs in setting synaptic strength. Collectively, these results demonstrate that spontaneous neurotransmission signals independently of stimulus-evoked release and highlight its role as a key regulator of postsynaptic efficacy.

Indexed as

AnimalsCells, CulturedElongation Factor 2 KinaseFemaleGlutamic AcidMaleMice, KnockoutNeuronsQb-SNARE ProteinsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateRNA InterferenceR-SNARE ProteinsSynapsesSynaptic TransmissionElongation Factor 2 KinaseGlutamic AcidQb-SNARE ProteinsReceptors, N-Methyl-D-AspartateR-SNARE ProteinsVamp7 protein, ratVti1a protein, rat

Identifiers

PMID28186166
PMCPMC5311059
OpenAlexW2587213236

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.