Evidence map›Paper›PMID 26208337›Full record

ArticleeLife2015

Spontaneous neurotransmission signals through store-driven Ca(2+) transients to maintain synaptic homeostasis.

Austin L Reese, Ege T Kavalali

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

61 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
  2. Lithium as a therapeutic strategy for SNAP25 encephalopathies via modulation of homeostatic plasticity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Spontaneous glutamate release activates mGluR signaling to drive rapid antidepressant responses.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Synaptic basis of rapid antidepressant action.European archives of psychiatry and clinical neuroscience · 2025
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Dorsal raphe dopaminergic neurons target CaMKIITranslational psychiatry · 2024
    Article
  15. Article
  16. Nano-organization of synaptic calcium signaling.Biochemical Society transactions · 2024
    Review
  17. Spatially non-overlapping CaCell reports · 2023
    Article
  18. Article
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

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 at 1 institution in 1 country.

Austin L ReeseDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, United States.
Ege T KavalaliDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, United States.
The University of Texas Southwestern Medical Center · US

Funding

Role of SNARE Interactions in Central Synapse FunctionR01MH066198 · NIMH · VANDERBILT UNIVERSITY · PI KAVALALI, EGE T · 2004 to 2023
$7.9M
The Cellular Biophysics of the Neuron Training ProgramT32NS069562 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI KAVALALI, EGE T · 2010 to 2014
$568k
NIMH NIH HHS MH066198NIMH NIH HHS R01 MH066198NINDS NIH HHS T32 NS069562
6 · The paper itself

Abstract

Spontaneous glutamate release-driven NMDA receptor activity exerts a strong influence on synaptic homeostasis. However, the properties of Ca(2+) signals that mediate this effect remain unclear. Here, using hippocampal neurons labeled with the fluorescent Ca(2+) probes Fluo-4 or GCAMP5, we visualized action potential-independent Ca(2+) transients in dendritic regions adjacent to fluorescently labeled presynaptic boutons in physiological levels of extracellular Mg(2+). These Ca(2+) transients required NMDA receptor activity, and their propensity correlated with acute or genetically induced changes in spontaneous neurotransmitter release. In contrast, they were insensitive to blockers of AMPA receptors, L-type voltage-gated Ca(2+) channels, or group I mGluRs. However, inhibition of Ca(2+)-induced Ca(2+) release suppressed these transients and elicited synaptic scaling, a process which required protein translation and eukaryotic elongation factor-2 kinase activity. These results support a critical role for Ca(2+)-induced Ca(2+) release in amplifying NMDA receptor-driven Ca(2+) signals at rest for the maintenance of synaptic homeostasis.

Indexed as

Action PotentialsHomeostasisAnimalsCalciumCells, CulturedMice, KnockoutNeuronsPatch-Clamp TechniquesRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateSynapsesCalciumReceptors, N-Methyl-D-AspartateCa2+ induced Ca2+ releasehomeostatic plasticitymouseneuroscienceNMDA receptor signalingratspontaneous neurotransmitter release

Identifiers

PMID26208337
PMCPMC4534843
OpenAlexW1763478481

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.