Evidence map›Paper›PMID 22243751›Full record

ArticleNeuron2012

Vti1a identifies a vesicle pool that preferentially recycles at rest and maintains spontaneous neurotransmission.

Denise M O Ramirez, Mikhail Khvotchev, Brent Trauterman, Ege T Kavalali

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 2 pooled it
10.4field-weighted citation impact, top 1% 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

113 citing papers in PubMed, 2 syntheses or guidelines pooled it, 163 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. The Synaptic Vesicle Priming Protein Munc13 Mediates Evoked Somatodendritic Dopamine Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  5. Munc13 serves as a molecular filter for SNARE sorting and assembly in active zone condensates.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Brain-derived neurotrophic factor scales presynaptic calcium transients to modulate excitatory neurotransmission.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. SV2B defines a subpopulation of synaptic vesicles.Journal of molecular cell biology · 2024
    Article
  14. Article
  15. Article
  16. Nanoelectrochemistry reveals how soluble AβProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  17. Early Endosomes Act as Local Exocytosis Hubs to Repair Endothelial Membrane Damage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  18. Article
  19. Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Denise M O RamirezDepartment of Neuroscience, UT Southwestern Medical Center, Dallas, TX 75390-9111, USA.
Mikhail Khvotchev
Brent Trauterman
Ege T Kavalali
Southwestern Medical Center · USSouthwestern Medical CenterThe 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
Role of the SNARE proteins Vti1a and VAMP7 in central synaptic transmissionF32MH093109 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI RAMIREZ, DENISE MARIE · 2010 to 2012
$100k
NIMH NIH HHS F32 MH093109NIMH NIH HHS F32MH093109NIMH NIH HHS R01 MH066198NIMH NIH HHS R01MH066198
6 · The paper itself

Abstract

Recent studies suggest that synaptic vesicles (SVs) giving rise to spontaneous neurotransmission are distinct from those that carry out evoked release. However, the molecular basis of this dichotomy remains unclear. Here, we focused on two noncanonical SNARE molecules, Vps10p-tail-interactor-1a (vti1a) and VAMP7, previously shown to reside on SVs. Using simultaneous multicolor imaging at individual synapses, we could show that compared to the more abundant vesicular SNARE synaptobrevin2, both vti1a and VAMP7 were reluctantly mobilized during activity. Vti1a, but not VAMP7, showed robust trafficking under resting conditions that could be partly matched by synaptobrevin2. Furthermore, loss of vti1a function selectively reduced high-frequency spontaneous neurotransmitter release detected postsynaptically. Expression of a truncated version of vti1a augmented spontaneous release more than full-length vti1a, suggesting that an autoinhibitory process regulates vti1a function. Taken together, these results support the premise that in its native form vti1a selectively maintains spontaneous neurotransmitter release.

Indexed as

Action PotentialsAnesthetics, LocalAnimalsAnimals, NewbornBiological TransportBiophysicsCalciumCells, CulturedElectric StimulationEnzyme InhibitorsExcitatory Postsynaptic PotentialsGreen Fluorescent ProteinsHippocampusHydrogen-Ion ConcentrationMacrolidesMicroscopy, ImmunoelectronAnesthetics, LocalCalciumconcanamycin AEnzyme InhibitorsGreen Fluorescent ProteinsMacrolidesPotassium ChlorideQb-SNARE ProteinsRNA, Small InterferingR-SNARE ProteinsSNARE ProteinsSynaptotagmin ITetrodotoxinVamp7 protein, ratVesicle-Associated Membrane Protein 2Vti1a protein, rat

Identifiers

PMID22243751
PMCPMC3259527
OpenAlexW1998116909

What OpenQuestion holds

Textmetadata
LicenceTDM
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.