Evidence map›Paper›PMID 15601945›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Augmentation increases vesicular release probability in the presence of masking depression at the frog neuromuscular junction.

Jonathan M Kalkstein, Karl L Magleby

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.7field-weighted citation impact, top 37% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. GABAProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  2. Article
  3. Dlg Is Required for Short-Term Memory and Interacts with NMDAR in theInternational journal of molecular sciences · 2022
    Article
  4. Article
  5. Doc2-mediated superpriming supports synaptic augmentation.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. A new kinetic framework for synaptic vesicle trafficking tested in synapsin knock-outs.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  11. Article
  12. Abnormal presynaptic short-term plasticity and information processing in a mouse model of fragile X syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  13. Article
  14. Article
  15. Article
  16. The role of presynaptic dynamics in processing of natural spike trains in hippocampal synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  17. Article
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  19. Article
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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 2 institutions in 2 countries.

Jonathan M KalksteinDepartment of Physiology and Biophysics and Neuroscience Program, University of Miami School of Medicine, Miami, Florida 33136, USA. jmk10@cornell.edu
Karl L Magleby
Cornell University · USUniversity of Miami · US

Funding

ADA3: a novel target for HPV16 E6 oncoproteinR01CA094143 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, VIMLA · 2002 to 2006
$1.7M
NCI NIH HHS R01 CA094143
6 · The paper itself

Abstract

Synaptic augmentation is a short-term component of synaptic plasticity that increases transmitter release during repetitive stimulation and decays thereafter with a time constant of approximately 7 sec. Augmentation has typically been observed under conditions where there is little or no depression because of depletion of synaptic vesicles from the readily releasable pool (RRP) of transmitter. We now study augmentation under conditions of pronounced depression at the frog neuromuscular junction to gain additional insight into mechanism. If augmentation reflects an increase in the size of the RRP of transmitter, then augmentation should not be present with depression. Our findings using four different experimental approaches suggested that augmentation was still present in the presence of pronounced depression: mathematical extraction of augmentation from the changes in transmitter release after repetitive stimulation, identification of augmentation with Ba2+, correction of the data for the measured depletion of the RRP, and identification of an augmentation component of residual Ca2+. We conclude that the augmentation machinery still acts to increase transmitter release when depression reduces the RRP sufficiently to mask obvious augmentation. The masked augmentation was found to increase transmitter release by increasing the probability of releasing individual vesicles from the depressed RRP, countering the effects of depression. Because augmentation and depression have similar time courses, either process can mask the other, depending on their relative magnitudes. Consequently, the apparent absence of one of the processes does not exclude that it is still contributing to short-term synaptic plasticity.

Indexed as

AnimalsBariumCalciumIn Vitro TechniquesModels, NeurologicalMotor EndplateNeuronal PlasticityNeurotransmitter AgentsRana pipiensSynaptic VesiclesTime FactorsBariumCalciumNeurotransmitter Agents

Identifiers

PMID15601945
PMCPMC6730369
OpenAlexW2043953994

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.