Evidence map›Paper›PMID 15111389›Full record

ArticleBiophysical journal2004

Facilitation through buffer saturation: constraints on endogenous buffering properties.

Victor Matveev, Robert S Zucker, Arthur Sherman

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
24.6field-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

58 citing papers in PubMed, 106 citations in OpenAlex.

  1. Presynaptic CaCell reports · 2026
    Article
  2. Presynaptic CabioRxiv : the preprint server for biology · 2026
    Article
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  14. Short-Term Facilitation at a Detonator Synapse Requires the Distinct Contribution of Multiple Types of Voltage-Gated Calcium Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Reduced endogenous Ca2+ buffering speeds active zone Ca2+ signaling.Proceedings of the National Academy of Sciences of the United States of America · 2015
    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

3 authors at 3 institutions in 1 country.

Victor MatveevDepartment of Mathematical Sciences, New Jersey Institute of Technology, Newark, New Jersey 07102, USA.
Robert S Zucker
Arthur Sherman
National Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · USUniversity of California, Berkeley · US

Funding

ELECTRICAL AND CHEMICAL OSCILLATIONS IN COUPLED CELL SYSTEMSZ01DK013020 · NIDDK · DIABETES, DIGESTIVE, KIDNEY DISEASES · PI SHERMAN, ARTHUR S · 1990 to 2006
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6 · The paper itself

Abstract

Synaptic facilitation (SF) is a ubiquitous form of short-term plasticity, regulating synaptic dynamics on fast timescales. Although SF is known to depend on the presynaptic accumulation of Ca(2+), its precise mechanism is still under debate. Recently it has been shown that at certain central synapses SF results at least in part from the progressive saturation of an endogenous Ca(2+) buffer (Blatow et al., 2003), as proposed by Klingauf and Neher (1997). Using computer simulations, we study the magnitude of SF that can be achieved by a buffer saturation mechanism (BSM), and explore its dependence on the endogenous buffering properties. We find that a high SF magnitude can be obtained either by a global saturation of a highly mobile buffer in the entire presynaptic terminal, or a local saturation of a completely immobilized buffer. A characteristic feature of BSM in both cases is that SF magnitude depends nonmonotonically on the buffer concentration. In agreement with results of Blatow et al. (2003), we find that SF grows with increasing distance from the Ca(2+) channel cluster, and increases with increasing external Ca(2+), [Ca(2+)](ext), for small levels of [Ca(2+)](ext). We compare our modeling results with the experimental properties of SF at the crayfish neuromuscular junction, and find that the saturation of an endogenous mobile buffer can explain the observed SF magnitude and its supralinear accumulation time course. However, we show that the BSM predicts slowing of the SF decay rate in the presence of exogenous Ca(2+) buffers, contrary to experimental observations at the crayfish neuromuscular junction. Further modeling and data are required to resolve this aspect of the BSM.

Indexed as

BuffersAnimalsAstacoideaBinding SitesBiophysicsCalciumCalcium ChannelsComputer SimulationFluorescent DyesFura-2KineticsModels, TheoreticalNeuromuscular JunctionTime FactorsBuffersCalciumCalcium ChannelsFluorescent DyesFura-2

Identifiers

PMID15111389
PMCPMC1304141
OpenAlexW2104969424

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.