Evidence map›Paper›PMID 9929478›Full record

ArticleBiophysical journal1999

Modeling study of the effects of overlapping Ca2+ microdomains on neurotransmitter release.

R Bertram, G D Smith, A Sherman

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 106 citations in OpenAlex.

  1. Review
  2. Stationary CaBiophysical journal · 2021
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  7. Review
  8. Review
  9. Nanodomain control of exocytosis is responsible for the signaling capability of a retinal ribbon synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  10. Article
  11. Ca2+ current versus Ca2+ channel cooperativity of exocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  12. Article
  13. Ca2+ from one or two channels controls fusion of a single vesicle at the frog neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006
    Article
  14. Article
  15. Article
  16. Three-dimensional reconstruction of a calyx of Held and its postsynaptic principal neuron in the medial nucleus of the trapezoid body.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    Article
  17. Article
  18. Calcium secretion coupling at calyx of Held governed by nonuniform channel-vesicle topography.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    Article
  19. Presynaptic Ca2+ channels and neurotransmitter release at the terminal of a mouse cortical neuron.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    Article
  20. Quantitative relationship between transmitter release and calcium current at the calyx of held synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    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 1 institution in 1 country.

R BertramSchool of Science and Center for Mathematical Biology, Pennsylvania State University, Erie, Pennsylvania 16563, USA. bertram@euler.bd.psu.edu
G D Smith
A Sherman
Pennsylvania State University · 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

Although single-channel Ca2+ microdomains are capable of gating neurotransmitter release in some instances, it is likely that in many cases the microdomains from several open channels overlap to activate vesicle fusion. We describe a mathematical model in which transmitter release is gated by single or overlapping Ca2+ microdomains produced by the opening of nearby Ca2+ channels. This model accounts for the presence of a mobile Ca2+ buffer, provided either that the buffer is unsaturable or that it is saturated near an open channel with Ca2+ binding kinetics that are rapid relative to Ca2+ diffusion. We show that the release time course is unaffected by the location of the channels (at least for distances up to 50 nm), but paired-pulse facilitation is greater when the channels are farther from the release sites. We then develop formulas relating the fractional release following selective or random channel blockage to the cooperative relationship between release and the presynaptic Ca2+ current. These formulas are used with the transmitter release model to study the dependence of this form of cooperativity, which we call Ca2+ current cooperativity, on mobile buffers and on the local geometry of Ca2+ channels. We find that Ca2+ current cooperativity increases with the number of channels per release site, but is considerably less than the number of channels, the theoretical upper bound. In the presence of a saturating mobile buffer the Ca2+ current cooperativity is greater, and it increases more rapidly with the number of channels. Finally, Ca2+ current cooperativity is an increasing function of channel distance, particularly in the presence of saturating mobile buffer.

Indexed as

Models, BiologicalCalciumCalcium ChannelsDiffusionElectrophysiologyKineticsNeurotransmitter AgentsProtein BindingCalciumCalcium ChannelsNeurotransmitter Agents

Identifiers

PMID9929478
PMCPMC1300078
OpenAlexW2119063345

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.