Evidence map›Paper›PMID 18832426›Full record

ArticleThe Journal of physiology2008

A limited contribution of Ca2+ current facilitation to paired-pulse facilitation of transmitter release at the rat calyx of Held.

Martin Müller, Felix Felmy, Ralf Schneggenburger

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.5field-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

45 citing papers in PubMed, 72 citations in OpenAlex.

  1. Presynaptic CaCell reports · 2026
    Article
  2. Article
  3. Article
  4. Presynaptic CabioRxiv : the preprint server for biology · 2026
    Article
  5. Synaptic Facilitation Enhances the Reliability and Precision of High-Frequency Neurotransmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. A sequential two-step priming scheme reproduces diversity in synaptic strength and short-term plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  11. Review
  12. The Role of CaCell reports · 2019
    Article
  13. Article
  14. Review
  15. Dynamics of volume-averaged intracellular CaThe Journal of physiology · 2017
    Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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 2 institutions in 2 countries.

Martin MüllerLaboratory of Synaptic Mechanisms, Ecole Polytechnique Fédérale de Lausanne, Brain-Mind Institute, 1015 Lausanne, Switzerland.
Felix Felmy
Ralf Schneggenburger
École Polytechnique Fédérale de Lausanne · CHLudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have suggested that transmitter release facilitation at synapses is largely mediated by presynaptic Ca(2+) current facilitation, but the exact contribution of Ca(2+) current facilitation has not been determined quantitatively. Here, we determine the contribution of Ca(2+) current facilitation, and of an increase in the residual free Ca(2+) concentration ([Ca(2+)](i)) in the nerve terminal, to paired-pulse facilitation of transmitter release at the calyx of Held. Under conditions of low release probability imposed by brief presynaptic voltage-clamp steps, transmitter release facilitation at short interstimulus intervals (4 ms) was 227 +/- 31% of control, Ca(2+) current facilitation was 113 +/- 4% of control, and the peak residual [Ca(2+)](i) was 252 +/- 18 nm over baseline. By inferring the 'local' [Ca(2+)](i) transients that drive transmitter release during these voltage-clamp stimuli with the help of a kinetic release model, we estimate that Ca(2+) current facilitation contributes to approximately 40% to paired-pulse facilitation of transmitter release. The remaining component of facilitation strongly depends on the build-up, and on the decay of the residual free [Ca(2+)](i), but cannot be explained by linear summation of the residual free [Ca(2+)](i), and the back-calculated 'local' [Ca(2+)](i) signal, which only accounts for approximately 10% of the total release facilitation. Further voltage-clamp experiments designed to compensate for Ca(2+) current facilitation demonstrated that about half of the observed transmitter release facilitation remains in the absence of Ca(2+) current facilitation. Our results indicate that paired-pulse facilitation of transmitter release at the calyx of Held is driven by at least two distinct mechanisms: Ca(2+) current facilitation, and a mechanism independent of Ca(2+) current facilitation that closely tracks the time course of residual free [Ca(2+)](i).

Indexed as

Calcium SignalingAction PotentialsAnimalsAuditory PathwaysBrain StemCalcium Channels, N-TypeCalcium Channels, R-TypeElectrophysiologyIn Vitro TechniquesModels, NeurologicalNeurotransmitter AgentsPatch-Clamp TechniquesRatsRats, WistarSynapsesCalcium Channels, N-TypeCalcium Channels, R-TypeNeurotransmitter Agents

Identifiers

PMID18832426
PMCPMC2655367
OpenAlexW2140592106

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.