Evidence map›Paper›PMID 18450780›Full record

ArticleThe Journal of physiology2008

Interactions between multiple sources of short-term plasticity during evoked and spontaneous activity at the rat calyx of Held.

Matthias H Hennig, Michael Postlethwaite, Ian D Forsythe, Bruce P Graham

Open access · greenAbstract 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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Nitric Oxide Signaling in the Auditory Pathway.Frontiers in neural circuits · 2021
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Theoretical models of synaptic short term plasticity.Frontiers in computational neuroscience · 2013
    Article
  12. Article
  13. 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
  14. Article
  15. Article
  16. Review
  17. 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

4 authors at 3 institutions in 1 country.

Matthias H HennigANC, School of Informatics, University of Edinburgh, 5 Forrest Hill, Edinburgh, EH1 2QL, UK. mhennig@inf.ed.ac.uk
Michael Postlethwaite
Ian D Forsythe
Bruce P Graham
University of Stirling · GBMRC Toxicology Unit · GBUniversity of Leicester · GB

Funding

Biotechnology and Biological Sciences Research Council BBS/B/07217Biotechnology and Biological Sciences Research Council BBS/B/07276Medical Research Council G0501327Medical Research Council MC_U132681855
6 · The paper itself

Abstract

Sustained activity at most central synapses is accompanied by a number of short-term changes in synaptic strength which act over a range of time scales. Here we examine experimental data and develop a model of synaptic depression at the calyx of Held synaptic terminal that combines many of these mechanisms (acting at differing sites and across a range of time scales). This new model incorporates vesicle recycling, facilitation, activity-dependent vesicle retrieval and multiple mechanisms affecting calcium channel activity and release probability. It can accurately reproduce the time course of experimentally measured short-term depression across different stimulus frequencies and exhibits a slow decay in EPSC amplitude during sustained stimulation. We show that the slow decay is a consequence of vesicle release inhibition by multiple mechanisms and is accompanied by a partial recovery of the releasable vesicle pool. This prediction is supported by patch-clamp data, using long duration repetitive EPSC stimulation at up to 400 Hz. The model also explains the recovery from depression in terms of interaction between these multiple processes, which together generate a stimulus-history-dependent recovery after repetitive stimulation. Given the high rates of spontaneous activity in the auditory pathway, the model also demonstrates how these multiple interactions cause chronic synaptic depression under in vivo conditions. While the magnitude of the depression converges to the same steady state for a given frequency, the time courses of onset and recovery are faster in the presence of spontaneous activity. We conclude that interactions between multiple sources of short-term plasticity can account for the complex kinetics during high frequency stimulation and cause stimulus-history-dependent recovery at this relay synapse.

Indexed as

AnimalsBrain StemComputer SimulationEvoked PotentialsMembrane PotentialsModels, BiologicalNeuronal PlasticityNeuronsRatsSynapsesTemperatureTime FactorsTissue Culture Techniques

Identifiers

PMID18450780
PMCPMC2538789
OpenAlexW2147170241

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.