Evidence map›Paper›PMID 15695246›Full record

ArticleThe Journal of physiology2005

Post-tetanic potentiation in the rat calyx of Held synapse.

Ron L P Habets, J Gerard G Borst

Open access · greenAbstract readComparative Study
In one paragraph

Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

64 citing papers in PubMed, 107 citations in OpenAlex.

  1. Munc13-1 couples DAG and CaScience advances · 2026
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  4. Munc13-1 is a CaNeuron · 2021
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  8. Presynaptic Calcium Channels.International journal of molecular sciences · 2019
    Review
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  11. Article
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  13. Emerging pathways driving early synaptic pathology in Alzheimer's disease.Biochemical and biophysical research communications · 2017
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Calcium-Dependent Protein Kinase C Is Not Required for Post-Tetanic Potentiation at the Hippocampal CA3 to CA1 Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  20. Article

4 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Ron L P HabetsDepartment of Neuroscience, Erasmus MC, University Medical Center Rotterdam, Dr. Molewaterplein 50, 3015 GE Rotterdam, The Netherlands.
J Gerard G Borst
Erasmus MC · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We studied synaptic plasticity in the calyx of Held synapse, an axosomatic synapse in the auditory brainstem, by making whole-cell patch clamp recordings of the principal cells innervated by the calyces in a slice preparation of 7- to 10-day-old rats. A 5 min 20 Hz stimulus train increased the amplitude of excitatory postsynaptic currents (EPSCs) on average more than twofold. The amplitude of the synaptic currents took several minutes to return to control values. The post-tetanic potentiation (PTP) was accompanied by a clear increase in the frequency, but not the amplitude, of spontaneous EPSCs, which returned to baseline more rapidly than the potentiation of evoked release. The size of the readily releasable pool of vesicles was increased by about 30%. In experiments in which presynaptic measurements of the intracellular calcium concentration were combined with postsynaptic voltage clamp recordings, PTP was accompanied by an increase in the presynaptic calcium concentration to about 210 nM. The decay of the PTP matched the decay of this increase. When the decay of the calcium transient was shortened by dialysing the terminal with EGTA, the PTP decay sped up in parallel. Our experiments suggest that PTP at the calyx of Held synapse is due to a long-lasting increase in the presynaptic calcium concentration following a tetanus, which results in an increase in the release probability of the vesicles of the readily releasable pool. Although part of the PTP can be explained by a direct activation of the calcium sensor for phasic release, other mechanisms are likely to contribute as well.

Indexed as

AnimalsBrain StemCalciumExcitatory Postsynaptic PotentialsIn Vitro TechniquesNeuronal PlasticityRatsRats, WistarSynapsesCalcium

Identifiers

PMID15695246
PMCPMC1456049
OpenAlexW2155781548

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.