Evidence map›Paper›PMID 38112713›Full record

ArticleThe Journal of general physiology2024

Interpretation of presynaptic phenotypes of synaptic plasticity in terms of a two-step priming process.

Erwin Neher

Abstract read
In one paragraph

Article in The Journal of general physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Article
  2. Article
  3. Thyroxine Disrupts Synaptic Plasticity via Non-genomic Action in the Hippocampus.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Depression of synaptic outputs by reduction of CaFrontiers in molecular neuroscience · 2026
    Article
  9. Interactions between long- and short-term synaptic plasticity transform temporal neural representations into spatial.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Different states of synaptic vesicle priming explain target cell type-dependent differences in neurotransmitter release.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  20. Complexin has a dual synaptic function as checkpoint protein in vesicle priming and as a promoter of vesicle fusion.Proceedings of the National Academy of Sciences of the United States of America · 2024
    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

1 author.

Erwin NeherMax Planck Institute for Multidisciplinary Sciences , Göttingen, Germany.ORCID 0000-0002-9758-7922

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies on synaptic proteins involved in neurotransmitter release often aim at distinguishing between their roles in vesicle priming (the docking of synaptic vesicles to the plasma membrane and the assembly of a release machinery) as opposed to the process of vesicle fusion. This has traditionally been done by estimating two parameters, the size of the pool of fusion-competent vesicles (the readily releasable pool, RRP) and the probability that such vesicles are released by an action potential, with the aim of determining how these parameters are affected by molecular perturbations. Here, it is argued that the assumption of a homogeneous RRP may be too simplistic and may blur the distinction between vesicle priming and fusion. Rather, considering priming as a dynamic and reversible multistep process allows alternative interpretations of mutagenesis-induced changes in synaptic transmission and suggests mechanisms for variability in synaptic strength and short-term plasticity among synapses, as well as for interactions between short- and long-term plasticity. In many cases, assigned roles of proteins or causes for observed phenotypes are shifted from fusion- to priming-related when considering multistep priming. Activity-dependent enhancement of priming is an essential element in this alternative view and its variation among synapse types can explain why some synapses show depression and others show facilitation at low to intermediate stimulation frequencies. Multistep priming also suggests a mechanism for frequency invariance of steady-state release, which can be observed in some synapses involved in sensory processing.

Indexed as

SynapsesSynaptic VesiclesAction PotentialsNeuronal PlasticityProteinsSynaptic TransmissionProteins

Identifiers

PMID38112713
PMCPMC10730358

What OpenQuestion holds

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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.