Evidence map›Paper›PMID 31216055›Full record

ArticleJournal of neurochemistry2019

Synaptophysin sustains presynaptic performance by preserving vesicular synaptobrevin-II levels.

Alexandros C Kokotos, Callista B Harper, Jamie R K Marland, Karen J Smillie, Michael A Cousin, Sarah L Gordon

Open access · hybridAbstract read
In one paragraph

Article in Journal of neurochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Aurantio-Obtusin Attenuates Aβ-Induced Cognitive Impairment and Synaptic Dysfunction by Suppressing Neuroinflammation in Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
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  15. Review
  16. Molecular architecture of synaptic vesicles.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  18. Article
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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

6 authors at 3 institutions in 2 countries.

Alexandros C KokotosCentre for Discovery Brain Sciences, Hugh Robson Building, University of Edinburgh, George Square, Edinburgh, Scotland, UK, EH8 9XD.ORCID 0000-0003-4024-9866
Callista B HarperCentre for Discovery Brain Sciences, Hugh Robson Building, University of Edinburgh, George Square, Edinburgh, Scotland, UK, EH8 9XD.
Jamie R K MarlandCentre for Discovery Brain Sciences, Hugh Robson Building, University of Edinburgh, George Square, Edinburgh, Scotland, UK, EH8 9XD.
Karen J SmillieCentre for Discovery Brain Sciences, Hugh Robson Building, University of Edinburgh, George Square, Edinburgh, Scotland, UK, EH8 9XD.
Michael A CousinCentre for Discovery Brain Sciences, Hugh Robson Building, University of Edinburgh, George Square, Edinburgh, Scotland, UK, EH8 9XD.ORCID 0000-0002-1762-160X
Sarah L GordonThe Florey Institute of Neuroscience and Mental Health, and Melbourne Dementia Research Centre, The Florey Institute for Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia.ORCID 0000-0003-2281-3160
Maxwell Institute for Mathematical Sciences · GBThe University of Melbourne · AUUniversity of Edinburgh · GB

Funding

Biotechnology and Biological Sciences Research Council BB/L019329/1Medical Research Council G1002117
6 · The paper itself

Abstract

The two most abundant molecules on synaptic vesicles (SVs) are synaptophysin and synaptobrevin-II (sybII). SybII is essential for SV fusion, whereas synaptophysin is proposed to control the trafficking of sybII after SV fusion and its retrieval during endocytosis. Despite controlling key aspects of sybII packaging into SVs, the absence of synaptophysin results in negligible effects on neurotransmission. We hypothesised that this apparent absence of effect may be because of the abundance of sybII on SVs, with the impact of inefficient sybII retrieval only revealed during periods of repeated SV turnover. To test this hypothesis, we subjected primary cultures of synaptophysin knockout neurons to repeated trains of neuronal activity, while monitoring SV fusion events and levels of vesicular sybII. We identified a significant decrease in both the number of SV fusion events (monitored using the genetically encoded reporter vesicular glutamate transporter-pHluorin) and vesicular sybII levels (via both immunofluorescence and Western blotting) using this protocol. This revealed that synaptophysin is essential to sustain both parameters during periods of repetitive SV turnover. This was confirmed by the rescue of presynaptic performance by the expression of exogenous synaptophysin. Importantly, the expression of exogenous sybII also fully restored SV fusion events in synaptophysin knockout neurons. The ability of additional copies of sybII to fully rescue presynaptic performance in these knockout neurons suggests that the principal role of synaptophysin is to mediate the efficient retrieval of sybII to sustain neurotransmitter release.

Indexed as

AnimalsCells, CulturedHippocampusMiceMice, Inbred C57BLMice, KnockoutNeuronsSynaptic TransmissionSynaptic VesiclesSynaptophysinVesicle-Associated Membrane Protein 2SynaptophysinVesicle-Associated Membrane Protein 2endocytosisneurotransmissionpresynapsesynaptophysinVAMP2vesicle

Identifiers

PMID31216055
PMCPMC6851701
OpenAlexW2951584685

What OpenQuestion holds

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LicenceCC BY-NC
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.