Evidence map›Paper›PMID 26805017›Full record

ArticleScientific reports2016

Botulinum neurotoxin type-A enters a non-recycling pool of synaptic vesicles.

Callista B Harper, Andreas Papadopulos, Sally Martin, Daniel R Matthews, Garry P Morgan, Tam H Nguyen, Tong Wang, Deepak Nair, Daniel Choquet, Frederic A Meunier

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. The Use of Botulinum Toxin in the Management of Headache Disorders.Handbook of experimental pharmacology · 2021
    Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Botulinum Neurotoxins: Mechanism of Action.Handbook of experimental pharmacology · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  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

10 authors at 3 institutions in 3 countries.

Callista B HarperThe University of Queensland, Queensland Brain Institute, Clem Jones Centre for Ageing Dementia Research, Brisbane, Queensland 4072, Australia.
Andreas PapadopulosThe University of Queensland, Queensland Brain Institute, Clem Jones Centre for Ageing Dementia Research, Brisbane, Queensland 4072, Australia.
Sally MartinThe University of Queensland, Queensland Brain Institute, Clem Jones Centre for Ageing Dementia Research, Brisbane, Queensland 4072, Australia.
Daniel R MatthewsThe University of Queensland, Queensland Brain Institute, Brisbane, Queensland 4072, Australia.
Garry P MorganThe University of Queensland, Centre for Microscopy and Microanalysis, Brisbane, Queensland 4072, Australia.
Tam H NguyenThe University of Queensland, Queensland Brain Institute, Clem Jones Centre for Ageing Dementia Research, Brisbane, Queensland 4072, Australia.
Tong WangThe University of Queensland, Queensland Brain Institute, Clem Jones Centre for Ageing Dementia Research, Brisbane, Queensland 4072, Australia.
Deepak NairInterdisciplinary Institute for Neuroscience, The University of Bordeaux, Bordeaux, 33000, France.
Daniel ChoquetInterdisciplinary Institute for Neuroscience, The University of Bordeaux, Bordeaux, 33000, France.
Frederic A MeunierThe University of Queensland, Queensland Brain Institute, Clem Jones Centre for Ageing Dementia Research, Brisbane, Queensland 4072, Australia.
University of Queensland · AUPark Centre for Mental Health · AUInstitut Interdisciplinaire de Neuroscience · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal communication relies on synaptic vesicles undergoing regulated exocytosis and recycling for multiple rounds of fusion. Whether all synaptic vesicles have identical protein content has been challenged, suggesting that their recycling ability may differ greatly. Botulinum neurotoxin type-A (BoNT/A) is a highly potent neurotoxin that is internalized in synaptic vesicles at motor nerve terminals and induces flaccid paralysis. Recently, BoNT/A was also shown to undergo retrograde transport, suggesting it might enter a specific pool of synaptic vesicles with a retrograde trafficking fate. Using high-resolution microscopy techniques including electron microscopy and single molecule imaging, we found that the BoNT/A binding domain is internalized within a subset of vesicles that only partially co-localize with cholera toxin B-subunit and have markedly reduced VAMP2 immunoreactivity. Synaptic vesicles loaded with pHrodo-BoNT/A-Hc exhibited a significantly reduced ability to fuse with the plasma membrane in mouse hippocampal nerve terminals when compared with pHrodo-dextran-containing synaptic vesicles and pHrodo-labeled anti-GFP nanobodies bound to VAMP2-pHluorin or vGlut-pHluorin. Similar results were also obtained at the amphibian neuromuscular junction. These results reveal that BoNT/A is internalized in a subpopulation of synaptic vesicles that are not destined to recycle, highlighting the existence of significant molecular and functional heterogeneity between synaptic vesicles.

Indexed as

AnimalsBotulinum Toxins, Type AExocytosisHippocampusMiceMotor NeuronsNeuromuscular JunctionNeurotoxinsProtein TransportSynaptic VesiclesBotulinum Toxins, Type ANeurotoxins

Identifiers

PMID26805017
PMCPMC4726273
OpenAlexW2275272626

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.