Evidence map›Paper›PMID 29445238›Full record

ArticleScientific reports2018

VPS35 depletion does not impair presynaptic structure and function.

Sonia Vazquez-Sanchez, Sander Bobeldijk, Marien P Dekker, Linda van Keimpema, Jan R T van Weering

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  6. Article
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  8. Review
  9. Article
  10. Article
  11. The Role of VPS35 in the Pathobiology of Parkinson's Disease.Cellular and molecular neurobiology · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Retromer in Synaptic Function and Pathology.Frontiers in synaptic neuroscience · 2018
    Review
  16. Review
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

5 authors at 2 institutions in 2 countries.

Sonia Vazquez-SanchezDepartment of Functional Genomics, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, Vrije Universiteit (VU), Amsterdam, Netherlands.
Sander BobeldijkDepartment of Functional Genomics, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, Vrije Universiteit (VU), Amsterdam, Netherlands.
Marien P DekkerClinical Genetics, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, VU medical center, Amsterdam, Netherlands.
Linda van KeimpemaDepartment of Functional Genomics, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, Vrije Universiteit (VU), Amsterdam, Netherlands.ORCID 0000-0001-6725-4599
Jan R T van WeeringClinical Genetics, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, VU medical center, Amsterdam, Netherlands. jan.van.weering@vu.nl.ORCID 0000-0001-5259-4945
Amsterdam Neuroscience · NLSylics (Netherlands) · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The endosomal system is proposed as a mediator of synaptic vesicle recycling, but the molecular recycling mechanism remains largely unknown. Retromer is a key protein complex which mediates endosomal recycling in eukaryotic cells, including neurons. Retromer is important for brain function and mutations in retromer genes are linked to neurodegenerative diseases. In this study, we aimed to determine the role of retromer in presynaptic structure and function. We assessed the role of retromer by knocking down VPS35, the core subunit of retromer, in primary hippocampal mouse neurons. VPS35 depletion led to retromer dysfunction, measured as a decrease in GluA1 at the plasma membrane, and bypassed morphological defects previously described in chronic retromer depletion models. We found that retromer is localized at the mammalian presynaptic terminal. However, VPS35 depletion did not alter the presynaptic ultrastructure, synaptic vesicle release or retrieval. Hence, we conclude that retromer is present in the presynaptic terminal but it is not essential for the synaptic vesicle cycle. Nonetheless, the presynaptic localization of VPS35 suggests that retromer-dependent endosome sorting could take place for other presynaptic cargo.

Indexed as

AnimalsCell MembraneCells, CulturedElectrical SynapsesHippocampusHumansMiceNeuronsParkinson DiseaseProtein TransportReceptors, AMPARNA, Small InterferingSynaptic VesiclesVesicular Transport ProteinsReceptors, AMPARNA, Small InterferingVesicular Transport ProteinsVps35 protein, mouse

Identifiers

PMID29445238
PMCPMC5812998
OpenAlexW2807265581

What OpenQuestion holds

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LicenceCC BY
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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.