Evidence map›Paper›PMID 28197078›Full record

ArticleFrontiers in molecular neuroscience2017

Redundant Postsynaptic Functions of SynCAMs 1-3 during Synapse Formation.

Daniel K Fowler, James H Peters, Carly Williams, Philip Washbourne

Abstract read
In one paragraph

Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Alterations of presynaptic proteins in autism spectrum disorder.Frontiers in molecular neuroscience · 2022
    Review
  5. Differential Contribution of Cadm1-Cadm3 Cell Adhesion Molecules to Peripheral Myelinated Axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. 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

4 authors.

Daniel K FowlerDepartment of Biology, Institute of Neuroscience, University of OregonEugene, OR, USA; Department of Integrative Physiology and Neuroscience, Washington State UniversityPullman, WA, USA.
James H PetersDepartment of Integrative Physiology and Neuroscience, Washington State University Pullman, WA, USA.
Carly WilliamsDepartment of Biology, Institute of Neuroscience, University of Oregon Eugene, OR, USA.
Philip WashbourneDepartment of Biology, Institute of Neuroscience, University of Oregon Eugene, OR, USA.

Funding

DEVELOPMENTAL BIOLOGY TRAINING PROGRAMT32HD007348 · NICHD · UNIVERSITY OF OREGON · PI Chris Q Doe, KRYN STANKUNAS · 1989 to 2026
$6.8M
Asynchronous Glutamate Release in Vagal Afferent to NTS NeurotransmissionR01DK092651 · NIDDK · WASHINGTON STATE UNIVERSITY · PI PETERS, JAMES HENRY · 2012 to 2016
$1.6M
NICHD NIH HHS T32 HD007348NIDDK NIH HHS R01 DK092651
6 · The paper itself

Abstract

Investigating the roles of synaptogenic adhesion molecules during synapse formation has proven challenging, often due to compensatory functions between additional family members. The synaptic cell adhesion molecules 1-3 (SynCAM1-3) are expressed both pre- and postsynaptically, share highly homologous domains and are synaptogenic when ectopically presented to neurons; yet their endogenous functions during synaptogenesis are unclear. Here we report that SynCAM1-3 are functionally redundant and collectively necessary for synapse formation in cultured hippocampal neurons. Only triple knockdown (KD) of SynCAM1-3 using highly efficient, chained artificial microRNAs (amiRNAs) reduced synapse density and increased synapse area. Electrophysiological recordings of quantal release events supported an increase in synapse size caused by SynCAM1-3 depletion. Furthermore, a combinatorial, mosaic lentiviral approach comparing wild type (WT) and SynCAM1-3 KD neurons in the same culture demonstrate that SynCAM1-3 set synapse number and size through postsynaptic mechanisms. The results demonstrate that the redundancy between SynCAM1-3 has concealed their synaptogenic function at the postsynaptic terminal.

Indexed as

adhesionartificial miRNAhippocampusknockdownmosaicredundancysynapse formationSynCAM

Identifiers

PMID28197078
PMCPMC5281628

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.