Evidence map›Paper›PMID 27219344›Full record

ArticleTranslational psychiatry2016

Developmental suppression of schizophrenia-associated miR-137 alters sensorimotor function in zebrafish.

J Giacomotto, A P Carroll, S Rinkwitz, B Mowry, M J Cairns, T S Becker

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. The evolutionarily conserved miRNA-137 targets the neuropeptide hypocretin/orexin and modulates the wake to sleep ratio.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  6. Review
  7. Review
  8. The αScientific reports · 2019
    Article
  9. BDNF, Brain, and Regeneration: Insights from Zebrafish.International journal of molecular sciences · 2018
    Review
  10. Article
  11. A comprehensive review of the genetic and biological evidence supports a role for MicroRNA-137 in the etiology of schizophrenia.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2018
    Review
  12. Review
  13. 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

6 authors at 4 institutions in 1 country.

J GiacomottoBrain and Mind Research Institute, Sydney Medical School, University of Sydney, Camperdown, NSW, Australia.
A P CarrollSchool of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, The University of Newcastle, Callaghan, NSW, Australia.
S RinkwitzBrain and Mind Research Institute, Sydney Medical School, University of Sydney, Camperdown, NSW, Australia.
B MowryPsychiatric Genomics Group, Queensland Brain Institute, The University of Queensland, Brisbane, QLD, Australia.
M J CairnsSchool of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, The University of Newcastle, Callaghan, NSW, Australia.
T S BeckerBrain and Mind Research Institute, Sydney Medical School, University of Sydney, Camperdown, NSW, Australia.
University of Newcastle Australia · AUUniversity of Sydney · AUQueensland Centre for Mental Health Research · AUUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The neurodevelopmentally regulated microRNA miR-137 was strongly implicated as risk locus for schizophrenia in the most recent genome wide association study coordinated by the Psychiatric Genome Consortium (PGC). This molecule is highly conserved in vertebrates enabling the investigation of its function in the developing zebrafish. We utilized this model system to achieve overexpression and suppression of miR-137, both transiently and stably through transgenesis. While miR-137 overexpression was not associated with an observable specific phenotype, downregulation by antisense morpholino and/or transgenic expression of miR-sponge RNA induced significant impairment of both embryonic and larval touch-sensitivity without compromising overall anatomical development. We observed miR-137 expression and activity in sensory neurons including Rohon-Beard neurons and dorsal root ganglia, two neuronal cell types that confer touch-sensitivity in normal zebrafish, suggesting a role of these cell types in the observed phenotype. The lack of obvious anatomical or histological pathology in these cells, however, suggested that subtle axonal network defects or a change in synaptic function and neural connectivity might be responsible for the behavioral phenotype rather than a change in the cellular morphology or neuroanatomy.

Indexed as

AnimalsAnimals, Genetically ModifiedGanglia, SpinalGene Expression Regulation, DevelopmentalMicroRNAsNeuronsPhenotypeSchizophreniaTouchZebrafishMicroRNAs

Identifiers

PMID27219344
PMCPMC5070046
OpenAlexW2402729538

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.