Evidence map›Paper›PMID 21151609›Full record

ArticlePloS one2010

Phenotypic characterization of transgenic mice overexpressing neuregulin-1.

Taisuke Kato, Atsushi Kasai, Makoto Mizuno, Liang Fengyi, Norihito Shintani, Sadaaki Maeda, Minesuke Yokoyama, Miwako Ozaki, Hiroyuki Nawa

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 110 citations in OpenAlex.

  1. Article
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  4. Review
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  6. What Can We Learn from Animal Models to Study Schizophrenia?Advances in experimental medicine and biology · 2022
    Article
  7. Article
  8. Article
  9. Neuregulins in Neurodegenerative Diseases.Frontiers in aging neuroscience · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Neuregulin in Health and Disease.International journal of brain disorders and treatment · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

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

9 authors at 5 institutions in 2 countries.

Taisuke KatoDepartment of Molecular Neurobiology, Brain Research Institute, Niigata University, Niigata, Japan.
Atsushi Kasai
Makoto Mizuno
Liang Fengyi
Norihito Shintani
Sadaaki Maeda
Minesuke Yokoyama
Miwako Ozaki
Hiroyuki Nawa
Niigata University · JPSetsunan University · JPNational University of Singapore · SGOsaka University · JPWaseda Bioscience Research Institute in Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuregulin-1 (NRG1) is one of the susceptibility genes for schizophrenia and implicated in the neurotrophic regulation of GABAergic and dopaminergic neurons, myelination, and NMDA receptor function. Postmortem studies often indicate a pathologic association of increased NRG1 expression or signaling with this illness. However, the psychobehavioral implication of NRG1 signaling has mainly been investigated using hypomorphic mutant mice for individual NRG1 splice variants. METHODOLOGY/PRINCIPAL

findingsTo assess the behavioral impact of hyper NRG1 signaling, we generated and analyzed two independent mouse transgenic (Tg) lines carrying the transgene of green fluorescent protein (GFP)-tagged type-1 NRG1 cDNA. The promoter of elongation-factor 1α gene drove ubiquitous expression of GFP-tagged NRG1 in the whole brain. As compared to control littermates, both heterozygous NRG1-Tg lines showed increased locomotor activity, a nonsignificant trend toward decreasing prepulse inhibition, and decreased context-dependent fear learning but exhibited normal levels of tone-dependent learning. In addition, social interaction scores in both Tg lines were reduced in an isolation-induced resident-intruder test. There were also phenotypic increases in a GABAergic marker (parvalbumin) as well as in myelination markers (myelin basic protein and 2',3'-cyclic nucleotide 3'-phosphodiesterase) in their frontal cortex, indicating the authenticity of NRG1 hyper-signaling, although there were marked decreases in tyrosine hydroxylase levels and dopamine content in the hippocampus.

conclusionsThese findings suggest that aberrant hyper-signals of NRG1 also disrupt various cognitive and behavioral processes. Thus, neuropathological implication of hyper NRG1 signaling in psychiatric diseases should be evaluated with further experimentation.

Indexed as

Gene Expression RegulationAlternative SplicingAnimalsDNA, ComplementaryDopamineFrontal LobeGenetic Predisposition to DiseaseHeterozygoteMiceMice, TransgenicMutationNeuregulin-1NeurogliaPhenotypePromoter Regions, GeneticDNA, ComplementaryDopamineNeuregulin-1

Identifiers

PMID21151609
PMCPMC3000321
OpenAlexW2052571439

What OpenQuestion holds

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Registered trials

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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.