Evidence map›Paper›PMID 33933000›Full record

ArticleBMC neuroscience2021

Oxytocin ameliorates impaired social behavior in a Chd8 haploinsufficiency mouse model of autism.

Stanislav M Cherepanov, Maria Gerasimenko, Teruko Yuhi, Kazumi Furuhara, Chiharu Tsuji, Shigeru Yokoyama, Keiichi I Nakayama, Masaaki Nishiyama, Haruhiro Higashida

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2021. 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
4.6field-weighted citation impact, top 5% 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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  5. Acute, chronic and conditioned effects of intranasal oxytocin in the mu-opioid receptor knockout mouse model of autism: Social context matters.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
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  14. Article
  15. Oxytocin in Women's Health and Disease.Frontiers in endocrinology · 2022
    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

9 authors at 2 institutions in 1 country.

Stanislav M Cherepanov *Department of Basic Research on Social Recognition and Memory, Research Center for Child Mental Development, Kanazawa University, Kanazawa, 920-8640, Japan.
Maria Gerasimenko *Department of Basic Research on Social Recognition and Memory, Research Center for Child Mental Development, Kanazawa University, Kanazawa, 920-8640, Japan.
Teruko YuhiDepartment of Basic Research on Social Recognition and Memory, Research Center for Child Mental Development, Kanazawa University, Kanazawa, 920-8640, Japan.
Kazumi FuruharaDepartment of Basic Research on Social Recognition and Memory, Research Center for Child Mental Development, Kanazawa University, Kanazawa, 920-8640, Japan.
Chiharu TsujiDepartment of Basic Research on Social Recognition and Memory, Research Center for Child Mental Development, Kanazawa University, Kanazawa, 920-8640, Japan.
Shigeru YokoyamaDepartment of Basic Research on Social Recognition and Memory, Research Center for Child Mental Development, Kanazawa University, Kanazawa, 920-8640, Japan.
Keiichi I NakayamaDepartment of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, 812-8582, Japan.
Masaaki NishiyamaDepartment of Histology and Cell Biology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, 920-8640, Japan.
Haruhiro HigashidaDepartment of Basic Research on Social Recognition and Memory, Research Center for Child Mental Development, Kanazawa University, Kanazawa, 920-8640, Japan. haruhiro@med.kanazawa-u.ac.jp.ORCID 0000-0002-1779-0606
Kanazawa University · JPKyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutism spectrum disorder (ASD) is characterized by the core symptoms of impaired social interactions. Increasing evidence suggests that ASD has a strong genetic link with mutations in chromodomain helicase DNA binding protein 8 (CHD8), a gene encoding a chromatin remodeler. It has previously been shown that Chd8 haplodeficient male mice manifest ASD-like behavioral characteristics such as anxiety and altered social behavior. Along with that, oxytocin (OT) is one of the main neuropeptides involved in social behavior. Administration of OT has shown improvement of social behavior in genetic animal models of ASD. The present study was undertaken to further explore behavioral abnormalities of Chd8 haplodeficient mice of both sexes, their link with OT, and possible effects of OT administration. First, we performed a battery of behavioral tests on wild-type and Chd8

resultsWe showed general anxiety phenotype in Chd8

conclusionsHere, we demonstrated that abnormal social behaviors were observed in both male and female Chd8

Indexed as

Social BehaviorAnimalsAutistic DisorderDNA-Binding ProteinsFemaleHaploinsufficiencyMaleMaze LearningMiceMice, TransgenicOxytocinDNA-Binding Proteinsduplin protein, mouseOxytocinAnxietyAutismCHD8OxytocinSocial novelty

Identifiers

PMID33933000
PMCPMC8088024
OpenAlexW3157987932

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.