Evidence map›Paper›PMID 38453903›Full record

ArticleTranslational psychiatry2024

Phenotypes for general behavior, activity, and body temperature in 3q29 deletion model mice.

Daisuke Mori, Ryosuke Ikeda, Masahito Sawahata, Sho Yamaguchi, Akiko Kodama, Takashi Hirao, Yuko Arioka, Hiroki Okumura, Chihiro Inami, Toshiaki Suzuki and 15 more

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. 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

25 authors at 7 institutions in 1 country.

Daisuke MoriDepartment of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan. d-mori@med.nagoya-u.ac.jp.ORCID 0000-0002-9072-2546
Ryosuke IkedaDepartment of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Masahito SawahataDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University, Graduate School of Medicine, Nagoya, Japan.
Sho YamaguchiDepartment of Neuropharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
Akiko KodamaDepartment of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Takashi HiraoDepartment of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yuko AriokaDepartment of Pathophysiology of Mental Disorders, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.ORCID 0000-0002-1792-8812
Hiroki OkumuraDepartment of Pathophysiology of Mental Disorders, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
Chihiro InamiDepartment of Pathophysiology of Mental Disorders, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
Toshiaki SuzukiDepartment of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID 0000-0002-0977-1317
Yu HayashiDepartment of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hidekazu KatoDepartment of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID 0000-0001-9995-504X
Yoshihiro NawaDepartment of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID 0000-0003-3164-2519
Seiko MiyataDepartment of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID 0000-0002-1144-5676
Hiroki KimuraDepartment of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Itaru KushimaDepartment of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID 0000-0002-0018-5178
Branko AleksicDepartment of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID 0000-0001-8982-4580
Hiroyuki MizoguchiDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University, Graduate School of Medicine, Nagoya, Japan.
Taku NagaiDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University, Graduate School of Medicine, Nagoya, Japan.ORCID 0000-0001-5050-7748
Takanobu NakazawaLaboratory of Molecular Biology, Department of Bioscience, Graduate School of Life Sciences, Tokyo University of Agriculture, Tokyo, Japan.ORCID 0000-0003-4863-1277
Ryota HashimotoDepartment of Pathology of Mental Diseases, National Institute of Mental Health, National Center of Neurology and Psychiatry, Tokyo, Japan.ORCID 0000-0002-5941-4238
Kozo KaibuchiDivision of Cell Biology, International Center for Brain Science, Fujita Health University, 1-98 Dengakugakubo, Kusukake-cho, Toyoake, Aichi, Japan.
Kazuhiko KumeDepartment of Neuropharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
Kiyofumi YamadaDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University, Graduate School of Medicine, Nagoya, Japan.
Norio OzakiDepartment of Pathophysiology of Mental Disorders, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.ORCID 0000-0002-7360-4898
Nagoya University · JPNagoya University Hospital · JPNagoya City University · JPFujita Health University · JPFujita Health University Hospital · JPNational Center of Neurology and Psychiatry · JPTokyo University of Agriculture · JP

Funding

Japan Agency for Medical Research and Development (AMED) JP19ak0101113Japan Agency for Medical Research and Development (AMED) JP19ak0101126Japan Agency for Medical Research and Development (AMED) JP19dm0207069Japan Agency for Medical Research and Development (AMED) JP19dm0207075Japan Agency for Medical Research and Development (AMED) JP20ek0109488Japan Agency for Medical Research and Development (AMED) JP21dk0307103Japan Agency for Medical Research and Development (AMED) JP21wm0425007Japan Agency for Medical Research and Development (AMED) JP22gm1410011Japan Agency for Medical Research and Development (AMED) JP22tm0424222Japan Agency for Medical Research and Development (AMED) JP23ak0101215Japan Agency for Medical Research and Development (AMED) JP23ek0109678Japan Agency for Medical Research and Development (AMED) JP23gm1910005Japan Agency for Medical Research and Development (AMED) P20dk0307099MEXT | Japan Society for the Promotion of Science (JSPS) 19K07384MEXT | Japan Society for the Promotion of Science (JSPS) 20K20602MEXT | Japan Society for the Promotion of Science (JSPS) 21H04815MEXT | Japan Society for the Promotion of Science (JSPS) 22K07369
6 · The paper itself

Abstract

Whole genome analysis has identified rare copy number variations (CNV) that are strongly involved in the pathogenesis of psychiatric disorders, and 3q29 deletion has been found to have the largest effect size. The 3q29 deletion mice model (3q29-del mice) has been established as a good pathological model for schizophrenia based on phenotypic analysis; however, circadian rhythm and sleep, which are also closely related to neuropsychiatric disorders, have not been investigated. In this study, our aims were to reevaluate the pathogenesis of 3q29-del by recreating model mice and analyzing their behavior and to identify novel new insights into the temporal activity and temperature fluctuations of the mouse model using a recently developed small implantable accelerometer chip, Nano-tag. We generated 3q29-del mice using genome editing technology and reevaluated common behavioral phenotypes. We next implanted Nano-tag in the abdominal cavity of mice for continuous measurements of long-time activity and body temperature. Our model mice exhibited weight loss similar to that of other mice reported previously. A general behavioral battery test in the model mice revealed phenotypes similar to those observed in mouse models of schizophrenia, including increased rearing frequency. Intraperitoneal implantation of Nano-tag, a miniature acceleration sensor, resulted in hypersensitive and rapid increases in the activity and body temperature of 3q29-del mice upon switching to lights-off condition. Similar to the 3q29-del mice reported previously, these mice are a promising model animals for schizophrenia. Successive quantitative analysis may provide results that could help in treating sleep disorders closely associated with neuropsychiatric disorders.

Indexed as

Developmental DisabilitiesIntellectual DisabilityAnimalsBody TemperatureChildChromosome DeletionDisease Models, AnimalDNA Copy Number VariationsHumansMicePhenotype

Identifiers

PMID38453903
PMCPMC10920862
OpenAlexW4392542694

What OpenQuestion holds

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LicenceCC BY
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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.