Evidence map›Paper›PMID 32498016›Full record

ArticleiScience2020

AUTS2 Regulation of Synapses for Proper Synaptic Inputs and Social Communication.

Kei Hori, Kunihiko Yamashiro, Taku Nagai, Wei Shan, Saki F Egusa, Kazumi Shimaoka, Hiroshi Kuniishi, Masayuki Sekiguchi, Yasuhiro Go, Shoji Tatsumoto and 14 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.2field-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

31 citing papers in PubMed, 49 citations in OpenAlex.

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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

24 authors at 7 institutions in 1 country.

Kei HoriDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan. Electronic address: khori@ncnp.go.jp.
Kunihiko YamashiroDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan.
Taku NagaiDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya 466-8560, Japan.
Wei ShanDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya 466-8560, Japan.
Saki F EgusaDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan.
Kazumi ShimaokaDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan.
Hiroshi KuniishiDepartment of Neuropsychopharmacology, National Institute of Mental Health, NCNP, Tokyo, 187-8502, Japan; Department of Degenerative Neurological Diseases, National Institute of Neuroscience, NCNP, Tokyo, 187-8502, Japan.
Masayuki SekiguchiDepartment of Degenerative Neurological Diseases, National Institute of Neuroscience, NCNP, Tokyo, 187-8502, Japan.
Yasuhiro GoCognitive Genomics Research Group, Exploratory Research Center on Life and Living Systems, National Institutes of Natural Sciences, Okazaki, Aichi 444-8585, Japan; School of Life Science, SOKENDAI (The Graduate University for Advanced Studies), Okazaki, Aichi 444-8585, Japan; Department of Physiological Sciences, National Institute for Physiological Sciences, Okazaki, Aichi 444-8585, Japan.
Shoji TatsumotoCognitive Genomics Research Group, Exploratory Research Center on Life and Living Systems, National Institutes of Natural Sciences, Okazaki, Aichi 444-8585, Japan.
Mitsuyo YamadaDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan; Department of Biomolecular Science, Faculty of Science, Toho University, Chiba 274-8510, Japan.
Reika ShiraishiDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan.
Kouta KannoDepartment of Humanities, Faculty of Law, Economics and the Humanities, Kagoshima University, Kagoshima 890-0065, Japan.
Satoshi MiyashitaDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan.
Asami SakamotoDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan.
Manabu AbeDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Nigata 951-8585, Japan.
Kenji SakimuraDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Nigata 951-8585, Japan.
Masaki SoneDepartment of Biomolecular Science, Faculty of Science, Toho University, Chiba 274-8510, Japan.
Kazuhiro SohyaDepartment of Mental Disorder Research, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan.
Hiroshi KunugiDepartment of Mental Disorder Research, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan.
Keiji WadaDepartment of Degenerative Neurological Diseases, National Institute of Neuroscience, NCNP, Tokyo, 187-8502, Japan.
Mitsuhiko YamadaDepartment of Neuropsychopharmacology, National Institute of Mental Health, NCNP, Tokyo, 187-8502, Japan.
Kiyofumi YamadaDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya 466-8560, Japan.
Mikio HoshinoDepartment of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan. Electronic address: hoshino@ncnp.go.jp.
National Center of Neurology and Psychiatry · JPNagoya University Hospital · JPNational Institutes of Natural Sciences · JPNiigata University · JPKagoshima University · JPNational Institute of Mental Health · JPToho University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Impairments in synapse development are thought to cause numerous psychiatric disorders. Autism susceptibility candidate 2 (AUTS2) gene has been associated with various psychiatric disorders, such as autism and intellectual disabilities. Although roles for AUTS2 in neuronal migration and neuritogenesis have been reported, its involvement in synapse regulation remains unclear. In this study, we found that excitatory synapses were specifically increased in the Auts2-deficient primary cultured neurons as well as Auts2 mutant forebrains. Electrophysiological recordings and immunostaining showed increases in excitatory synaptic inputs as well as c-fos expression in Auts2 mutant brains, suggesting that an altered balance of excitatory and inhibitory inputs enhances brain excitability. Auts2 mutant mice exhibited autistic-like behaviors including impairments in social interaction and altered vocal communication. Together, these findings suggest that AUTS2 regulates excitatory synapse number to coordinate E/I balance in the brain, whose impairment may underlie the pathology of psychiatric disorders in individuals with AUTS2 mutations.

Indexed as

Behavioral NeuroscienceMolecular NeuroscienceNeuroscienceTranscriptomics

Identifiers

PMID32498016
PMCPMC7267731
OpenAlexW3026770356

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.