Evidence map›Paper›PMID 37612363›Full record

ReviewMolecular psychiatry2023

Social circuits and their dysfunction in autism spectrum disorder.

Masaaki Sato, Nobuhiro Nakai, Shuhei Fujima, Katrina Y Choe, Toru Takumi

Open access · hybridAbstract readReview
In one paragraph

Review in Molecular psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
36.0field-weighted citation impact, top 1% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.

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4 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

5 authors at 4 institutions in 2 countries.

Masaaki SatoDepartment of Neuropharmacology, Hokkaido University Graduate School of Medicine, Kita, Sapporo, 060-8638, Japan.
Nobuhiro NakaiDepartment of Physiology and Cell Biology, Kobe University School of Medicine, Chuo, Kobe, 650-0017, Japan.ORCID 0000-0002-7171-230X
Shuhei FujimaDepartment of Physiology and Cell Biology, Kobe University School of Medicine, Chuo, Kobe, 650-0017, Japan.
Katrina Y ChoeDepartment of Psychology, Neuroscience & Behaviour, McMaster University, Hamilton, ON, Canada.
Toru TakumiDepartment of Physiology and Cell Biology, Kobe University School of Medicine, Chuo, Kobe, 650-0017, Japan. takumit@med.kobe-u.ac.jp.ORCID 0000-0001-7153-266X
Kobe University · JPHokkaido University · JPMcMaster University · CARIKEN Center for Biosystems Dynamics Research · JP

Funding

Japan Society for the Promotion of Science London (JSPS London) 17H05985,MEXT | Japan Society for the Promotion of Science (JSPS) 16H06316
6 · The paper itself

Abstract

Social behaviors, how individuals act cooperatively and competitively with conspecifics, are widely seen across species. Rodents display various social behaviors, and many different behavioral paradigms have been used for investigating their neural circuit bases. Social behavior is highly vulnerable to brain network dysfunction caused by neurological and neuropsychiatric conditions such as autism spectrum disorders (ASDs). Studying mouse models of ASD provides a promising avenue toward elucidating mechanisms of abnormal social behavior and potential therapeutic targets for treatment. In this review, we outline recent progress and key findings on neural circuit mechanisms underlying social behavior, with particular emphasis on rodent studies that monitor and manipulate the activity of specific circuits using modern systems neuroscience approaches. Social behavior is mediated by a distributed brain-wide network among major cortical (e.g., medial prefrontal cortex (mPFC), anterior cingulate cortex, and insular cortex (IC)) and subcortical (e.g., nucleus accumbens, basolateral amygdala (BLA), and ventral tegmental area) structures, influenced by multiple neuromodulatory systems (e.g., oxytocin, dopamine, and serotonin). We particularly draw special attention to IC as a unique cortical area that mediates multisensory integration, encoding of ongoing social interaction, social decision-making, emotion, and empathy. Additionally, a synthesis of studies investigating ASD mouse models demonstrates that dysfunctions in mPFC-BLA circuitry and neuromodulation are prominent. Pharmacological rescues by local or systemic (e.g., oral) administration of various drugs have provided valuable clues for developing new therapeutic agents for ASD. Future efforts and technological advances will push forward the next frontiers in this field, such as the elucidation of brain-wide network activity and inter-brain neural dynamics during real and virtual social interactions, and the establishment of circuit-based therapy for disorders affecting social functions.

Indexed as

Autism Spectrum DisorderAnimalsBrainMiceNucleus AccumbensPrefrontal CortexSocial Behavior

Identifiers

PMID37612363
PMCPMC10618103
OpenAlexW4386100739

What OpenQuestion holds

Textmetadata
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.