Evidence map›Paper›PMID 35908593›Full record

ReviewNeuroscience and biobehavioral reviews2022

Prefrontal circuits guiding social preference: Implications in autism spectrum disorder.

Abigail V Fortier, Olivia C Meisner, Amrita R Nair, Steve W C Chang

Abstract readReview
In one paragraph

Review in Neuroscience and biobehavioral reviews, 2022. 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
–field-weighted citation impact
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.

  1. Review
  2. Article
  3. Article
  4. Biomolecules · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Dopamine D1 receptor in medial prefrontal cortex mediates the effects of TAAR1 activation on chronic stress-induced cognitive and social deficits.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
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  16. 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

4 authors.

Abigail V FortierDepartment of Psychology, Yale University, New Haven, CT 06520, USA; Department of Molecular, Cellular, Developmental Biology, New Haven, CT 06520, USA.
Olivia C MeisnerDepartment of Psychology, Yale University, New Haven, CT 06520, USA; Department of Neuroscience, Yale University School of Medicine, New Haven, CT 06510, USA. Electronic address: olivia.meisner@yale.edu.
Amrita R NairDepartment of Psychology, Yale University, New Haven, CT 06520, USA.
Steve W C ChangDepartment of Psychology, Yale University, New Haven, CT 06520, USA; Department of Neuroscience, Yale University School of Medicine, New Haven, CT 06510, USA; Kavli Institute for Neuroscience, Yale University School of Medicine, New Haven, CT 06510, USA; Wu Tsai Institute, Yale University, New Haven, CT 06510, USA.

Funding

Behavioral and Neural Bases of Combining Oxytocin and Naloxone for Optimally Enhancing Interactive Social AttentionR01MH120081 · NIMH · YALE UNIVERSITY · PI CHANG, STEVE W. C. · 2019 to 2023
$2.7M
Toward A Macaque Model Of Social Brain Dysfunction In Real-Life Social InteractionsR01MH110750 · NIMH · YALE UNIVERSITY · PI CHANG, STEVE W. C. · 2016 to 2020
$2.5M
NIMH NIH HHS R01 MH110750NIMH NIH HHS R01 MH120081
6 · The paper itself

Abstract

Although Autism Spectrum Disorder (ASD) is increasing in diagnostic prevalence, treatment options are inadequate largely due to limited understanding of ASD's underlying neural mechanisms. Contributing to difficulties in treatment development is the vast heterogeneity of ASD, from physiological causes to clinical presentations. Recent studies suggest that distinct genetic and neurological alterations may converge onto similar underlying neural circuits. Therefore, an improved understanding of neural circuit-level dysfunction in ASD may be a more productive path to developing broader treatments that are effective across a greater spectrum of ASD. Given the social preference behavioral deficits commonly seen in ASD, dysfunction in circuits mediating social preference may contribute to the atypical development of social cognition. We discuss some of the animal models used to study ASD and examine the function and effects of dysregulation of the social preference circuits, notably the medial prefrontal cortex-amygdala and the medial prefrontal cortex-nucleus accumbens circuits, in these animal models. Using the common circuits underlying similar behavioral disruptions of social preference behaviors as an example, we highlight the importance of identifying disruption in convergent circuits to improve the translational success of animal model research for ASD treatment development.

Indexed as

Autism Spectrum DisorderAnimalsDisease Models, AnimalPrefrontal CortexSocial BehaviorSocial Behavior DisordersAmygdalaAutismCircuitsNucleus accumbensPrefrontal cortexSocial behaviorSocial preference

Identifiers

PMID35908593
PMCPMC10122914

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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.