Evidence map›Paper›PMID 34253921›Full record

ArticleNature neuroscience2021

Reduced sociability and social agency encoding in adult Shank3-mutant mice are restored through gene re-expression in real time.

Daniel K Lee, S William Li, Firas Bounni, Gabriel Friedman, Mohsen Jamali, Leah Strahs, Omer Zeliger, Pauline Gabrieli, Michael A Stankovich, Jack Demaree and 1 more

Open access · greenAbstract read
In one paragraph

Article in Nature neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 30 citations in OpenAlex.

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  14. Neural circuits regulating prosocial behaviors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
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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

11 authors at 4 institutions in 1 country.

Daniel K Lee *Harvard-MIT Division of Health Sciences and Technology, Boston, MA, USA.
S William Li *Department of Neurosurgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Firas Bounni *Department of Neurosurgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Gabriel Friedman *Department of Neurosurgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Mohsen JamaliDepartment of Neurosurgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-1750-7591
Leah StrahsNortheastern University, Boston, MA, USA.
Omer ZeligerNortheastern University, Boston, MA, USA.
Pauline GabrieliHarvard University, Cambridge, MA, USA.
Michael A StankovichDepartment of Neurosurgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Jack DemareeNortheastern University, Boston, MA, USA.
Ziv M WilliamsHarvard-MIT Division of Health Sciences and Technology, Boston, MA, USA. zwilliams@mgh.harvard.edu.ORCID http://orcid.org/0000-0002-0017-0048
Harvard University · USNortheastern University · USBoston University · USHarvard University Press · US

Funding

Neuroscience Resident Research ProgramUE5NS065743 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI SYDNEY S CASH, Ziv Williams · 2024 to 2026
$2.6M
Using game theory in primates to study the distributed neuronal and time-casual underpinnings of interactive social behaviorR01MH112846 · NIMH · MASSACHUSETTS GENERAL HOSPITAL · PI WILLIAMS, ZIV · 2017 to 2021
$2.0M
Neuronal based prosthetic control of volitional movementR01HD059852 · NICHD · MASSACHUSETTS GENERAL HOSPITAL · PI WILLIAMS, ZIV · 2009 to 2015
$2.0M
Studying Memory Retrieval at the Dynamic Neural Network LevelR01NS091390 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI WILLIAMS, ZIV · 2015 to 2019
$1.8M
Howard Hughes Medical InstituteNICHD NIH HHS R01 HD059852NIMH NIH HHS R01 MH112846NINDS NIH HHS R01 NS091390NINDS NIH HHS UE5 NS065743
6 · The paper itself

Abstract

Despite a growing understanding of the molecular and developmental basis of autism spectrum disorder (ASD), how the neuronal encoding of social information is disrupted in ASD and whether it contributes to abnormal social behavior remains unclear. Here, we disrupted and then restored expression of the ASD-associated gene Shank3 in adult male mice while tracking the encoding dynamics of neurons in the medial prefrontal cortex (mPFC) over weeks. We find that Shank3 disruption led to a reduction of neurons encoding the experience of other mice and an increase in neurons encoding the animal's own experience. This shift was associated with a loss of ability by neurons to distinguish other from self and, therefore, the inability to encode social agency. Restoration of Shank3 expression in the mPFC reversed this encoding imbalance and increased sociability over 5-8 weeks. These findings reveal a neuronal-encoding process that is necessary for social behavior and that may be disrupted in ASD.

Indexed as

Social BehaviorAnimalsAutism Spectrum DisorderMaleMiceMice, Inbred C57BLMicrofilament ProteinsNerve Tissue ProteinsNeuronsPrefrontal CortexMicrofilament ProteinsNerve Tissue ProteinsShank3 protein, mouse

Identifiers

PMID34253921
PMCPMC8410666
OpenAlexW3179442887

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.