Evidence map›Paper›PMID 31988060›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020

Interneuron Transplantation Rescues Social Behavior Deficits without Restoring Wild-Type Physiology in a Mouse Model of Autism with Excessive Synaptic Inhibition.

Derek G Southwell, Helia Seifikar, Ruchi Malik, Karen Lavi, Daniel Vogt, John L Rubenstein, Vikaas S Sohal

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. 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
1.9field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

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  15. [Advances on GABAergic interneurons in autism spectrum disorders].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020
    Review
  16. Review
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

7 authors at 2 institutions in 3 countries.

Derek G SouthwellDepartment of Neurological Surgery, derek.southwell@duke.edu vikaas.sohal@ucsf.edu.ORCID 0000-0001-6465-3869
Helia SeifikarWeill Institute for Neurosciences.
Ruchi MalikWeill Institute for Neurosciences.ORCID 0000-0003-0611-8790
Karen LaviWeill Institute for Neurosciences.
Daniel VogtWeill Institute for Neurosciences.
John L RubensteinWeill Institute for Neurosciences.ORCID 0000-0002-4414-7667
Vikaas S SohalWeill Institute for Neurosciences, derek.southwell@duke.edu vikaas.sohal@ucsf.edu.ORCID 0000-0002-2238-4186
University of California, San Francisco · USKavli Institute for Theoretical Sciences · CN

Funding

Genetic Control of Basal Telencephalic DevelopmentR01MH081880 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUBENSTEIN, JOHN L. R. · 2009 to 2023
$8.1M
Genetic Regulation of Telencephalon DevelopmentR37MH049428 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUBENSTEIN, JOHN L. R. · 2008 to 2017
$5.9M
STRUCTURE, EXPRESSION &FUNCTION OF THE DLX GENE FAMILYR01MH049428 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUBENSTEIN, JOHN L. R. · 1992 to 2022
$5.8M
Reverse engineering the prefrontal microcircuitDP2MH100011 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SOHAL, VIKAAS SINGH · 2012 to 2012
$2.4M
Restoring cognition by optogenetically rescuing gamma rhythms in PFC interneuronsR01MH106507 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SOHAL, VIKAAS SINGH · 2015 to 2019
$2.0M
Identification of enhancers whose activity defines cortical interneuron typesU01MH105948 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUBENSTEIN, JOHN L. R., SOHAL, VIKAAS SINGH · 2014 to 2016
$1.5M
NIMH NIH HHS DP2 MH100011NIMH NIH HHS R01 MH049428NIMH NIH HHS R01 MH081880NIMH NIH HHS R01 MH106507NIMH NIH HHS R37 MH049428NIMH NIH HHS U01 MH105948
6 · The paper itself

Abstract

Manipulations that enhance GABAergic inhibition have been associated with improved behavioral phenotypes in autism models, suggesting that autism may be treated by correcting underlying deficits of inhibition. Interneuron transplantation is a method for increasing recipient synaptic inhibition, and it has been considered a prospective therapy for conditions marked by deficient inhibition, including neuropsychiatric disorders. It is unknown, however, whether interneuron transplantation may be therapeutically effective only for conditions marked by reduced inhibition, and it is also unclear whether transplantation improves behavioral phenotypes solely by normalizing underlying circuit defects. To address these questions, we studied the effects of interneuron transplantation in male and female mice lacking the autism-associated gene,

Indexed as

Brain Tissue TransplantationFetal Tissue TransplantationSocial BehaviorAnimalsAutistic DisorderDisease Models, AnimalElectroencephalographyExploratory BehaviorFemaleGABAergic NeuronsInterneuronsMaleMaze LearningMedian EminenceMiceMice, KnockoutPTEN PhosphohydrolasePten protein, mouseautismexcitatory/inhibitory balanceinterneuron transplantation

Identifiers

PMID31988060
PMCPMC7083289
OpenAlexW3002050219

What OpenQuestion holds

Textmetadata
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.