Evidence map›Paper›PMID 26748053›Full record

ArticleNeuropharmacology2016

Reversal of social deficits by subchronic oxytocin in two autism mouse models.

Brian L Teng, Viktoriya D Nikolova, Natallia V Riddick, Kara L Agster, James J Crowley, Lorinda K Baker, Beverly H Koller, Cort A Pedersen, Michael B Jarstfer, Sheryl S Moy

Open access · hybridAbstract read
In one paragraph

Article in Neuropharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
11.5field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

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  5. Acute, chronic and conditioned effects of intranasal oxytocin in the mu-opioid receptor knockout mouse model of autism: Social context matters.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
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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

10 authors at 1 institution in 1 country.

Brian L TengCarolina Institute for Developmental Disabilities, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Eshelman School of Pharmacy, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.
Viktoriya D NikolovaCarolina Institute for Developmental Disabilities, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Department of Psychiatry, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.
Natallia V RiddickCarolina Institute for Developmental Disabilities, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Department of Psychiatry, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.
Kara L AgsterCarolina Institute for Developmental Disabilities, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Department of Psychiatry, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.
James J CrowleyDepartment of Genetics, University of North Carolina, Chapel Hill, NC 27599, USA.
Lorinda K BakerCarolina Institute for Developmental Disabilities, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Department of Psychiatry, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.
Beverly H KollerDepartment of Genetics, University of North Carolina, Chapel Hill, NC 27599, USA.
Cort A PedersenCarolina Institute for Developmental Disabilities, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Department of Psychiatry, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.
Michael B JarstferCarolina Institute for Developmental Disabilities, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Eshelman School of Pharmacy, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.
Sheryl S MoyCarolina Institute for Developmental Disabilities, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Department of Psychiatry, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA. Electronic address: ssmoy@med.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

UNC MRDD Research CenterP30HD003110 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI HATTON, DEBORAH · 1985 to 2012
$28.7M
Preclinical CoreU54HD079124 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MOY, SHERYL S · 2013 to 2019
$8.0M
Early Intervention in a mouse model of NMDA hypofunctionR01MH080069 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MOY, SHERYL S · 2008 to 2012
$1.4M
Systems Genetics of Fluoxetine-Induced Neurogenesis and Antidepressant ResponseK01MH094406 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CROWLEY, JAMES JOSEPH · 2012 to 2015
$588k
NICHD NIH HHS P30 HD003110NICHD NIH HHS U54 HD079124NIMH NIH HHS K01 MH094406NIMH NIH HHS R01 MH080069
6 · The paper itself

Abstract

Social deficits are a hallmark feature of autism spectrum disorder (ASD) and related developmental syndromes. Although there is no standard treatment for social dysfunction, clinical studies have identified oxytocin as a potential therapeutic with prosocial efficacy. We have previously reported that peripheral oxytocin treatment can increase sociability and ameliorate repetitive stereotypy in adolescent mice from the C58/J model of ASD-like behavior. In the present study, we determined that prosocial oxytocin effects were not limited to the adolescent period, since C58/J mice, tested in adulthood, demonstrated significant social preference up to 2 weeks following subchronic oxytocin treatment. Oxytocin was also evaluated in adult mice with underexpression of the N-methyl-d-aspartate receptor NR1 subunit (encoded by Grin1), a genetic model of autism- and schizophrenia-like behavior. Subchronic oxytocin had striking prosocial efficacy in male Grin1 knockdown mice; in contrast, chronic regimens with clozapine (66 mg/kg/day) or risperidone (2 mg/kg/day) failed to reverse deficits in sociability. Neither the subchronic oxytocin regimen, nor chronic treatment with clozapine or risperidone, reversed impaired prepulse inhibition in the Grin1 knockdown mice. Overall, these studies demonstrate oxytocin can enhance sociability in mouse models with divergent genotypes and behavioral profiles, adding to the evidence that this neurohormone could have therapeutic prosocial efficacy across a spectrum of developmental disorders.

Indexed as

Social BehaviorAnimalsAutism Spectrum DisorderBehavior, AnimalChoice BehaviorDisease Models, AnimalFemaleGene Knockdown TechniquesHyperkinesisMaleMiceNerve Tissue ProteinsOxytocinPrepulse InhibitionReceptors, N-Methyl-D-AspartateGprin1 protein, mouseNerve Tissue ProteinsOxytocinReceptors, N-Methyl-D-AspartateAutism spectrum disordersClozapineOxytocinRisperidoneSchizophreniaSociability

Identifiers

PMID26748053
PMCPMC4873352
OpenAlexW2197651963

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.