Cited by 246Genetics and Neurodevelopmental DisordersAutism Spectrum Disorder ResearchNeuroendocrine regulation and behavior

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Social approach in genetically engineered mouse lines relevant to autism

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Moy, S. S., Nadler, J. J., Young, N. B., Nonneman, R. J., Grossman, A. W., Murphy, D. L., D’Ercole, A. J., Crawley, J. N., Magnuson, T. R., Lauder, J. M.·2009·Genes, Brain and Behavior

DOI 10.1111/j.1601-183x.2008.00452.xPMC PMC2659808

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Abstract

Profound impairment in social interaction is a core symptom of autism, a severe neurodevelopmental disorder. Deficits can include a lack of interest in social contact and low levels of approach and proximity to other children. In this study, a three‐chambered choice task was used to evaluate sociability and social novelty preference in five lines of mice with mutations in genes implicated in autism spectrum disorders. Fmr1 tm1Cgr/Y(Fmr1−/y) mice represent a model for fragile X, a mental retardation syndrome that is partially comorbid with autism. We tested Fmr1−/ymice on two genetic backgrounds, C57BL/6J and FVB/N‐129/OlaHsd (FVB/129). Targeted disruption of Fmr1 resulted in low sociability on one measure, but only when the mutation was expressed on FVB/129. Autism has been associated with altered serotonin levels and polymorphisms in SLC6A4 (SERT), the serotonin transporter gene. Male mice with targeted disruption of Slc6a4 displayed significantly less sociability than wild‐type controls. Mice with conditional overexpression of Igf‐1 (insulin‐like growth factor‐1) offered a model for brain overgrowth associated with autism. Igf‐1 transgenic mice engaged in levels of social approach similar to wild‐type controls. Targeted disruption in other genes of interest, En2 (engrailed‐2) and Dhcr7, was carried on genetic backgrounds that showed low levels of exploration in the choice task, precluding meaningful interpretations of social behavior scores. Overall, results show that loss of Fmr1 or Slc6a4 gene function can lead to deficits in sociability. Findings from the fragile X model suggest that the FVB/129 background confers enhanced susceptibility to consequences of Fmr1 mutation on social approach.

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Authors: Moy, S. S., Nadler, J. J., Young, N. B., Nonneman, R. J., Grossman, A. W., Murphy, D. L., D’Ercole, A. J., Crawley, J. N., Magnuson, T. R., & Lauder, J. M.
Affiliations: University of North Carolina at Chapel Hill (US)
University of Illinois Urbana-Champaign (US)
National Institutes of Health (US)
National Institute of Mental Health (US)
Corresponding author: Moy, S. S.
ORCID: Moy, S. S.
Grossman, A. W.
Crawley, J. N.
Magnuson, T. R.
Venue: Genes, Brain and Behavior
Publisher: Wiley
Published: 2009-03
Volume: 8
Issue: 2
Pages: 129-142
ISSN: 1601-183X (ISSN-L)
1601-1848
DOI: 10.1111/j.1601-183x.2008.00452.x
PMC: PMC2659808
OpenAlex: W2076599994
Cited by: 246
References: 110
Citations by year: 2026: 5 · 2025: 5 · 2024: 3 · 2023: 9 · 2022: 10 · 2021: 9 · 2020: 12 · 2019: 15 · 2018: 10 · 2017: 14 · 2016: 20 · 2015: 11 · 2014: 23 · 2013: 15 · 2012: 25
FWCI: 11.43
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Genes Brain & Behavior (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
UNC Libraries
Funders: Autism Speaks (AS1847)
FRAXA Research Foundation
National Institutes of Health (5u54mh066418-05, HD 03110)
National Institute of Mental Health (U54-MH066418, U54 MH 66418, R01MH035321, R37MH035321, MH035321)
National Institute of Child Health and Human Development (P30-HD03110, HD03110)
Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD008299, P30-HD03110, P30HD003110, R01HD008299)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroendocrine regulation and behavior
Keywords: autism spectrum disorder, social behavior, sociability, social novelty preference, Fmr1 knockout mice, fragile X syndrome, serotonin transporter, brain overgrowth, EN2, DHCR7, genetic background effects, social approach
MeSH terms: Engrailed 2 Protein, Animals, Anxiety, Autistic Disorder, Behavior, Animal, Postural Balance, Exploratory Behavior, Female, Food Deprivation, Genetic Engineering, Insulin-Like Growth Factor I, Male, Mice, Inbred C57BL, Motor Activity, Nerve Tissue Proteins, Pregnancy, Sex Characteristics, Smell, Social Behavior, Mice, Knockout, Homeodomain Proteins, Oxidoreductases Acting on CH-CH Group Donors, Serotonin Plasma Membrane Transport Proteins, Mice, Fragile X Mental Retardation Protein, Fragile X Messenger Ribonucleoprotein 1

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