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Social approach in genetically engineered mouse lines relevant to autism
Open accessAbstract
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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“Studies aimed at modeling, in animals, the core phenotypes associated with ASDs have focused on studying social and repetitive behaviors in mice [530-532] and pair-bonding behaviors in the prairie vole (Microtus ochrogaster) [533,534].”
From Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings (2012) · cites this paper as [531]
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“The physical features can include: a long narrow face with large protruding ears, connective tissue abnormalities (i.e. hyperextensive joints), macroorchidism, macrocephaly, obesity (especially in young males), loose skin over the hands, a high arched palate, a vertical plantar crease and flat feet (Moy et al., 2009; Schapiro et al., 1995).”
From Oxytocin and vasopressin systems in genetic syndromes and neurodevelopmental disorders (2014) · cites this paper as Moy et al., 2009
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Metadata
- 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.
- Venue
- Genes, Brain and Behavior
- Publisher
- Wiley
- Published
- 2009-03
- Volume
- 8
- Issue
- 2
- Pages
- 129-142
- ISSN
- 1601-183X (ISSN-L)
- 1601-1848
- 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
- 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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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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