Genetic-background modulation of core and variable autistic-like symptoms in Fmr1 knock-out mice
Open accessAbstract
BACKGROUND: No animal models of autism spectrum disorders (ASD) with good construct validity are currently available; using genetic models of pathologies characterized by ASD-like deficits, but with known causes, may be therefore a promising strategy. The Fmr1-KO mouse is an example of this approach, modeling Fragile X syndrome, a well-known genetic disorder presenting ASD symptoms. The Fmr1-KO is available on different genetic backgrounds (FVB versus C57BL/6), which may explain some of the conflicting results that have been obtained with these mutants up till now. METHODS: Fmr1 KO and their wild-type littermates on both the FVB and C57BL/6 genetic backgrounds were examined on a battery of tests modeling the clinical symptoms of ASD, including the triad of core symptoms (alterations in social interaction and communication, presence of repetitive behaviors), as well as the secondary symptoms (disturbances in sensori-motor reactivity and in circadian patterns of activity, epileptic events). RESULTS: Fmr1-KO mice displayed autistic-like core symptoms of altered social interaction and occurrence of repetitive behaviors with additional hyperactivity. The genetic background modulated the effects of the Fmr1 deletion and it appears that the C57BL/6 background may be more suitable for further research on core autistic-like symptoms. CONCLUSIONS: The Fmr1-mouse line does not recapitulate all of the main core and secondary ASD symptoms, but still can be useful to elucidate the neurobiological mechanisms underlying specific ASD-like endophenotypes.
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Fmr1 KO mice, compared to wild-type, have lower than normal levels of initial social interactions, fail to show a preference for social novelty, and display inappropriate social responses.
“Fmr1 KO, in comparison to the wild-type (WT) strain, are described as having lower than normal levels of initial social interactions (Mineur et al., 2006), fail to show a preference for social novelty, and display inappropriate social responses (Pietropaolo et al., 2011).”
From Oxytocin and vasopressin systems in genetic syndromes and neurodevelopmental disorders (2014) · cites this paper as Pietropaolo et al., 2011
In research by Pietropaolo et al. (2011), the Fmr1 KO on the B6 background was found to be a good model for Fragile X syndrome and a suitable model for ASD.
“They found the Fmr1 KO on the B6 background to be a good model for FXS and a suitable model for ASD (Pietropaolo et al., 2011; Yan et al., 2004).”
From Oxytocin and vasopressin systems in genetic syndromes and neurodevelopmental disorders (2014) · cites this paper as Pietropaolo et al., 2011
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Self-citation
- Authors
- Pietropaolo, S., Guilleminot, A., Martin, B., D'Amato, F. R., & Crusio, W. E.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Inserm (FR)
- National Research Council (IT)
- Corresponding author
- Crusio, Wim E.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2011-02-22
- Volume
- 6
- Issue
- 2
- Pages
- e17073
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3043074
- OpenAlex
- W2002465714
- Cited by
- 178
- References
- 82
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 15 · 2023: 11 · 2022: 13 · 2021: 12 · 2020: 10 · 2019: 12 · 2018: 10 · 2017: 10 · 2016: 15 · 2015: 15 · 2014: 15 · 2013: 9 · 2012: 11
- FWCI
- 8.18
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- March of Dimes Foundation (12-FY05-1198)
- Institut National de la Santé et de la Recherche Médicale
- Centre National de la Recherche Scientifique (12-FY05-1198)
- Université de Bordeaux (12-FY05-1198)
- 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 › Developmental Neuroscience › Williams Syndrome Research
- Keywords
- autism spectrum disorder, Fmr1 knockout mice, fragile X syndrome, genetic background, FVB mice, C57BL/6 mice, social interaction deficits, repetitive behavior, hyperactivity, circadian activity, animal models of autism, endophenotypes
- MeSH terms
- Animals, Autistic Disorder, Behavior, Animal, Disease Models, Animal, Learning, Male, Mice, Inbred C57BL, Motor Activity, Phenotype, Mice, Knockout, Genetic Heterogeneity, Genetic Predisposition to Disease, Mice, Fragile X Messenger Ribonucleoprotein 1, Endophenotypes
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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