Communication impairments in mice lacking Shank1: reduced levels of ultrasonic vocalizations and scent marking behavior
Open accessAbstract
Autism is a neurodevelopmental disorder with a strong genetic component. Core symptoms are abnormal reciprocal social interactions, qualitative impairments in communication, and repetitive and stereotyped patterns of behavior with restricted interests. Candidate genes for autism include the SHANK gene family, as mutations in SHANK2 and SHANK3 have been detected in several autistic individuals. SHANK genes code for a family of scaffolding proteins located in the postsynaptic density of excitatory synapses. To test the hypothesis that a mutation in SHANK1 contributes to the symptoms of autism, we evaluated Shank1(-/-) null mutant mice for behavioral phenotypes with relevance to autism, focusing on social communication. Ultrasonic vocalizations and the deposition of scent marks appear to be two major modes of mouse communication. Our findings revealed evidence for low levels of ultrasonic vocalizations and scent marks in Shank1(-/-) mice as compared to wildtype Shank1(+/+) littermate controls. Shank1(-/-) pups emitted fewer vocalizations than Shank1(+/+) pups when isolated from mother and littermates. In adulthood, genotype affected scent marking behavior in the presence of female urinary pheromones. Adult Shank1(-/-) males deposited fewer scent marks in proximity to female urine than Shank1(+/+) males. Call emission in response to female urinary pheromones also differed between genotypes. Shank1(+/+) mice changed their calling pattern dependent on previous female interactions, while Shank1(-/-) mice were unaffected, indicating a failure of Shank1(-/-) males to learn from a social experience. The reduced levels of ultrasonic vocalizations and scent marking behavior in Shank1(-/-) mice are consistent with a phenotype relevant to social communication deficits in autism.
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Behavioral analyses revealed subtle impairments in social interaction and communication as well as increased repetitive behaviors in Shank1 mutant mice.
“Behavioral analyses revealed subtle impairments in social interaction and communication as well as increased repetitive behaviors (Silverman et al., 2011; Wohr et al., 2011).”
From Modeling Autism by SHANK Gene Mutations in Mice (2013) · cites this paper as Wohr et al., 2011
Shank1 mutant mice with a deletion of exons 14-15 encoding the PDZ domain were first reported in 2007, and more extensive behavioral analyses were conducted subsequently.
“Shank1 mutant mice with a deletion of exons 14-15 encoding the PDZ domain were first reported in 2007 (Hung et al., 2008) (Figure 3C) and more extensive behavioral analyses were conducted subsequently (Silverman et al., 2011; Wohr et al., 2011).”
From Modeling Autism by SHANK Gene Mutations in Mice (2013) · cites this paper as Wohr et al., 2011
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- Authors
- Wöhr, M., Roullet, F. I., Hung, A. Y., Sheng, M., & Crawley, J. N.
- Affiliations
- National Institutes of Health (US)
- Massachusetts Institute of Technology (US)
- Corresponding author
- Wöhr, Markus
- Crawley, Jacqueline N.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2011-06-09
- Volume
- 6
- Issue
- 6
- Pages
- e20631
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3111434
- OpenAlex
- W2115330604
- Cited by
- 220
- References
- 126
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 10 · 2023: 11 · 2022: 14 · 2021: 14 · 2020: 10 · 2019: 11 · 2018: 9 · 2017: 16 · 2016: 21 · 2015: 23 · 2014: 21 · 2013: 19 · 2012: 22
- FWCI
- 13.17
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, public-domain)
- PubMed Central (publishedVersion, public-domain)
- PubMed (publishedVersion)
- Lirias (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc)
- Funders
- National Institutes of Health
- National Institute of Mental Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Keywords
- Shank1, autism spectrum disorder, social communication, ultrasonic vocalizations, scent marking, urinary pheromones, postsynaptic scaffolding proteins, social learning, social behavior deficits
- MeSH terms
- Aging, Animals, Body Temperature, Body Weight, Female, Male, Membrane Proteins, Nerve Tissue Proteins, Odorants, Reflex, Ultrasonics, Vocalization, Animal, Mice
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.
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