Sociability and motor functions in Shank1 mutant mice
Open accessAbstract
Autism is a neurodevelopmental disorder characterized by aberrant reciprocal social interactions, impaired communication, and repetitive behaviors. While the etiology remains unclear, strong evidence exists for a genetic component, and several synaptic genes have been implicated. SHANK genes encode a family of synaptic scaffolding proteins located postsynaptically on excitatory synapses. Mutations in SHANK genes have been detected in several autistic individuals. To understand the consequences of SHANK mutations relevant to the diagnostic and associated symptoms of autism, comprehensive behavioral phenotyping on a line of Shank1 mutant mice was conducted on multiple measures of social interactions, social olfaction, repetitive behaviors, anxiety-related behaviors, motor functions, and a series of control measures for physical abilities. Results from our comprehensive behavioral phenotyping battery indicated that adult Shank1 null mutant mice were similar to their wildtype and heterozygous littermates on standardized measures of general health, neurological reflexes and sensory skills. Motor functions were reduced in the null mutants on open field activity, rotarod, and wire hang, replicating and extending previous findings (Hung et al., 2008). A partial anxiety-like phenotype was detected in the null mutants in some components of the light ↔ dark task, as previously reported (Hung et al., 2008) but not in the elevated plus-maze. Juvenile reciprocal social interactions did not differ across genotypes. Interpretation of adult social approach was confounded by a lack of normal sociability in wildtype and heterozygous littermates. All genotypes were able to discriminate social odors on an olfactory habituation/dishabituation task. All genotypes displayed relatively high levels of repetitive self-grooming. Our findings support the interpretation that Shank1 null mice do not demonstrate autism-relevant social interaction deficits, but confirm and extend a role for Shank1 in motor functions.
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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 Silverman et al., 2011
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 Silverman et al., 2011
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Self-citation
- Authors
- Silverman, J. L., Turner, S. M., Barkan, C. L., Tolu, S. S., Saxena, R., Hung, A. Y., Sheng, M., & Crawley, J. N.
- Affiliations
- National Institutes of Health (US)
- Massachusetts Institute of Technology (US)
- Corresponding author
- Silverman, Jill L.
- ORCID
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2011-03
- Volume
- 1380
- Pages
- 120-137
- ISSN
- 0006-8993 (ISSN-L)
- PMC
- PMC3041833
- OpenAlex
- W2065643355
- Cited by
- 218
- References
- 108
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 12 · 2023: 10 · 2022: 10 · 2021: 16 · 2020: 13 · 2019: 10 · 2018: 7 · 2017: 22 · 2016: 15 · 2015: 23 · 2014: 19 · 2013: 16 · 2012: 26
- FWCI
- 9.26
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc-nd)
- Funders
- National Institute of Mental Health Intramural Research Program and by a Simons Foundation grant to A.H. and M.S.
- 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 › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Shank1, autism spectrum disorder, synaptic scaffolding proteins, sociability, motor function, anxiety-like behavior, open field behavior, rotarod test, social interaction deficits
- MeSH terms
- Animals, Autistic Disorder, Mental Disorders, Disease Models, Animal, Female, Male, Membrane Proteins, Mice, Inbred C57BL, Mice, Mutant Strains, Movement Disorders, Nerve Tissue Proteins, Social Behavior, Transplantation Chimera, Mice, Knockout, Genetic Predisposition to Disease, Animals, Genetically Modified, Mice, Mice, 129 Strain
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