Sociability and motor functions in Shank1 mutant mice
Name
nihms239618.pdf
Description
Accepted version
Size
2.15 MB
Format
Unknown
Checksum (MD5)
7fc0eb7c26b431f314d8b774e1ce0c83
Author(s)
Silverman, Jill L.
Turner, Sarah M.
Barkan, Charlotte L.
Tolu, Seda S.
Saxena, Roheeni
Hung, Albert Y.
Sheng, Morgan
Crawley, Jacqueline N.
Date Issued
September 2010
Journal
Brain Research
Publisher
Elsevier BV
Citation
Silverman, Jill L., et al. "Sociability and Motor Functions in Shank1 Mutant Mice." Brain Research 1380 (2011): 120-37.
Version
Author's final manuscript
Abstract
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.
MIT Department
Picower Institute for Learning and Memory
Terms of Use
Creative Commons Attribution-NonCommercial-NoDerivs License
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1016/j.brainres.2010.09.026
