Sociability and motor functions in Shank1 mutant mice

Jill L Silverman, Sarah M. Turner, Charlotte L. Barkan, Seda S. Tolu, Roheeni Saxena, Albert Y. Hung, Morgan Sheng, Jacqueline Crawley

Research output: Contribution to journalArticle

128 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)120-137
Number of pages18
JournalBrain Research
Volume1380
DOIs
StatePublished - Mar 22 2011
Externally publishedYes

Fingerprint

Interpersonal Relations
Autistic Disorder
Genotype
Anxiety
Genes
Grooming
Mutation
Aptitude
Smell
Synapses
Reflex
Communication
Phenotype
Light
Health
Proteins

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Neurology
  • Developmental Biology
  • Molecular Biology

Cite this

Sociability and motor functions in Shank1 mutant mice. / Silverman, Jill L; Turner, Sarah M.; Barkan, Charlotte L.; Tolu, Seda S.; Saxena, Roheeni; Hung, Albert Y.; Sheng, Morgan; Crawley, Jacqueline.

In: Brain Research, Vol. 1380, 22.03.2011, p. 120-137.

Research output: Contribution to journalArticle

Silverman, JL, Turner, SM, Barkan, CL, Tolu, SS, Saxena, R, Hung, AY, Sheng, M & Crawley, J 2011, 'Sociability and motor functions in Shank1 mutant mice', Brain Research, vol. 1380, pp. 120-137. https://doi.org/10.1016/j.brainres.2010.09.026
Silverman JL, Turner SM, Barkan CL, Tolu SS, Saxena R, Hung AY et al. Sociability and motor functions in Shank1 mutant mice. Brain Research. 2011 Mar 22;1380:120-137. https://doi.org/10.1016/j.brainres.2010.09.026
Silverman, Jill L ; Turner, Sarah M. ; Barkan, Charlotte L. ; Tolu, Seda S. ; Saxena, Roheeni ; Hung, Albert Y. ; Sheng, Morgan ; Crawley, Jacqueline. / Sociability and motor functions in Shank1 mutant mice. In: Brain Research. 2011 ; Vol. 1380. pp. 120-137.
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