Characterizing social behavior in genetically targeted mouse models of brain disorders

Methods Mol Biol. 2013:1017:95-104. doi: 10.1007/978-1-62703-438-8_7.

Abstract

Fragile X syndrome, the leading inherited cause of mental retardation and autism spectrum disorders worldwide, is caused by a tandem repeat expansion in the FMR1 (fragile X mental retardation 1) gene. It presents with a distinct behavioral phenotype which overlaps significantly with that of autism. Emerging evidence suggests that tandem repeat polymorphisms (TRPs) might also play a key role in modulating disease susceptibility for a range of common polygenic disorders, including the broader autism spectrum of disorders (ASD) and other forms of psychiatric illness such as schizophrenia, depression, and bipolar disorder [1]. In order to understand how TRPs and associated gene mutations mediate pathogenesis, various mouse models have been generated. A crucial step in such functional genomics is high-quality behavioral and cognitive phenotyping. This chapter presents a basic behavioral battery for standardized tests for assaying social phenotypes in mouse models of brain disorders, with a focus on aggression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autistic Disorder* / genetics
  • Autistic Disorder* / metabolism
  • Autistic Disorder* / pathology
  • Autistic Disorder* / physiopathology
  • Disease Models, Animal
  • Fragile X Mental Retardation Protein* / genetics
  • Fragile X Mental Retardation Protein* / metabolism
  • Fragile X Syndrome* / genetics
  • Fragile X Syndrome* / metabolism
  • Fragile X Syndrome* / pathology
  • Fragile X Syndrome* / physiopathology
  • Humans
  • Mice
  • Mice, Transgenic
  • Social Behavior*
  • Trinucleotide Repeat Expansion*

Substances

  • Fmr1 protein, mouse
  • Fragile X Mental Retardation Protein