Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 102, Issue 52, Pages 19132-19137Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0509635102
Keywords
22q11; habituation; hyperactivity; mouse model; schizophrenia
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Funding
- NIDCD NIH HHS [R01DC005186, R01 DC005186] Funding Source: Medline
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Human chromosome 22q11.2 has been implicated in various behavioral abnormalities, including schizophrenia and other neuropsychiatric/behavioral disorders. However, the specific genes within 22q11.2 that contribute to these disorders are still poorly understood. Here, we show that an approximate to 200-kb segment of human 22q11.2 causes specific behavioral abnormalities in mice. Mice that overexpress an approximate to 200-kb region of human 22q11.2, containing CDCrel, GP1B beta, TBX1, and WDR14, exhibited spontaneous sensitization of hyperactivity and a lack of habituation. These effects were ameliorated by antipsychotic drugs. The transgenic mice were also impaired in nesting behavior. Although Tbx1 has been shown to be responsible for many physical defects associated with 22q11.2 haploinsufficiency, Tbx1 heterozygous mice did not display these behavioral abnormalities. Our results show that the approximate to 200-kb region of 22q11.2 contains a gene(s) responsible for behavioral abnormalities and suggest that distinct genetic components within 22q11.2 mediate physical and behavioral abnormalities.
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