Analysis of self-other recognition in mice model for autism
| Project/Area Number |
24700380
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | The Institute of Physical and Chemical Research (2013-2014)
Hiroshima University (2012) |
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Principal Investigator |
TAMADA Kota 独立行政法人理化学研究所, 脳科学総合研究センター, 研究員 (10550957)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 自閉症 / 自他認識 / モデルマウス / セリン / 発達障害 / 行動異常 / アミノ酸 / 行動 / セロトニン |
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| Outline of Final Research Achievements |
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by less social interaction / communication or repetitive behaviors. Despite recent intensive researches, its molecular mechanism remains largely unclear. Recently, our research group succeeded to generate mice model (patDp/+) for ASD that have duplicated chromosome 7B to C region, corresponding to human chromosome 15q11-13 which is one of the responsible locus for ASD. In this study, we addressed the self-other recognition mechanism by using this model and tried to find causative molecule in the brain. Compared to WT mice, patDp/+ mice showed altered brain activity stimulated by the odor of other mice or self. PatDp/+ mice had decreased levels of a specific amino acid in the brain both in adult and postnatal developmental period. These results suggest that the imbalance of amino acids in brain might be a critical role in the social abnormalities found in ASD.
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Report
(4 results)
Research Products
(1 results)
