| Project/Area Number |
17591232
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | University of the Air |
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Principal Investigator |
SEMBA Juni'chi Faculty of Liberal Arts, University of the Air, Professor, 教養学部, 教授 (30183429)
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| Co-Investigator(Kenkyū-buntansha) |
SUHARA Tetsuya University of the Air, National Institute of Radiological Medicine, Senior Researcher, 分子イメージング研究センター, 特別上席研究員 (90216490)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 2006: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | neurodevelopmental disorder / schizophrenia / animal model / dopamine transporter / apoptosis / Bcl-2 / Bax |
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| Research Abstract |
Methylazoxymethanol (MAM) is known to cause neurodeveolpmental abnormalities in the brain when administered to pregnant rats. We assessed the validity of prenatal exposure of MAM as an animal model of schizophrenia. MAM was administered to pregnant rats at GD 17 at a dose of 25 mg/kg intraperitoneally. The brain of rats at PD 21 showed an disrupted array of granular cell layer in the hippocampus and reduced width of the cortex. Thus, we confirmed the validity of prenatal MAM exposure as an animal model for schizophrenia. In next experiment, rats were exposed with MAM in their prenatal period and were challenged with 5 mg/kg methamphetamine daily for 5 days from PD 7. This period is considered to be equivalent with human pubertal period. The function of dopamine transporter (DAT) was examined by the expression of DAT mRNA in the ventral tegmental area or substantia nigra as a measure. DAT mRNA expression was not altered by MAM pretreatment. At the same time, the expressions of Bcl-2 and Bax protein, both of which are related to apoptosis of the neurons, were also examined. The expressions of Bcl-2 and Bax in the striatum were not changed by MAM pretreatment. These findings suggest that prenatal MAM exposure induce an abnormal development of neurons in the brain, but did not change either the function of DAT or the expression of apoptosis-related proteins (Bcl-2 and Bax).
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