| Project/Area Number |
23510072
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Risk sciences of radiation/Chemicals
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| Research Institution | Gunma University |
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Principal Investigator |
IWASAKI TOSHIHARU 群馬大学, 医学(系)研究科(研究院), 講師 (80375576)
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| Co-Investigator(Kenkyū-buntansha) |
KOIBUCHI Noriyuki 群馬大学, 大学院医学系研究科, 教授 (80234681)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 甲状腺ホルモン / 脳発達 / アストロサイト / 環境化学物質 / 神経成長因子 / 甲状腺ホルモン受容体 / 転写共役因子 / Purkinje細胞 / アクチン重合化 / 脱ヨード活性 |
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| Research Abstract |
We showed that PBDE, BP-6, HBCD and PFOS impaired TH-mediated Purkinje cell dendrite arborization using primary culture of rat cerebellar cells. On the other hand, 4-NP increased the dendrite arborization. PBDE, BP-6 and HBCD inpaired TH-mediated granule cell neurite development, while 4-NP incresed. PBDE, BP-6 and HBCD suppressed the TR-mediated transcription due to dissociation of TR-TRE binding. PFOS may suppressed the dendrite arborization though a novel pathway such as effects of astrocyte function. 4-NP may recruit the cofactors to TR. Lipopolysacchalide (LPS) suppressed the actin polymerization and D2 activity through p38 MAP kinase pathway. We analyzed mice expressing a dominant-negative TRbeta1 (G345R) specifically in the cerebellar Purkinje cells. Homo mice showed aberrant cerebellar development. We investigated functions of a newly cloned corepressor, brain-derived repressive molecule (B-ReM).
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