| Project/Area Number |
15H04667
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General anatomy (including histology/embryology)
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
NAMBU ATSUSHI 生理学研究所, 統合生理研究系, 教授 (80180553)
CHIKEN SATOMI 生理学研究所, 統合生理研究系, 助教 (30396262)
SANO HIROMI 生理学研究所, 統合生理研究系, 助教 (00363755)
HORIE MASAO 鹿児島大学, 医歯学系, 准教授 (70322716)
BIZEN NORIHISA 新潟大学, 医歯学系, 助教 (40751053)
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| Research Collaborator |
HOSSAIN MD IBRAHIM 新潟大学, 医歯学系, 大学院生
MORI YUKIKO 新潟大学, 医学部, 研究補助員
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2017: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2016: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2015: ¥9,230,000 (Direct Cost: ¥7,100,000、Indirect Cost: ¥2,130,000)
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| Keywords | ジストニン / 三叉神経運動核 / 運動神経 / 咬筋 / マクロファージ / 運動ニューロン / オリゴデンドロサイト前駆細胞 / 増殖 / ジストニア / モデルマウス / dystonin / 神経科学 / dystonin (Dst) |
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| Outline of Final Research Achievements |
Dystonia musculorum (dt) mice have a loss-of-function mutation in the Dystonin (Dst) gene, which encodes a cytoskeleton regulator. Dt mice show movement disorders, such as cerebellar ataxia and dystonia, as well as sensory neuropathy. Since dt mice die around four weeks old, we investigated why they show growth retardation and die at premature stage. We observed neuronal cell death in the trigeminal motor nucleus (Mo5 nucleus). We also report atrophy and weak contraction of the masseter muscles in dt mice by histological analyses and electromyographic recording, which are innervated by Mo5 motoneurons. Taken together, our findings strongly suggest that mastication in dt mice is affected due to abnormalities of Mo5 motoneurons and masseter muscles, which is one possible reason of growth retardation at the post-weaning stages. In addition, we observed reduced proliferation of oligodendrocyte progenitor cells in the brain of dt mice.
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