| Project/Area Number |
12671699
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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 |
Ophthalmology
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| Research Institution | Niigata University |
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Principal Investigator |
ABE Haruki Graduate School of Medical and Dental Sciences, Niigata University, Professor, 大学院・医歯学総合研究科, 教授 (40018875)
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| Co-Investigator(Kenkyū-buntansha) |
SAKIMURA Kenji Brain Research Institute, Niigata University, Professor, 脳研究所, 教授 (40162325)
SHIRAKASHI Motohiro University Medical Hospital, Niigata University, Lecturer, 医学部・附属病院, 講師 (50242417)
FUKUCHI Takeo University Medical Hospital, Niigata University, Assistant, 医学部・附属病院, 助手 (90240770)
YAMAMOTO Tadashi Faculty of Medicine, Niigata University, Professor, 医学部, 教授 (30092737)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2000: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | NMDA receptor / glutamate / knockout mice / ischemia-reperfusion model / retinal ganglion cell / glaucoma / brain-derived neurotrophic factor / 網膜 / 眼圧 / ラット / 神経節細胞 / ε1サブユニット / ε2サブユニット |
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| Research Abstract |
Cell death has been thought to be induced by glutamate that stimulates the N-methyl-d-aspatate (NMDA) receptor present on retinal ganglion cells and on cells in the inner nuclear layer. Knock out mice were used to elucidate the role of the NR2A and NR2B subunit of the NMDA receptor. Wild type and NR2A and NR2B subunit knock out mice were used. Transient retinal ischemia was induced by raising intraocular pressure (IOP) to 120mmHg. In the Wild type mice, all the retinal ganglion cells were lost after 14 days. The number of cells in the inner nuclear layer was decreased. The thickness of the inner plexiform layer was reduced. By contrast, the retina appeared to be normal, unaffected by the insult in the NR2A subunit knockout mice. While the NR2B subunit knock out mice also showed the same tendency. These results suggest that the subunit may have a direct role in the retinal cell death induced by ischemia-reperfusion.
We quantifies the level of brain-derived neurotrophic factor (BDNF) in the retina of experimental ocular hypertension model rat. To induce unilateral IOP elevation, we used a model developed by Ueda et al. (1998). Fellow eyes were served as control. IOP was measured by pneumatonometer. After the duration of IOP elevation above 22 mmHg for 1, 2, 4 and 12 weeks, retinas were dissected out from both experimental and control eyes and used as samples. To quantify BDNF protein level, we used enzyme-linked immunosorbant assay. Retinal BDNF levels of hypertensive eye compared to control after 1, 2, 4 and 12 weeks of IOP elevation were 277%, 102%, 59% and 24%, respectively. This study clarifies that BDNF levels were dramatically altered in the retina of experimental ocular hypertension model rat.
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