| Project/Area Number |
24592666
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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 |
Ophthalmology
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| Research Institution | Akita University |
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Principal Investigator |
ISHIKAWA Makoto 秋田大学, 医学(系)研究科(研究院), 准教授 (10212854)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHITOMI Takeshi 秋田大学, 大学院医学研究科病態制御系眼科学講座, 准教授 (60191623)
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| Research Collaborator |
TAKASEKI Sanae 秋田大学, 大学院医学研究科病態制御系眼科学講座, 実験補助員
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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 |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 緑内障 / 眼圧 / グルタミン酸毒性 / グルタミン酸輸送体 / グルタミン合成酵素 / 神経ステロイド / 神経保護 / GABA受容体 / 加圧障害 / グルタミン酸 / 興奮毒性 / GABA / グルタミン酸代謝 |
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| Outline of Final Research Achievements |
Glutamate transporter (GT) regulates extracellular glutamate accumulation and prevents excitotoxicity. Acute exposure to elevated hydrostatic pressure can cause axonal impairments of retinal ganglion cells via down-regulation of GT expression. 17β-Estradiol (E2) and tamoxifen (TX), a selective estrogen modulator, have been shown to possess neuroprotection by increase in expression of GT and glutamine syntheses (GS). We have tested our hypothesis that E2 and TX reverse pressure-induced decrease of GT and GS, and results in the protection of axonal damage in the rat ex vivo and in vivo glaucoma model. Additionally, we reveal that neurosteroid, allopregnanolone, may serve as potential therapeutic target for the prevention of pressure-induced excitotoxicity in glaucoma.
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