Role of retinal neuronal cells in the architecture and functional regulation of retinal blood vessels
| Project/Area Number |
15K08242
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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 |
General pharmacology
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| Research Institution | Kitasato University |
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Principal Investigator |
Mori Asami 北里大学, 薬学部, 助教 (80453504)
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 微小循環 / 緑内障 / 血管生物学 / 網膜血管 / 網膜神経‐グリア‐血管連関 / 一酸化窒素 / プロスタグランジン / 薬理学 / 神経‐グリア‐血管連関 / NO / 網膜神経 |
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| Outline of Final Research Achievements |
The purpose of this study was to investigate interactions between blood vessels and neuronal cells in the retina. Intravitreal injection of low dose of NMDA (6 nmol) facilitated neuronal nitric oxide (NO) synthase-derived NO production in retinal ganglion and amacrine cells. NO released from neuronal cells acted on retinal glial cells, thereby dilating retinal blood vessels. Intravitreal injection of high dose of NMDA (200 nmol) induced damage to retinal neuronal cells and blood vessels. In the injured retina, NMDA (6 nmol)-induced vasodilation was mediated by inducible NO synthase-derived NO. These results suggest that NO released from neuronal and glial cells plays an important role in the vasodilatory mechanisms of blood vessels in the retina.
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Report
(4 results)
Research Products
(14 results)
