| Project/Area Number |
23592586
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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 | Kitasato University |
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Principal Investigator |
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| Research Collaborator |
ASAKAWA Ken 北里大学, 医療衛生学部, 助教 (60582749)
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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 |
¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2013: ¥130,000 (Direct Cost: ¥100,000、Indirect Cost: ¥30,000)
Fiscal Year 2012: ¥260,000 (Direct Cost: ¥200,000、Indirect Cost: ¥60,000)
Fiscal Year 2011: ¥260,000 (Direct Cost: ¥200,000、Indirect Cost: ¥60,000)
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| Keywords | メラノプシン / 網膜神経節細胞 / 対光反射 / 変異型ロドプシン遺伝子トランスジェニック家兎 / 神経節細胞 |
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| Research Abstract |
Recently, a new photosensitive pigment, melanopsin, was found in 1998. Later, melanopsin-containing retinal ganglion cells (mRGCs) were discovered and revealed that mRGCs would depolarize without input from the photoreceptors, meaning that these cells were photosensitive. The mRGCs mediate the pupillary light reflex. We investigated the mechanisms of photoreception by retinal photoreceptor cells, and to evaluate the relative contribution of pupil light response using the control, pharmacological blockade of neurotransmission (PB) model and a transgenic model of retinal degeneration (Tg) rabbit. Although rod and cone photoreceptors were disappeared in the PB and Tg model, miosis was still induced during exposure to blue light (470nm). Our study also indicated that some histologically-identified RGCs were consistent with the characteristics and structures of mRGC. The greater sustained constriction of pupils to blue light in eyes with outer retinal damage reflects mRGC activation.
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