| Project/Area Number |
07671942
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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 | Kansai Medical University |
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Principal Investigator |
YAMAGISHI Kazuya Kansai Medical University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (90174599)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1996: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1995: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Tachykinin receptor / Retrograde cell labeling / Optic nerve crush / Ganglion cell layr / Inner nuclear layr / 神経節細胞 / 単純ヘルペス / 眼内炎 / アンチセンスオリゴ核酸 / 遺伝子治療 |
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| Research Abstract |
Substance P receptor is known to provide a principal interface between tachykinin peptides and tachykinin-sensitive cells in retinal circuitry and to produce several physiological functions such as excitation of ganglion cells. We reported results of in situ hybridization analysis of substance P receptor in rat retina using digoxigenin-labeled RNA probes to yield discrete cell labeling. Distinct hybridization signal was present in a great majority of ganglion cells that provide retinal fibers to a central target. It was also present in a subpopulation of amacrine cells. Following optic nerve crush, ganglion cells lost hybridization signal in a time-dependent manner, while hybridization-positive amacrine cells were persistently seen. From the results, we identified hybridization message distinctly localized to two systems, output cells and intrinsic cells in retinal circuitry.
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