| Project/Area Number |
07680831
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | Nippon Medical School |
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Principal Investigator |
IMAKI Junko Nippon Medical School, Medical Department, Assistant professor, 医学部, 講師 (20223323)
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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 |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1996: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1995: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | retina / CREB / in situ hybridization / c-fos mRNA / immunocytochemistry / phosphorylation / rat / Ca^<2+> / カルシウム イオン / 燐酸化CREB / ウエスタンブロット |
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| Research Abstract |
The signal pathway of the light-induced gene expression in retinal cells was investigated. Flashing light induced c-fos and somatostatin in the cells of the inner border of the inner nuclear layr (INL) and the ganglion nuclear layr (GNL). As both c-fos and somatostatin genes have cAMP responsive element (CRE) in their promoters, CREB phosphorylation in retinal cells was examined with phospho-CREB specific antibody. One min exposure to flashing light induced maximum phosphorylation of CREB showing close correlation with c-fos and somatostatin mRNA expression in the same portion of the retina. Administration of L-type Ca^<2+> channel activator Bay K 8644 also induced CREB phosphorylation and c-fos and somatostatin expression in the rat retina. The distribution of calmodulin kinase II immunoreactive retina cells was in good accordance with the phospho-CREB immunoreactivity. Thus we propose that transcriptional response to light stimulation is regulated via CREB phosphorylation catalyzed by Ca^<2+>/calmodulin-dependent protein kinase in neural retina.
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