| Project/Area Number |
15591818
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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 |
Otorhinolaryngology
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| Research Institution | Kochi Medical School |
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Principal Investigator |
TAKEDA Taizo Kochi Medical School, Medicine, Professor, 医学部, 教授 (50115763)
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| Co-Investigator(Kenkyū-buntansha) |
OKADA Teruhiko Kochi Medical School, Medicine, Associate Professor, 医学部, 助教授 (00025628)
KAKIGI Akinobu Kochi Medical School, Medicine, Asistant Professor, 医学部, 講師 (60243820)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2003: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | aquaporin2 / aquaporin3 / vasopressin / V2-receptor / OPC-31260 / lithium / Meniere's disease / endolymphatic hydrops / Meniere' s disease / aquaporin 2 / 炭酸リチュウム |
|---|
| Research Abstract |
Aquaporin 2(AQP2) protein and renal type vasopressin receptor are histochemically confirmed to express in the basal cells of the stria vascularis and in the endolymphatic sac. AQP1 is also localized in the intermediate cells of the stria vascularis. The intermediate cells are well known to connect to the basal cells via the gap junctions. Therefore, these cells are thought to operate in a body in the AVP-AQP2 system of the inner ear. As previously reported, the AVP-AQP2 system in the inner ear mediates the water homeostasis in the endolymphatic fluid. In the present study, OPC-31260, V2-antagonist, and lithium, an inhibitor of cyclic AMP, resulted in the down-regulation of AQP2 mRNA in the cochlea and endolymphatic sac and produced collapse of the endolymphatic space. AQP3 is also confirmed to express in the endolymphatic sac, but the expression in the cochlea did not arrive at a conclusion.
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