| Project/Area Number |
23592361
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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 |
Urology
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| Research Institution | University of Yamanashi |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIYAMA Mitsuharu 山梨大学, 医学工学総合研究部, 教授 (20422694)
TAKEDA Masayuki 山梨大学, 医学工学総合研究部, 教授 (80197318)
NAKAGOMI Hiroshi 山梨大学, 医学部附属病院, 助教 (80418714)
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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 |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 膀胱上皮 / TRPV４ / ATP / メカノセンサー / ＴＲＰＶ４ / Piezo1 / TRPV4 / 求心性シグナル伝達 / 蓄尿障害 |
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| Research Abstract |
These studies using transient receptor potential vanilloid (TRPV)1-knock out (KO) mice and TRPV4-KO mice were conducted to examine functional roles of TRPV1 and TRPV4 channels in regulation of lower urinary tract activity. Analysis of voiding behavior with novel metabolic cages showed that TRPV4-KO mice have markedly higher voiding frequency and TRPV1-KO mice exhibit similar VFD.Evaluation of reflex micturition under decerebrate unanesthetized conditions using in vivo cystometrograms revealed that both TRPV1-KO and TRPV4-KO mice exhibit a large number of non-voiding bladder contractions (NVCs) whereas WT hardly show NVCs. These results suggested the possibilities that TRPV1 and TRPV4 channels are involved in modulation to stabilize detrusor activity during urine storage and that conscious TRPV4-KO mice are more vulnerable to NVCs, which are transient but repeatedly-bothering events, than TRPV1-KO mice, therefore leading to urinary incontinence more easily.
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