Project/Area Number |
25462513
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Urology
|
Research Institution | Tottori University |
Principal Investigator |
HONDA Masashi 鳥取大学, 医学部附属病院, 講師 (20362890)
|
Co-Investigator(Kenkyū-buntansha) |
TAKENAKA Atsushi 鳥取大学, 医学部, 教授 (50368669)
SAITO Motoaki 高知大学, 医歯学系, 教授 (60273893)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 下部尿路機能障害 / 新規受容体 / SNSR / シクロホスファミド誘発膀胱炎 / 膀胱内圧測定 / 膀胱内注入 / 下部尿路機能 |
Outline of Final Research Achievements |
A novel family of G-protein-coupled receptors has been identified in rat dorsal root ganglia and named as sensory neuron-specific receptors (SNSRs). Intravenous or intrathecal administration of BAM8-22, a selective rat SNSR1 agonist, can suppress cyclophosphamide-induced bladder overactivity, probably due to suppression of bladder afferent activity. In urethane-anesthetized rats, intravesical administration of BAM8-22 can ameliorate cyclophosphamide-induced bladder overactivity via suppression of capsaicin sensitive C-fiber afferent pathways in rats. Thus, SNSRs could be an effective target for the treatment of bladder dysfunction such as overactive bladder and bladder pain syndrome/interstitial cystitis, for which C-fiber afferent hyperexcitability has been proposed to be an important pathophysiological basis.
|