Adverse effects of vasopressin receptor deficiency on the male reproductive defect

Research Project

Project/Area Number	24790259
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	General pharmacology
Research Institution	Jichi Medical University
Principal Investigator	TSUCHIYA Hiroyoshi 自治医科大学, 医学部, 助教 (80508755)
Project Period (FY)	2012-04-01 – 2015-03-31
Project Status	Completed (Fiscal Year 2014)
Budget Amount *help	¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000) Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000) Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000) Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Keywords	バソプレッシン / V1a受容体 / 精巣上体 / 子宮 / 分娩 / in situ hybridization法 / バソプレッシンV1a受容体 / 欠損マウス / オキシトシン受容体
Outline of Final Research Achievements	In vasopressin V1a receptor deficient mice, we observed the decrease of the number of birth, delay of the initiation of parturition, and the prolongation of the duration of labor. These changes were dependent on the maternal genetic background of mice, rather than paternal or fetal genetic background. We also revealed by in situ hybridization analyzes with male reproductive organs that there were intense V1a receptor expressions in bladder, testis, vas deference and epididymis, most of which were interstitial tissue. In female reproductive organs, V1a receptor was also observed in ovary and uterus. These results suggest that V1a receptor has important roles in male and female reproductive physiology and could provide important information in the elucidation of the pathophysiology associated with vasopressin.