| Project/Area Number |
23659118
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
General physiology
|
|---|
| Research Institution | National Institute for Physiological Sciences |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SATO Kaori (NUMATA Kaori) 生理学研究所, 細胞器官研究系, NIPS リサーチフェロー (60614196)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
UETA Yoichi 産業医科大学, 医学部, 教授 (10232745)
|
|---|
| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
|---|
| Keywords | 浸透圧センサー / バソプレシン視索上核 / アニオンチャネル / タウリン / グリシンレセプター / 低浸透圧センサー / バソプレシン / 視索上核 |
|---|
| Research Abstract |
Arginine-vasopressin (AVP), an antidiuretic hormone, is secreted from AVP neurons in a manner sensitive to body fluid osmolarity. The current view for the hypotonicity-induced suppression mechanism consists of following two hypotheses: Reduced depolarization due to inactivation of stretch-inactivated cation channel (SIC) in osmotically swollen AVP neurons, and increased hyperpolarization due to glycine receptor (GlyR) activation in AVP neurons in response to taurine released from osmotically swollen glial cells. In rat AVP neurons, in the present study, the SIC activity was not observed, and taurine-induced activation of GlyR brought about depolarization but not hyperpolarization under hypotonic conditions. Also, the present study showed that taurine-releasing anion channel activated by cell swelling serves as a sensor for hypoosmolarity.
|
