| Project/Area Number |
24790229
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General physiology
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| Research Institution | National Institute for Physiological Sciences |
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Principal Investigator |
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| Research Collaborator |
OKADA Yasunobu 総合研究大学院大学, 学長 (10025661)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 高浸透圧センサー / バソプレシン分泌 / 容積調節能 / バソプレシンニューロン / 浸透圧センサー / バソプレシン / カチオンチャネル |
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| Outline of Final Research Achievements |
It is well known that many types of mammalian cell sense the change of plasma osmolarity and regulate their cell volume to keep cell volume homeostasis under hyperosmolarity. On the other hand, it was reported that osmosensory SON neurons, including arginine-vasopressin (AVP) neurons which are necessary for regulation of body fluid osmolarity, failed to exhibit cell volume regulation under hypseosmotic conditions. In the present study, in contrast, we find that AVP neurons also have the mechanism of cell volume regulation called regulatory volume increase (RVI). Also, it is suggested that a cation channel activated by hyperosmolarity is involved not only in inhibition of the RVI mechanism but also in the promotion of AVP release from AVP neurons.
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