Studies on molecular and physiological properties of the Na-level sensor and osmosensor.
Project Area | Molecular interaction and modal shift of cellular sensors |
Project/Area Number |
18077007
|
Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
|
Allocation Type | Single-year Grants |
Review Section |
Biological Sciences
|
Research Institution | National Institute for Basic Biology |
Principal Investigator |
HIYAMA Takeshi National Institute for Basic Biology, 統合神経生物学研究部門, 助教 (90360338)
|
Project Period (FY) |
2006 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥63,700,000 (Direct Cost: ¥63,700,000)
Fiscal Year 2010: ¥12,000,000 (Direct Cost: ¥12,000,000)
Fiscal Year 2009: ¥12,200,000 (Direct Cost: ¥12,200,000)
Fiscal Year 2008: ¥13,500,000 (Direct Cost: ¥13,500,000)
Fiscal Year 2007: ¥12,900,000 (Direct Cost: ¥12,900,000)
Fiscal Year 2006: ¥13,100,000 (Direct Cost: ¥13,100,000)
|
Keywords | セルセンサー / 神経科学 / イオンチャンネル / ナノバイオ / 生体分子 / グリア / 恒常性 / ノックアウトマウス |
Research Abstract |
We showed direct interaction between Na_x channels and alpha subunits of Na^+/K^+-ATPase, which brings about Na-dependent activation of the metabolic state of the glial cells. The metabolic enhancement leading to extensive lactate production was observed in the subfornical organ (SFO). Furthermore, lactate, as well as Na, stimulated the activity of GABAergic neurons in the SFO. These results suggest that the information on a physiological increase in the Na level of body fluids, which is sensed by Na_x in glial cells, is transmitted to neurons by lactate as a mediator to regulate neural activities of the SFO. We further demonstrated that a ganglioneuroma formed in the PNS triggered an autoimmune channelopathy targeting Na_x, the Na-level sensor of body fluids in the brain, leading to essential hypernatremia.
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Report
(7 results)
Research Products
(52 results)
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[Presentation] 脳のナトリウムセンサー2008
Author(s)
渡辺英治, 檜山武史, 野田昌晴
Organizer
日本味と匂い学会第42大会
Place of Presentation
富山市民プラザ(富山市)
Year and Date
2008-09-19
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