2017 Fiscal Year Final Research Report
Study of brain mechanisms controlling body-fluid homeostasis
Project/Area Number |
24220010
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Research Category |
Grant-in-Aid for Scientific Research (S)
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Allocation Type | Single-year Grants |
Research Field |
Neuroscience in general
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Research Institution | National Institute for Basic Biology |
Principal Investigator |
Noda Masaharu 基礎生物学研究所, 統合神経生物学研究部門, 教授 (60172798)
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Co-Investigator(Renkei-kenkyūsha) |
HIYAMA Takeshi 基礎生物学研究所, 統合神経生物学研究部門, 助教 (90360338)
SAKUTA Hiraki 基礎生物学研究所, 統合神経生物学研究部門, 助教 (40343743)
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Project Period (FY) |
2012-05-31 – 2017-03-31
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Keywords | 神経科学 / 脳・神経 / 体液恒常性 / イオンチャネル / シグナル伝達 / 水分摂取 / 塩分摂取 / 脳弓下器官 |
Outline of Final Research Achievements |
Body-fluid conditions are continuously monitored in the brain to regulate thirst and salt appetite. We revealed that thirst and salt appetite are driven by two distinct groups of angiotensin II receptor type 1a(AT1a)-positive excitatory neurons in the SFO. We named them “water neurons” and “salt neurons”, respectively. Water neurons were cholecystokinin-dependently controlled by specific GABAergic inhibitory neurons, and projected to the vBNST. On the other hand, salt neurons were controlled by distinct population of GABAergic neurons through body-fluid [Na+], and projected to the OVLT. We also found that the sensitivity of Nax, the brain [Na+] sensor, was dose-dependently enhanced by endothelin-3. In addition, our investigation of water intake induced by intracerebroventricular administration of a hypertonic NaCl solution revealed that Nax-positive glial cells in the OVLT secreted epoxyeicosatrienoic acids as gliotransmitter to activate TRPV4-positive neurons to generate thirst.
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Free Research Field |
分子神経生物
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