| Budget Amount *help |
¥223,600,000 (Direct Cost: ¥172,000,000、Indirect Cost: ¥51,600,000)
Fiscal Year 2016: ¥40,690,000 (Direct Cost: ¥31,300,000、Indirect Cost: ¥9,390,000)
Fiscal Year 2015: ¥41,080,000 (Direct Cost: ¥31,600,000、Indirect Cost: ¥9,480,000)
Fiscal Year 2014: ¥44,980,000 (Direct Cost: ¥34,600,000、Indirect Cost: ¥10,380,000)
Fiscal Year 2013: ¥51,480,000 (Direct Cost: ¥39,600,000、Indirect Cost: ¥11,880,000)
Fiscal Year 2012: ¥45,370,000 (Direct Cost: ¥34,900,000、Indirect Cost: ¥10,470,000)
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| 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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