| Budget Amount *help |
¥15,860,000 (Direct Cost: ¥12,200,000、Indirect Cost: ¥3,660,000)
Fiscal Year 2016: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
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| Outline of Final Research Achievements |
In this research project, we investigated neural mechanisms underlying thirst and salt appetite. We identified neurons driving thirst and salt appetite in the subfornical organ and named them water neurons and salt neurons, respectively. Our results show that they are distinct groups of angiotensin II receptor type 1a-positive excitatory neurons. Water neurons were suppressed by cholecystokinin via GABAergic inhibitory neurons. On the other hand, salt neurons were suppressed by another GABAergic population, which are downstream of the glial Na+-level sensor (Nax) in the brain. In addition, Nax is also involved in thirst control: The Na+ signals generated in Nax-positive cells lead to the activation of TRPV4-positive neurons by using epoxyeicosatrienoic acids as gliotransmitters, and stimulated water intake. Finally, our data indicate that the generation of antoantibodies targeting the subfornical organ elicit adipsic hypernatremia without structural anomalies in the hypothalamus.
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