Studies on the regulatory mechanisms for water / salt appetite

2017 Fiscal Year Final Research Report

• Project/Area Number: 26293043
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: General physiology
• Research Institution: National Institute for Basic Biology
• Principal Investigator: Hiyama Takeshi 基礎生物学研究所, 統合神経生物学研究部門, 助教 (90360338)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: 生理学 / 循環器・高血圧 / 行動学 / 生物物理 / 脳・神経 / 神経疾患 / イオンチャネル / 体液

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.

Free Research Field

分子神経生物学