Representation and sensing mechanisms of gut osmolality in the peripheral sensory ganglia

2023 Fiscal Year Final Research Report

• Project/Area Number: 22K15223
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 46030:Function of nervous system-related
• Research Institution: Niigata University
• Principal Investigator: Ichiki Takako 新潟大学, 医歯学系, 助教 (30778519)
• Project Period (FY): 2022-04-01 – 2024-03-31
• Keywords: 飲水抑制機構 / 肝門脈 / 迷走神経

Outline of Final Research Achievements

Emerging evidence suggests that gut osmolality sensing rapidly inhibits thirst neurons upon water intake. Nevertheless, it remains unclear the mechanisms of how visceral sensory neurons detect gut osmolality changes. We established in vivo optical recording to show that the vagal pathway mediates visceral osmolality responses. We demonstrate that hypotonic responses are mediated by vagal afferents innervating the hepatic portal area (HPA). Water stimuli to the intestine induce osmolality responses in vagal neurons which is mediated by sensory afferents from the HPA. This signal modulates thirst satiation and may recruits Vasoactive intestinal peptide(VIP) - VIP receptor 2(VIPR2) signaling. Together, our results revealed gut hypoosmolality as an important vagal sensory modality to regulate thirst circuit activity through the HPA pathway.

Free Research Field

神経科学

Academic Significance and Societal Importance of the Research Achievements

飲水後に消化管内で浸透圧変化が感知されることで、飲水抑制が起こることが示唆されてきたが、そのメカニズムは長らく不明だった。我々は、消化管を制御する迷走神経の感覚神経節をリアルタイムに観察することで、腸管内の水による低浸透圧刺激に特異的に反応する神経群を見出した。さらに、この低浸透圧感知には、肝門脈が主要な働きをしていることを明らかにした。本研究により、長らく不明であった消化管における飲水抑制回路が明らかとなった。