Nature：喝水解渴，肠道如何给大脑发信号？
- ①向小鼠肠道注水引起的肠道低渗透压，可激活肠-脑途径中的迷走神经（而非背根神经节）的特定神经亚群；
- ②肝门区（HPA）是传递渗透压信号的主要区域，阻断支配该区域的迷走神经分支可消除迷走神经对肠道低渗的反应；
- ③通过小鼠行为实验和对大脑口渴神经元活动的记录表明，源自HPA的渗透压信号对于饮水后的口渴消除是必须的；
- ④该信号由血管活性肠肽（VIP，一种激素）介导，小鼠饮水后，VIP被分泌到门静脉，进而激活HPA的迷走神经。
主编推荐语
口渴时喝杯水往往足以解渴。然而，机体补水的过程实际上需要较长时间，之所以口渴的感觉能在喝水后几分钟内就被止住，是因为大脑收到来自肠道的渗透压感知信号，从而快速抑制大脑中的口渴神经元。这一过程中，肠道信号是如何传递给大脑的尚不清楚。Nature发表的这项最新研究，揭示了介导这一过程的主要感觉途径，表明饮水后肠道的渗透压变化信号被转化成特定的激素信号，经支配肝门区的迷走神经传递至大脑，从而调控小鼠的渴感和饮水行为。
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Sensory representation and detection mechanisms of gut osmolality change
肠道渗透压变化的感觉表现和检测机制
10.1038/s41586-021-04359-5
2022-01-26, Article
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Ingested food and water stimulate sensory systems in the oropharyngeal and gastrointestinal areas before absorption1,2. These sensory signals modulate brain appetite circuits in a feed-forward manner3,4,5. Emerging evidence suggests that osmolality sensing in the gut rapidly inhibits thirst neurons upon water intake. Nevertheless, it remains unclear how peripheral sensory neurons detect visceral osmolality changes, and how they modulate thirst. Here we use optical and electrical recording combined with genetic approaches to visualize osmolality responses from sensory ganglion neurons. Gut hypotonic stimuli activate a dedicated vagal population distinct from mechanical-, hypertonic- or nutrient-sensitive neurons. We demonstrate that hypotonic responses are mediated by vagal afferents innervating the hepatic portal area (HPA), through which most water and nutrients are absorbed. Eliminating sensory inputs from this area selectively abolished hypotonic but not mechanical responses in vagal neurons. Recording from forebrain thirst neurons and behavioural analyses show that HPA-derived osmolality signals are required for feed-forward thirst satiation and drinking termination. Notably, HPA-innervating vagal afferents do not sense osmolality itself. Instead, these responses are mediated partly by vasoactive intestinal peptide secreted after water ingestion. Together, our results reveal visceral hypoosmolality as an important vagal sensory modality, and that intestinal osmolality change is translated into hormonal signals to regulate thirst circuit activity through the HPA pathway.
First Authors:
Takako Ichiki
Correspondence Authors:
Yuki Oka
All Authors:
Takako Ichiki,Tongtong Wang,Ann Kennedy,Allan-Hermann Pool,Haruka Ebisu,David J Anderson,Yuki Oka
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