A neural circuit mechanism for mechanosensory feedback control of ingestion
Dong-Yoon Kim,
Gyuryang Heo,
Minyoo Kim,
Hyunseo Kim,
Ju Ae Jin,
Hyun-Kyung Kim,
Sieun Jung,
Myungmo An,
Benjamin H. Ahn,
Jong Hwi Park,
Han-Eol Park,
Myungsun Lee,
Jung Weon Lee,
Gary J. Schwartz and
Sung-Yon Kim ()
Additional contact information
Dong-Yoon Kim: Seoul National University
Gyuryang Heo: Seoul National University
Minyoo Kim: Seoul National University
Hyunseo Kim: Seoul National University
Ju Ae Jin: Seoul National University
Hyun-Kyung Kim: Seoul National University
Sieun Jung: Seoul National University
Myungmo An: Seoul National University
Benjamin H. Ahn: Seoul National University
Jong Hwi Park: Seoul National University
Han-Eol Park: Seoul National University
Myungsun Lee: Seoul National University
Jung Weon Lee: Seoul National University
Gary J. Schwartz: Albert Einstein College of Medicine
Sung-Yon Kim: Seoul National University
Nature, 2020, vol. 580, issue 7803, 376-380
Abstract:
Abstract Mechanosensory feedback from the digestive tract to the brain is critical for limiting excessive food and water intake, but the underlying gut–brain communication pathways and mechanisms remain poorly understood1–12. Here we show that, in mice, neurons in the parabrachial nucleus that express the prodynorphin gene (hereafter, PBPdyn neurons) monitor the intake of both fluids and solids, using mechanosensory signals that arise from the upper digestive tract. Most individual PBPdyn neurons are activated by ingestion as well as the stimulation of the mouth and stomach, which indicates the representation of integrated sensory signals across distinct parts of the digestive tract. PBPdyn neurons are anatomically connected to the digestive periphery via cranial and spinal pathways; we show that, among these pathways, the vagus nerve conveys stomach-distension signals to PBPdyn neurons. Upon receipt of these signals, these neurons produce aversive and sustained appetite-suppressing signals, which discourages the initiation of feeding and drinking (fully recapitulating the symptoms of gastric distension) in part via signalling to the paraventricular hypothalamus. By contrast, inhibiting the same population of PBPdyn neurons induces overconsumption only if a drive for ingestion exists, which confirms that these neurons mediate negative feedback signalling. Our findings reveal a neural mechanism that underlies the mechanosensory monitoring of ingestion and negative feedback control of intake behaviours upon distension of the digestive tract.
Date: 2020
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DOI: 10.1038/s41586-020-2167-2
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