A neural basis for tonic suppression of sodium appetite

• Published in: Nature neuroscience Vol. 23; no. 3; pp. 423 - 432
• Main Authors: Park, Seahyung, Williams, Kevin W., Liu, Chen, Sohn, Jong-Woo
• Format: Journal Article
• Language: English
• Published: New York Nature Publishing Group US 01-03-2020; Nature Publishing Group
• Subjects: 631/378/3920; 631/443/376; Amygdala - cytology; Amygdala - physiology; Animal Genetics and Genomics; Animals; Appetite; Appetite - physiology; Behavioral Sciences; Biological Techniques; Biomedical and Life Sciences; Biomedicine; Brachial Plexus - physiology; Brain stem; Control; Feeding Behavior; Glutamates - physiology; Health aspects; Homeostasis; Hypovolemia - psychology; Ingestion; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Motivation; Neural circuitry; Neurobiology; Neurological research; Neurons; Neurosciences; Observations; Parabrachial nucleus; Patch-Clamp Techniques; Population studies; Primates; Receptor, Serotonin, 5-HT2C - genetics; Receptor, Serotonin, 5-HT2C - physiology; Serotonergic Neurons - physiology; Serotonin; Sodium; Sodium - metabolism; Sodium in the body; Sodium, Dietary; United States
• ISSN: 1097-6256; 1546-1726; 1546-1726
• DOI: 10.1038/s41593-019-0573-2

Sodium appetite is a powerful form of motivation that can drive ingestion of high, yet aversive concentrations of sodium in animals that are depleted of sodium. However, in normal conditions, sodium appetite is suppressed to prevent homeostatic deviations. Although molecular and neural mechanisms underlying the stimulation of sodium appetite have received much attention recently, mechanisms that inhibit sodium appetite remain largely obscure. Here we report that serotonin 2c receptor (Htr2c)-expressing neurons in the lateral parabrachial nucleus (LPBN
Htr2c
neurons) inhibit sodium appetite. Activity of these neurons is regulated by bodily sodium content, and their activation can rapidly suppress sodium intake. Conversely, inhibition of these neurons specifically drives sodium appetite, even during euvolemic conditions. Notably, the physiological role of Htr2c expressed by LPBN neurons is to disinhibit sodium appetite. Our results suggest that LPBN
Htr2c
neurons act as a brake against sodium appetite and that their alleviation is required for the full manifestation of sodium appetite.
High concentrations of sodium are normally unpalatable. This study shows a neural population in the brainstem that suppresses appetite for sodium. Reducing the activity of these neurons can drive ingestion of high concentrations of sodium.