HSD2 neurons in the hindbrain drive sodium appetite

Activation of putative aldosterone-sensitive neurons in the hindbrain drives mice to drink sodium solutions, and this appetite is distinct from thirst and hunger. These neurons are critical for animals to fully develop a sodium appetite following sodium depletion, although there is likely redundant circuitry. Sodium-depleted animals develop an appetite for aversive concentrations of sodium. Here we show that chemogenetic activation of aldosterone-sensitive neurons that express 11β-hydroxysteroid dehydrogenase type 2 (HSD2) in the nucleus of the solitary tract is sufficient to drive consumption of sodium-containing solutions in mice, independently of thirst or hunger. These HSD2-positive neurons are necessary for full expression of sodium appetite and have distinct downstream targets that are activated during sodium depletion.