The overconsumption of sodium contributes to a wide range of detrimental health conditions. Thus, it is imperative to gain a better understanding of the neural mechanisms driving sodium appetite. Here, we combined neuroanatomic, transgenic, behavioral, and chemogenetic approaches to investigate the role of bed nucleus of stria terminalis (BNST) enkephalin neurons (BNSTENK) in sodium appetite in male and female pENK-Cre mice. Our results demonstrate that Gi-mediated signaling onto BNSTENK neurons regulates salt consumption following sodium depletion but does not impact upon taste preference when replete. Further, Gi-mediated signaling onto BNSTENK neurons had no effect on deprivation-induced food or water intake or anxiety-like behavior.





