Low bodily sodium levels can lead to a rise in sodium appetite but how is the drive to ingest sodium regulated to prevent overconsumption of this mineral? Park et al. found that, in mice, 5-hydroxytryptamine receptor 2C-expressing (5HTR2C+) neurons in the lateral parabracial nucleus (LPBN) increased or decreased their activity when bodily sodium levels were high or low, respectively. Moreover, activation of LPBN 5HTR2C+ neurons suppressed sodium intake, whereas their inhibition induced sodium intake, suggesting that these neurons are key regulators of sodium appetite in mice.