Sodium deficiency increases angiotensin II (ATII) and aldosterone, which synergistically stimulate sodium retention and consumption. Recently, ATII-responsive neurons in the subfornical organ (SFO) and aldosterone-sensitive neurons in the nucleus of the solitary tract (NTS(HSD2) neurons) were shown to drive sodium appetite. Here we investigate the basis for NTS(HSD2) neuron activation, identify the circuit by which NTS(HSD2) neurons drive appetite, and uncover an interaction between the NTS(HSD2) circuit and ATII signaling. NTS(HSD2) neurons respond to sodium deficiency with spontaneous pacemaker-like activity-the consequence of "cardiac" HCN and Nav1.5 channels. Remarkably, NTS(HSD2) neurons are necessary for sodium appetite, and with concurrent ATII signaling their activity is sufficient to produce rapid consumption. Importantly, NTS(HSD2) neurons stimulate appetite via projections to the vlBNST, which is also the effector site for ATII-responsive SFO neurons. The interaction between angiotensin signaling and NTS(HSD2) neurons provides a neuronal context for the long-standing "synergy hypothesis" of sodium appetite regulation.
This research output has an Altmetric Attention Score of 118. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 06 February 2024.
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