| First Author | Resch JM | Year | 2017 |
| Journal | Neuron | Volume | 96 |
| Issue | 1 | Pages | 190-206.e7 |
| PubMed ID | 28957668 | Mgi Jnum | J:256132 |
| Mgi Id | MGI:6114493 | Doi | 10.1016/j.neuron.2017.09.014 |
| Citation | Resch JM, et al. (2017) Aldosterone-Sensing Neurons in the NTS Exhibit State-Dependent Pacemaker Activity and Drive Sodium Appetite via Synergy with Angiotensin II Signaling. Neuron 96(1):190-206.e7 |
| abstractText | 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. |
