Aldosterone-Sensing Neurons in the NTS Exhibit State-Dependent Pacemaker Activity and Drive Sodium Appetite via Synergy with Angiotensin II Signaling.

ABSTRACT: 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 Na_v1.5 channels. Remarkably, NTS^HSD2 neurons are necessary for sodium appetite

SUBMITTER: Resch JM 

PROVIDER: S-EPMC5637454 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature