The influence of opioid dependence on salt consumption and related psychological parameters in mice and humans.

Background: The consumption of dietary salt (NaCl) is controlled by neuronal pathways that are modulated by endogenous opioid signalling. The latter is disrupted by chronic use of exogenous opioid receptor agonists, such as morphine. Therefore, opioid dependence may influence salt consumption, which we investigated in two complimentary studies in humans and mice.

Phenotyping neurons activated in the mouse brain during restoration of salt debt.

Salt overconsumption contributes to hypertension, which is a major risk factor for stroke, heart and kidney disease. Characterising neuronal pathways that may control salt consumption is therefore important for developing novel approaches for reducing salt overconsumption. Here, we identify neurons within the mouse central amygdala (CeA), lateral parabrachial nucleus (LPBN), intermediate nucleus of the solitary tract (iNTS), and caudal NTS (cNTS) that are activated and display Fos immunoreactivity in mice that have consumed salt in order to restore a salt debt, relative to salt replete and salt depleted controls.