Characterising the neuronal circuitry that underlies salt appetite

While we need to consume salt, too much can be harmful and is in fact directly linked to ~5% of deaths annually in Australia. We have identified a system in the brain that regulates salt intake. Going forwards we will fully elucidate the pathway(s) implicated in regulation of salt intake, thereby identifying strategies to reduce excessive salt consumption.

Aims

Our findings therefore provide compelling evidence for the crucial role played by this CeA-MOR pathway in controlling salt seeking and consumption. Using established mouse models we will:

  • Determine whether CeA-MOR signalling increases salt intake by increasing the motivation for salt and/or its palatability. 
  • Characterise the anatomical circuitry involved in CeA-MOR-dependent salt appetite.
  • Determine whether salt deprivation is detected by NTS and/or CVO sources to drive CeA-MOR-dependent salt intake.

We have recently identified an endogenous signalling system that drives salt consumption. This system requires mu-opioid receptor (MOR) signalling within the central amygdala (CeA). We hypothesise that this CeA-MOR pathway increases the motivation for salt and/or its palatability, and is activated by the nucleus of the solitary tract (NTS) and/or circumventricular (CVO) brain regions that detect salt depletion. To test this hypothesis, we have identified that intrinsic CeA enkephalin-containing neurons are the putative source of opioid ligand that drives CeA-MOR-mediated salt intake following salt depletion. This system may therefore detect peripheral salt depletion via both NTS and CVO sources.

 

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