Sensitization of sodium appetite: evidence for sustained molecular changes in the lamina terminalis

307: R1405–R1412, 2014. First published November 5, 2014; doi:10.1152/ajpregu.00210.2014.—Animals with a history of sodium depletions exhibit increases in salt intake, a phenomenon described as the sensitization of sodium appetite. Using a novel experimental design, the present experiments investigated whether putative molec-ular markers of neural plasticity and changes in the message for components of the brain renin-angiotensin-aldosterone-system (RAAS) accompany the sensitization of sodium appetite. An initial set of experiments examined whether the glutamatergic N-methyl-D-aspartate receptor antagonist MK-801 would attenuate sodium appe-tite sensitization and prevent changes in mRNA expression associated with sensitization. Rats with repeated sodium depletions exhibited enhanced sodium appetite and mRNA expression for components of the RAAS in areas along the lamina terminalis (LT), a region of the brain that is important for the regulation of body fluid homeostasis