Physiological, biochemical and molecular mechanisms of salt appetite control by mineralocorticoid action in brain.

Adrenocortical hormone effects in the central nervous system depend on steroid interaction with intracellular receptors, which belong to a superfamily of ligand-activated transcription factors. Using a combination of biochemical and molecular biology techniques, we have demonstrated: 1. the localization of mineralocorticoid receptors in the brain, with highest density present in hippocampus, lateral septum and some amygdaloid nuclei; 2. the arousal of a mineralocorticoid-specific behavior such as salt appetite, coincident with inhibition of the biosynthesis/activity of (Na+K)ATPase in some amygdaloid and hypothalamic nuclei; 3. the modulation of the biosynthesis/activity of the sodium pump by glucocorticoids, although for these hormones changes are stimulatory, as shown in the spinal cord and brain; 4. the reported steroid effects on the (Na+K)ATPase constitute an important mechanism of control of nervous system function, involving behavior, changes in excitability and neurotropism.