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

Braz J Med Biol Res. 1992;25(12):1153-62.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Appetite Regulation / drug effects
  • Appetite Regulation / physiology*
  • Brain / drug effects
  • Brain / physiology*
  • Glucocorticoids / pharmacology
  • Mineralocorticoids / metabolism*
  • Rats
  • Receptors, Mineralocorticoid / drug effects
  • Receptors, Mineralocorticoid / metabolism
  • Sodium Chloride, Dietary / metabolism*
  • Sodium-Potassium-Exchanging ATPase / drug effects
  • Sodium-Potassium-Exchanging ATPase / metabolism

Substances

  • Glucocorticoids
  • Mineralocorticoids
  • Receptors, Mineralocorticoid
  • Sodium Chloride, Dietary
  • Sodium-Potassium-Exchanging ATPase