Inhibition of glucocorticoid secretion is achieved primarily through the action of glucocorticoids themselves. This negative feedback inhibition is achieved partly by glucocorticoid binding to specific corticoid receptors in the brain. Based on biochemical and functional characteristics, two types of corticoid receptors have been described (Reul & De Kloet, 1985). The glucocorticoid receptor (GR) is widely distributed in the brain but is most abundant in hypothal-amic CRH neurons and pituitary corticotrophs. The min-eralocorticoid receptor (MR) is densely localized in hip-pocampal and septal neurons. The MR binds glucocorticoids with a tenfold higher affinity than the GR. The receptor characteristics and distribution complement each other, thus providing the organism with the ability to modulate HPA responses. The MR operates at low glucocorticoid concentrations and exerts a tonic inhibition. When glucocorticoid levels are high, the MR receptors become saturated and the corticosteroids then bind to GR receptors, thereby ensuring a return to homeostasis.
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