Altered expression of glucocorticoid receptor and corticotropin-releasing factor in the central amygdala in response to elevated corticosterone.

The amygdala is not only a critical site for the generation of anxiety and fear, but is involved in the affective processing of sensory information including nociception. Previously, we demonstrated that the stress hormone corticosterone (CORT) localized to the central nucleus of the amygdala (CeA) induces anxiety-like behavior and increases the sensitivity to visceral or somatic stimuli in rats. Here we test the hypothesis that exposure of the CeA to elevated CORT alters the expression of key receptors and ion channels that are implicated in anxiety and pain processing.