novel situations and the selection of appropriate responses to deal with challenges (18). Research on these functions, combined with rodent data indicating that mineralocorticoid receptor overexpression in the amygdala reduces corticosterone release and anxiety-like behavior (19), highlights the potentially powerful influence of variability in mineralocorticoid receptor signaling, including that resulting from genetic polymorphisms, on the expression of individual differences in threat-related amygdala reactivity. Moreover, such mineralocorticoid receptor-mediated effects on reactivity may be contingent on the experience of stress.