Extensive evidence indicates that glucocorticoid hormones administered or released during or shortly after training on emotionally arousing tasks enhance the long-term storage of this newly acquired information. Findings of our laboratory indicate that the basolateral complex of the amygdala (BLA) is a critical component of the neural circuitry mediating emotional arousal and stress hormone effects on memory consolidation [1]. Evidence that lesions of the BLA block the modulatory effects of systemic or intrahippocampal glucocorticoid administration on memory consolidation suggests that BLA activity is essential for enabling glucocorticoid effects in other brain regions to modulate memory consolidation. Furthermore, the finding that a beta-adrenoceptor antagonist infused into the BLA blocks memory enhancement induced by posttraining systemic or intra-cerebral glucocorticoid administration indicates that noradrenergic activation of the BLA is a co-requirement in regulating glucocorticoid-induced modulatory influences on memory consolidation. These findings are consistent with recent evidence suggesting that glucocorticoids do not uniformly modulate memory of all kinds of information but, rather, preferentially influence the consolidation of emotionally arousing information. In recent experiments investigating glucocorticoid effects on memory of object recognition training we found that glucocorticoid effects on memory consolidation depend on emotional arousal because of such critical interactions with training-induced noradrenergic activation of the amygdala [2]. However, glucocorticoids not only influence the formation of long-lasting memory; there is now extensive evidence that they impair the retrieval of previously acquired information [3]. In recent experiments we found that the integrity of the BLA and noradrenergic neurotransmission within the BLA are also essential for enabling such glucocorticoid effects on memory retrieval impairment [4]. These findings are in accordance with recent evidence suggesting that glucocorticoids also require a certain degree of emotional arousal in influencing memory retrieval. Stress exposure or glucocorticoid administration further impairs working memory, a dynamic process whereby information is continuously updated. Working memory relies on the medial prefrontal cortex (mPFC). We recently reported that the BLA interacts with the mPFC in regulating glucocorticoid effects on delayed alternation performance in a T-maze, a task commonly used to investigate spatial working memory functions in rodents. A glucocorticoid receptor agonist infused into the mPFC induces impairment in working memory, and BLA lesions block the working memory impairment induced by the glucocorticoid receptor agonist [5]. Additionally, systemic administration of the beta-adrenoceptor antagonist propranolol blocks glucocorticoid-induced impairment of working memory. As our findings indicate that BLA influences on other brain regions in regulating glucocorticoid effects on memory are not restricted to consolidation of long-term memories but extend to memory retrieval and working memory, they provide compelling evidence that the BLA is part of an integrated network of cortical and subcortical brain regions engaged in regulating different, and often opposite, stress hormone effects on memory processes.