GLUCOCORTICOID ENHANCEMENT OF MEMORY STORAGE INVOLVES NORADRENERGIC ACTIVATION IN THE BASOLATERAL AMYGDALA

Evidence indicates that the modulatory effects of the adrenergic stres s hormone epinephrine as well as several other neuromodulatory systems on memory storage are mediated by activation of beta-adrenergic mecha nisms in the amygdala. In view of our recent findings indicating that the amygdala is involved in mediating the effects of glucocorticoids o n memory storage, the present stud examined whether the glucocorticoid -induced effects on memory storage depend on beta-adrenergic activatio n within the amygdala. Microinfusions (0.5 mu g in 0.2 mu l) of either propranolol (a nonspecific beta-adrenergic antagonist), atenolol (a b eta(1)-adrenergic antagonist), or zinterol (a beta(2)-adrenergic antag onist) administered bilaterally into the basolateral nucleus of the am ygdala (BLA) of male Sprague-Dawley rats 10 min before training blocke d the enhancing effect of posttraining systemic injections of dexameth asone (0.3 mg/kg) on 48-h memory for inhibitory avoidance training. In fusions of these beta-adrenergic antagonists into the central nucleus of the amygdala did not block the dexamethasone-induced memory enhance ment. Furthermore, atenolol (0.5 mu g) blocked the memory-enhancing ef fects of the specific glucocorticoid receptor (GR or type II) agonist RU 25362 infused concurrently into the BLA immediately posttraining. T hese results strongly suggest that beta-adrenergic activation is an es sential step in mediating glucocorticoid effects on memory storage and that the BLA is a locus of interaction for these tno systems.