Evidence indicates that the modulatory effects of the adrenergic stress hormone epinephrine as well as several other neuromodulatory systems on memory storage are mediated by activation of ␤-adrenergic mechanisms in the amygdala. In view of our recent findings indicating that the amygdala is involved in mediating the effects of glucocorticoids on memory storage, the present study examined whether the glucocorticoid-induced effects on memory storage depend on ␤-adrenergic activation within the amygdala. Microinfusions (0.5 g in 0.2 l) of either propranolol (a nonspecific ␤-adrenergic antagonist), atenolol (a ␤ 1 -adrenergic antagonist), or zinterol (a ␤ 2 -adrenergic antagonist) administered bilaterally into the basolateral nucleus of the amygdala (BLA) of male Sprague-Dawley rats 10 min before training blocked the enhancing effect of posttraining systemic injections of dexamethasone (0.3 mg͞kg) on 48-h memory for inhibitory avoidance training. Infusions of these ␤-adrenergic antagonists into the central nucleus of the amygdala did not block the dexamethasone-induced memory enhancement. Furthermore, atenolol (0.5 g) blocked the memory-enhancing effects of the specific glucocorticoid receptor (GR or type II) agonist RU 28362 infused concurrently into the BLA immediately posttraining. These results strongly suggest that ␤-adrenergic activation is an essential step in mediating glucocorticoid effects on memory storage and that the BLA is a locus of interaction for these two systems.Extensive evidence from studies of memory of inhibitory avoidance training in rats indicates that several neuromodulatory systems interact with the noradrenergic system in the amygdala in modulating memory storage (1-8). Intraamygdala infusions of the ␤-adrenergic antagonist propranolol or depletion of norepinephrine in the amygdala by the neurotoxin N-2-chloroethyl-N-ethyl-bromobenzylamine (DSP-4) block the memory-enhancing effect of the adrenergic stress hormone epinephrine (5, 6). Moreover, intra-amygdala infusions of propranolol as well as specific ␤ 1 -or ␤ 2 -adrenergic antagonists also block the effects, on memory, of drugs affecting opioid peptidergic and GABAergic systems (4, 7). Norepinephrine and other ␤-adrenergic agonists administered to the amygdala after training dose-dependently enhance retention (5, 9-11). These effects are also time-dependent; they affect retention when given shortly after training but have no effect if given several hours later. These findings are consistent with evidence from recent experiments using in vivo microdialysis indicating that norepinephrine is released in the amygdala by footshock stimulation of the kind typically used in inhibitory avoidance training (12). Furthermore, adrenergic and opioid peptidergic systems influence the training-induced release of norepinephrine (13,14).Findings of a series of recent experiments from our laboratory indicate that the amygdala is involved in mediating the memory-modulating effects of glucocorticoids (15). Excitotoxically induced lesions of the ba...

Infusion of a beta-adrenoceptor antagonist into the basolateral nucleus of the amygdala (BLA) blocks memory enhancement induced by systemic or intra-BLA administration of a glucocorticoid receptor (GR) agonist. As there is evidence that glucocorticoids interact with the noradrenergic signalling pathway in activating adenosine 3prime prime or minute,5prime prime or minute-cyclic monophosphate (cAMP), the present experiments examined whether glucocorticoids influence the beta-adrenoceptor--cAMP system in the BLA in modulating memory consolidation. Male, Sprague--Dawley rats received bilateral infusions of atenolol (a beta-adrenoceptor antagonist), prazosin (an alpha1-adrenoceptor antagonist) or Rp-cAMPS (a protein kinase A inhibitor) into the BLA 10 min before inhibitory avoidance training and immediate post-training intra-BLA infusions of the GR agonist, RU 28362. Atenolol and Rp-cAMPS, but not prazosin, blocked 48-h retention enhancement induced by RU 28362. A second series of experiments investigated whether a GR antagonist alters the effect of noradrenergic activation in the BLA on memory consolidation. Bilateral intra-BLA infusions of the GR antagonist, RU 38486, administered 10 min before inhibitory avoidance training completely blocked retention enhancement induced by alpha1-adrenoceptor activation and attenuated the dose--response effects of post-training intra-BLA infusions of clenbuterol (a beta-adrenoceptor agonist). However, the GR antagonist did not alter retention enhancement induced by post-training intra-BLA infusions of 8-Br-cAMP (a synthetic cAMP analogue). These findings suggest that glucocorticoids influence the efficacy of noradrenergic stimulation in the BLA on memory consolidation via an interaction with the beta-adrenoceptor--cAMP cascade, at a locus between the membrane-bound beta-adrenoceptor and the intracellular cAMP formation site.

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Previous findings indicate that the memory-impairing effects of posttraining amygdala lesions are attenuated by increasing the number of training trials given prior to the induction of the lesion. The aim of this experiment was to determine whether the degree of impairment is also influenced by the footshock intensity used during training. Rats were given 1 trial of inhibitory avoidance (IA) training with either no footshock or a footshock at 1 of 3 intensities. Sham or neurotoxic amygdala lesions were induced 1 week later. On a retention test performed 4 days after surgery, the performance of all amygdala-lesioned rats given footshock training, including those given the lowest training footshock, was better than that of amygdala-lesioned rats given no training footshock. These findings of preserved retention of IA learning in rats given posttraining amygdala lesions do not support a general hypothesis that the amygdala is a locus of permanent changes underlying aversively motivated learning.

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There is little doubt that all experiences are not equally well remembered. Most of our experiences are uneventful events that are generally quickly forgotten or, at best, poorly remembered. Extensive evidence indicates that experiences that are emotionally arousing tend to be well remembered. The strength of memories of events reflects the significance of the event. Although it might be argued that enhanced remembrance of emotionally arousing events results simply from increased attention to these situations or from subsequent thinking about or rehearsing the experiences, considerable evidence supports the hypothesis that emotional responses influence memory, at least in part, by modulating long-term memory storage.Research in our laboratory has focused on the hormonal and brain systems that mediate the effects of emotional arousal on memory storage. This chapter reviews the findings of our experiments using laboratory animals to investigate the effects of stress-released hormones on memory storage. Our findings suggest that stress hormones influence memory storage by activating the amygdala, a brain system known to be involved in emotionally based memory (Davis, this volume; LeDoux, this volume). Furthermore, our findings suggest that the amygdala modulates memory storage in other brain regions. The findings have implications for understanding the role of emotional arousal, stress hormones, and brain systems in normal-human memory as well as pathological memory in patients with posttraumatic stress disorder (YTSD) (Cahill, this volume).' MODULATION OF MEMORY STORAGEIt is well established that recently acquired information is susceptible to modulating influences for a period of time after learning. The hypothesis that memory traces

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