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Bermúdez-Rattoni F, editor. Neural Plasticity and Memory: From Genes to Brain Imaging. Boca Raton (FL): CRC Press/Taylor & Francis; 2007.

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Neural Plasticity and Memory: From Genes to Brain Imaging.

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Chapter 13Adrenal Stress Hormones and Enhanced Memory for Emotionally Arousing Experiences

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Emotionally significant experiences tend to be well remembered.1,2 We know this from personal experiences as well as from extensive research findings. Significant experiences such as birthdays, graduation ceremonies, or the loss of a loved one typically leave lasting and vivid memories. Findings of experimental studies indicate that people have good recollections of where they were and what they were doing when they experienced earthquakes3 or witnessed accidents.4 Similarly, a rat remembers the place in an apparatus where it received a footshock or the location of an escape platform in a tank filled with water.5,6 Such memory enhancement is not limited to experiences that are unpleasant or aversive. Pleasurable events also tend to be well remembered. Our research focuses on understanding the role of emotional responses induced by such arousing experiences in enabling the significance of events to regulate their remembrance.

Extensive evidence indicates that stress hormones released from the adrenal glands are critically involved in memory consolidation of emotionally arousing experiences. Epinephrine, glucocorticoids, and specific agonists for their receptors administered after exposure to emotionally arousing experiences enhance the consolidation of long-term memories of these experiences.7–10

Do stress hormones also enhance memories of experiences that are not emotionally arousing? The findings of recent experiments suggest that this may not be the case. As discussed below, we recently reported that the endogenous glucocorticoid corticosterone enhanced memory consolidation of object recognition training when administered to rats that were emotionally aroused by an unfamiliar training apparatus. However, the treatment had no effect when administered to rats that had extensive prior habituation to the training context in order to reduce novelty-induced arousal.11 In studies of human memory, epinephrine or cortisol treatment also appear to selectively enhance memory for emotionally arousing material.12–15

These findings thus provide some important clues concerning the neurobiological mechanism(s) underlying adrenal hormone effects on memory consolidation and suggest that at least some degree of training-associated endogenous emotional arousal is essential for enabling their effects on memory consolidation. Our findings indicate that adrenal stress hormones influence memory consolidation of emotional experiences via interactions with arousal-induced activation of noradrenergic mechanisms within the amygdala.


It is well established that hormones of the adrenal medulla (epinephrine) and adrenal cortex (corticosterone, cortisol in humans) are released during and immediately after stressful stimulation of the kind used in emotionally arousing learning tasks. The degree to which these hormonal systems are activated depends on the severity as well as type of stressor employed.16 As removal of endogenous hormones by adrenalectomy impairs memory consolidation for emotionally arousing experiences,5,17–19 such evidence indicates that stress hormones released by the training experience may act as endogenous modulators of memory consolidation.

In support of this view, single injections of epinephrine or glucocorticoids administered after training enhance the long-term retention of many different kinds of training experiences typically used in animal memory studies including inhibitory avoidance, active avoidance, contextual and cued fear conditioning, spatial discrimination, conditioned taste aversion, object recognition, and appetitively motivated tasks.11,20–23 Further, antagonists of adrenoceptors or adrenal steroid receptors as well as drugs that disrupt glucocorticoid functioning (i.e., metyrapone) impair memory consolidation.5,17,24,25 Injections of stress hormones at doses that enhance memory when administered shortly after training are generally ineffective when administered several hours after training.26,27 Such findings indicate that the hormones affect memory by modulating the storage or “consolidation” phase. Extensive evidence also indicates that epinephrine and glucocorticoids or stressful conditions that stimulate their release enhance memory consolidation in human subjects when administered shortly before or after learning.12,13,28,29

Although epinephrine and glucocorticoids interact in influencing memory consolidation,24,30,31 their effects are initiated through different mechanisms. Because epinephrine does not readily cross the blood–brain barrier, a peripheral central pathway must be involved in mediating epinephrine effects on brain activity in modulating memory consolidation. The findings of many experiments indicate that epinephrine effects on memory consolidation are initiated by activation of peripheral β-adrenoceptors located on vagal afferents that project to the nucleus of the solitary tract (NTS) in the brain stem. Noradrenergic projections originating in the NTS innervate forebrain structures involved in learning and memory, including the amygdala,32,33 but may also influence norepinephrine release via projections to the nucleus paragigantocellularis in the lower medulla, which projects to the locus coeruleus. The locus coeruleus noradrenergic system is viewed as a broad system with projections to many areas involved in memory processing including the amygdala, hippocampus, and prefrontal cortex.34–36

Glucocorticoids are highly lipophilic and readily enter the brain to bind to mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs). These two receptor types differ in their affinities for corticosterone and synthetic ligands. MRs have a high affinity for the natural steroids and are almost saturated during basal levels of corticosterone and cortisol, whereas GRs have a high affinity for synthetic ligands such as dexamethasone and RU 28362.37 In contrast to MRs, GRs become occupied only during stress and at the circadian peak. Several studies using pharmacological and genetic techniques indicate that the memory–modulatory effects of glucocorticoids selectively involve activation of GRs.17,38–41 GRs are considered classical intra-somatic receptors that, after their activation, translocate to the nucleus and regulate gene transcription by binding of receptor homodimers to DNA or other nuclear proteins.42–45 However, glucocorticoids or specific GR agonists also have rapid (milliseconds to minutes) effects on the brain and behavior, suggesting that they may also produce fast-acting, nongenomic effects, presumably involving an activation of membrane receptors.46–48


Stress hormone effects on memory consolidation follow an inverted-U shaped doseresponse effect. Moderate doses of epinephrine or glucocorticoids enhance memory consolidation but lower or higher doses are less effective or may even impair memory consolidation.49,50 Other variables such as gender and age may also influence the direction of the effects of stress hormones on memory consolidation due to differences in stress responses and vulnerability across populations.51–53

Stress hormone effects on memory consolidation depend further on the level of emotional arousal induced by the training experience. For example, posttraining injections of moderate doses of corticosterone or dexamethasone, a synthetic ligand, enhance memory consolidation in a water-maze spatial task.54 However, the same glucocorticoid treatment impairs memory consolidation when the task becomes more aversive by lowering the water temperature.54,55 Similarly, epinephrine and glucocorticoids, as well as drugs affecting many other neurotransmitter systems, are known to enhance memory of inhibitory avoidance training when administered after a mild, low-arousing foot shock, but to impair memory consolidation when given after a strong, highly aversive foot shock that produces robust memory in control animals.56 Thus, these findings indicate that the efficacy and even the direction of the effects of exogenous drug administration on memory consolidation depend on the level of endogenous emotional arousal evoked by the training experience.

To address the question raised earlier in this chapter of whether stress hormone effects on memory consolidation require emotional arousal, we recently investigated the importance of emotional arousal in influencing stress hormone effects on memory consolidation in rats trained on an object recognition task.11 Learning tasks in animal experiments are often emotionally arousing because of the punishment or reward necessary to elicit changes in behavior. It is obvious that with the use of such experimental conditions, it is not possible to determine whether emotional arousal is a prerequisite in regulating stress hormone influences on memory processes. Although no rewarding or aversive stimulation is used during object recognition training,57 such training induces modest novelty-induced stress or arousal. However, extensive habituation of rats to the training apparatus (in the absence of any objects) prior to the training reduces the arousal level induced by object recognition training. Thus, object recognition training may be performed under two distinct conditions in which rats are either exposed to the objects while in a state of heightened arousal or in a less aroused state. We found that corticosterone administered systemically immediately after training enhanced 24-hour retention performance of rats that were not previously habituated to the experimental context (i.e., emotionally aroused rats). In contrast, corticosterone did not affect 24-hour retention of rats that received extensive prior habituation to the experimental context and thus had decreased novelty-induced emotional arousal during training.11 Clearly, these findings indicate that at least some degree of training-associated endogenous emotional arousal is essential for enabling stress hormone effects on memory consolidation.

Recent studies of human memory have also investigated interactions of stress hormones with training-associated emotional arousal. Decreasing glucocorticoid levels below baseline with the cortisol synthesis inhibitor metyrapone impaired long-term memory for both emotionally arousing and emotionally neutral information,58 presumably involving a reduced MR occupancy. However, cortisol administration selectively enhance long-term memory of emotionally arousing, but not emotionally neutral, pictures.12,15 Consistent with these findings, Abercrombie and colleagues14 reported that levels of endogenous cortisol correlated with enhanced memory consolidation only in individuals who were emotionally aroused.

The memory-enhancing effects of epinephrine administration or stress exposure immediately after learning also appear to depend on the arousal level.13,29 For example, Cahill and Alkire13 recorded electrodermal skin responses in human subjects as they viewed standard nonarousing slides, followed by infusions of epinephrine or saline. They reported that epinephrine-treated subjects showed enhanced memory for the first slides (i.e., primacy effect). Likewise, electrodermal skin responses to those slides were significantly greater than responses to slides shown at a later time. Therefore, the authors concluded that epinephrine effects on memory depend on the level of arousal at the time of encoding.


Why do stress hormones selectively enhance memory for emotionally arousing experiences? The findings described above suggest that stress hormones must interact with some other component of emotional arousal in mediating memory enhancement. Our findings indicate that stress hormone effects on memory consolidation require amygdala activity. It is well established that emotional experiences that induce the release of adrenal stress hormones also activate the amygdala.59

Lesions or temporary inactivation of the amygdala block the memory-modulatory effects induced by posttraining systemic injections of drugs affecting a variety of neuromodulatory systems including norepinephrine, opioid peptides, GABA, vasopressin, and ACTH.9,60 Furthermore, as noted above, the amygdala mediates epinephrine as well as glucocorticoid effects on memory consolidation.20,61 Selective NMDA-induced lesions of the amygdala restricted to the basolateral complex (BLA; consisting of the lateral, basal, and accessory basal nuclei) block inhibitory avoidance memory enhancement induced by posttraining systemic injections of the synthetic glucocorticoid dexamethasone.39 In contrast, lesions of the adjacent central nucleus (CEA) do not block the dexamethasone-induced memory enhancement. Moreover, posttraining infusions of the specific GR agonist RU 28362 administered into the BLA, but not the CEA, enhanced memory consolidation in a dose-dependent fashion, whereas intra-BLA infusions of the GR antagonist RU 38486 impaired memory consolidation.39 Corticotropin-releasing hormone (CRH) is another neurotransmitter that is released into the amygdala as well as several other brain regions in response to arousing or stressful stimulation. Blockade of endogenous CRH in the BLA with infusions of a CRH receptor antagonist impaired memory for emotionally arousing training,62 whereas preliminary findings indicate that infusions of CRH into the BLA dose-dependently enhance memory consolidation. This evidence indicates that BLA activation by emotional arousal is a general gateway in mediating stress hormone and neurotransmitter effects on memory consolidation.

13.4.1. Amygdala Interacts With Other Brain Regions

Other evidence indicates that the BLA is not a site of permanent storage of the enhanced memory trace but rather is involved in strengthening consolidation processes in other brain regions.9,60 The evidence that lesions of the stria terminalis, a major amygdala input–output pathway, block the memory-modulatory effects of systemic drug infusions and of drugs infused directly into the amygdala63–65 strongly suggests that the amygdala regulates memory consolidation by influencing the storage of information in efferent brain regions. The BLA interacts with many brain regions, including the hippocampus, caudate nucleus and insular, entorhinal, and anterior cingulate cortices in regulating the consolidation of different types of information.60 It also interacts with the hippocampus in regulating stress (hormone) effects on memory consolidation of contextual/spatial components of training. Hippocampal GRs play a role in neuroplasticity66–69 and posttraining activation of hippocampal GRs enhances memory consolidation for both appetitive and aversive training.40,70,71 However, BLA lesions block the memory enhancement produced by posttraining intra-hippocampal infusions of a GR agonist.40 Similarly, electrophysiological findings indicate that BLA lesions or temporary blockade of BLA functioning impair stress- or perforant path stimulation-induced long-term potentiation in the dentate gyrus.72,73 These findings indicate that BLA neuronal activity is required for enabling memory modulation induced by local GR activation in the hippocampus. Since the BLA is normally activated by emotional arousal, such evidence may provide an explanation for the findings that stress hormones selectively influence memory consolidation of emotionally arousing experiences.

Other findings indicate the existence of interactions between the BLA and medial prefrontal cortex (mPFC). The mPFC is implicated in higher cognitive functions such as thought, decision-making, and working memory74,75 and also plays a role in memory consolidation.76 The BLA interacts with the mPFC via reciprocal inhibitory connections.77,78 In a recent study, we examined whether the BLA and mPFC interact in regulating glucocorticoid effects on memory consolidation.79 A GR agonist infused posttraining into either the mPFC or the BLA enhanced memory consolidation of inhibitory avoidance training. The same GR agonist administered into the mPFC also increased BLA neuronal activity, as assessed by elevated phosphorylation levels of the transcription factor mitogen-activated protein kinase (MAPK) in the BLA. Importantly, the GR agonist infused into the mPFCs of animals that had not received inhibitory avoidance training did not increase MAPK levels in the BLA, supporting the hypothesis that glucocorticoid effects on memory consolidation and brain activity require training-associated emotional arousal. Because the inhibition of this MAPK activation in the BLA with infusions of a MEK inhibitor blocked the memory enhancement induced by intra-mPFC infusions of the GR agonist,79 these findings further indicate that BLA activity is essential in regulating stress hormone effects on the consolidation of emotionally arousing memories.

13.4.2. Amygdala Involvement In Human Studies

Considerable evidence from human studies indicates that the enhancing influence of emotional arousal on memory involves activation of the amygdala. Human studies, however, have not yet investigated a possible selective involvement of the BLA. The evidence that emotionally arousing stimulation does not enhance long-term memory in human subjects with amygdala lesions supports the view that amygdala activation may be critical for emotionally enhanced memory.80 Interestingly, the reactions of amygdala-damaged subjects to the emotional material in these studies appeared normal, suggesting that the amygdala in humans may not be as critical for the production of emotional reactions per se.

The involvement of amygdala activation in emotionally influenced memory has also been investigated in many studies using positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) in healthy humans.81–84 These studies reported that activity of the amygdala assessed during the presentation of emotionally arousing stimuli correlated highly with memory of the stimuli tested weeks later. Further, the relationship between amygdala activity during encoding and subsequent long-term memory was greatest for the most emotionally arousing stimuli. Human studies indicate that the enhanced memory for emotionally arousing events (versus non-arousing events) involves amygdala modulation of the hippocampal formation.85–87 Collectively, these studies of emotionally influenced memory in human subjects are consistent with findings of animal experiments and indicate that emotional arousal-induced amygdala (BLA) activation may be a critical step in enabling stress hormone effects in modulating memory processes involving other brain regions including hippocampus-dependent explicit/declarative memory.


The enhancing effects of adrenal stress hormones on memory consolidation depend on the integrity of the amygdala noradrenergic system. Infusions of β-adrenoceptor antagonists administered into the amygdala block the memory-enhancing effects of peripherally administered epinephrine that, as discussed above, are known to be mediated by activation of the noradrenergic cells of the NTS and locus coeruleus.61 Glucocorticoids also require noradrenergic activation within the amygdala to influence memory for emotionally arousing training. A β-adrenoceptor antagonist infused into the BLA blocks the memory-enhancing effect of systemically administered glucocorticoids.88,89 Furthermore, a β-adrenoceptor antagonist infused into the BLA blocked memory enhancement induced by a GR agonist infused into the hippocampus.90

Studies using in vivo microdialysis indicate that stress induced by prolonged immobilization or tail pinch increased amygdala norepinephrine levels.91,92 Even a single mild foot shock of the kind typically used in inhibitory avoidance training increased amygdala norepinephrine levels93 and the increase in norepinephrine varied with footshock intensity.94 Furthermore, as shown in Figure 13.1, amygdala norepinephrine levels assessed following inhibitory avoidance training correlated with retention latencies tested 24 hours later,95 whereas posttraining infusions of norepinephrine or β-adrenoceptor agonists administered into the BLA enhanced memory consolidation.96,97

FIGURE 13.1. Norepinephrine levels in the amygdala are significantly correlated with retention latency scores.


Norepinephrine levels in the amygdala are significantly correlated with retention latency scores. Each line represents norepinephrine levels as a percentage of baseline for an individual rat. Latency to enter the dark compartment on the retention test (more...)

Such findings suggest that systemically administered stress hormones may influence noradrenergic function by altering the synthesis, release, and/or reuptake of norepinephrine. In accord with this hypothesis, Williams and colleagues33 showed that epinephrine administered immediately after inhibitory avoidance training increased norepinephrine levels in the amygdala.

Brainstem noradrenergic cells in the locus coeruleus and NTS are involved not only in mediating epinephrine effects on memory consolidation but also express high levels of GRs.98 Posttraining infusions of a GR agonist into the NTS dose-dependently enhanced memory consolidation of inhibitory avoidance training and the memory enhancement was blocked by intra-BLA infusions of the β-adrenoceptor antagonist atenolol.50 The findings of a recent in vivo microdialysis experiment support the view that glucocorticoids may influence norepinephrine release in the BLA. Corticosterone administration after inhibitory avoidance training increased norepinephrine levels in the amygdala.99 In contrast, corticosterone did not increase norepinephrine levels in the amygdala when administered to naive rats that did not receive inhibitory avoidance training, indicating that glucocorticoids facilitate, but cannot initiate, the release of norepinephrine in the amygdala.

At a postsynaptic level, glucocorticoids may enhance memory consolidation by potentiating β-adrenoceptor-cAMP/PKA efficacy in the BLA.100 Activation of β-adrenoceptors in the BLA enhanced memory consolidation via stimulation of the cAMP/PKA pathway.101,102 We found that intra-BLA infusions of a GR antagonist attenuated the dose-response effects of a β-adrenoceptor agonist on retention enhancement for inhibitory avoidance training. The GR antagonist had no effect on memory enhancement induced by posttraining intra-BLA infusions of the synthetic cAMP analog 8-Br-cAMP.100 These findings suggest that glucocorticoids facilitate the efficacy of noradrenergic stimulation in the BLA on memory consolidation via an interaction with the β-adrenoceptor-cAMP cascade. A model of this interaction is illustrated in Figure 13.2.

FIGURE 13.2. Summary of interactions of glucocorticoids with the noradrenergic system of the basolateral amygdala at both presynaptic and post-synaptic sites as suggested by the findings of our experiments.


Summary of interactions of glucocorticoids with the noradrenergic system of the basolateral amygdala at both presynaptic and post-synaptic sites as suggested by the findings of our experiments. α1 = α1-adrenoceptor. β =β-adrenoceptor. (more...)

13.5.1. Role Of Emotional Arousal-Induced Noradrenergic Activation

The findings summarized above indicate that emotional arousal induces the release of norepinephrine in the BLA and that adrenal stress hormones may facilitate this training-induced noradrenergic activation. Such findings suggest that emotional arousal-induced noradrenergic activation within the BLA may be essential in enabling stress hormone effects on memory consolidation.

In a recent experiment we investigated this hypothesis.89 As addressed above, corticosterone enhanced memory consolidation of object recognition training only in emotionally aroused rats that were not previously habituated to the context. Object recognition training in these rats also induced marked increases in noradrenergic activity within the BLA, as assessed by immunoreactivity for phosphorylated tyrosine hydroxylase (the rate-limiting enzyme in the biosynthesis of norepinephrine). As shown in Figure 13.3, a β-adrenoceptor antagonist administered either systemically or into the BLA blocked this corticosterone-induced memory enhancement. In contrast, infusion of a β-adrenoceptor antagonist into the hippocampus did not prevent the corticosterone-induced memory enhancement of object recognition training. These findings further indicate that glucocorticoids require noradrenergic activity in the BLA in regulating memory consolidation.

FIGURE 13.3. Glucocorticoid effects on memory consolidation for object recognition training require noradrenergic activation.


Glucocorticoid effects on memory consolidation for object recognition training require noradrenergic activation. Data represent discrimination index (%) on a 24-hour retention trial, expressed as mean ± SEM. (A) Effects of immediate posttraining (more...)

Importantly, training of context-habituated rats on the object recognition task did not induce significant increases in noradrenergic activation within the BLA.89 If the failure of corticosterone to enhance memory consolidation in context-habituated rats is due selectively to insufficient arousal-induced noradrenergic activation, then posttraining pharmacological augmentation of noradrenergic activity should provide the activation normally produced by novelty stress and enable glucocorticoid enhancement of memory consolidation. To examine this implication, a low dose of the α2-adrenoceptor antagonist yohimbine, which increases norepinephrine levels in the brain, was administered to habituated rats either alone or together with corticosterone immediately after object recognition training. Yohimbine administered alone did not affect retention performance. However, as shown in Figure 13.3, corticosterone administered concurrently with yohimbine induced dose-dependent retention enhancement. Posttraining injections of the two drugs separated by a 4-hour delay did not induce a preference for the novel object on the retention. These findings thus indicate that arousal-induced noradrenergic activation is necessary to mediate glucocorticoid effects on memory consolidation but that pharmacologically stimulated noradrenergic activity mimics the effects of emotional arousal in enabling glucocorticoid enhancement of memory consolidation under low-arousing training conditions.89 These finding support the notion that the noradrenergic component of emotional arousal is critical for memory enhancement induced by glucocorticoids and possibly by epinephrine.

13.5.2. Interactions At Cellular Level

Synergistic effects of glucocorticoids and the noradrenergic system in peripheral tissues including the lungs and liver have been implicated in the regulation of several cellular functions.103 Is there molecular evidence for interactions between these two systems in regulating memory consolidation? We recently reported that corticoster-one interacts with emotion-induced noradrenergic activation in activating the cAMP response-element binding (CREB) pathway in the BLA.89 Several findings have implicated CREB phosphorylation in the BLA in the modulation of memory consolidation.104,105 We found that corticosterone administered immediately after object recognition training significantly increased the number of pCREB-positive neurons in the BLA. Corticosterone did not alter the number of pCREB-positive BLA neurons in rats that received prior habituation to the training context. Importantly, however, corticosterone administered together with the noradrenergic stimulant yohimbine after object recognition training significantly increased pCREB immunoreactivity in the BLA. Thus, these findings are in accord with behavioral studies and indicate that corticosterone activates the CREB pathway in the BLA only with training conditions that induce sufficient noradrenergic activation.

Other studies have indicated that glucocorticoids may interact with noradrenergic mechanisms in increasing the expression and enzymatic activity of the MAPK pathway, leading to an increased expression of the immediate early gene Egr1 (early growth response-1).106 Like CREB, phosphorylation of MAPKs is considered critical for memory consolidation and long-term neuronal plasticity.107,108 Blockade of MAPK signaling in the hippocampus abolishes the enhancing effect of systemically administered corticosterone on contextual fear conditioning.106 Glucocorticoid effects on MAPK activation may be modulated by β-adrenoceptor activation. Activation of β-adrenoceptors by epinephrine and norepinephrine leads to the dissociation of G protein subunits β and γ. It has been demonstrated that β G protein subunits interact with phosphoinositide-3 kinase to stimulate the MAPK pathway.109,110 Further, epinephrine and norepinephrine were found to potentiate ligand-dependent GR transactivation in cultured hippocampal cells via β2-adrenoceptors.111


The evidence summarized in this chapter indicates that adrenal stress hormones influence memory processes in various animal and human memory tasks. Acutely administered or released epinephrine or glucocorticoids dose-dependently enhance the consolidation of long-term memory. However, the effects of stress hormones on the storage of long-term memories depend critically on the arousal state and noradrenergic activation of the BLA. These findings may help to explain why stress hormones do not uniformly modulate memory for all kinds of information but rather, preferentially influence the consolidation of emotionally arousing information. As adrenal stress hormones also play a critical role in the development of traumatic memories and posttraumatic stress disorder (PTSD),112–114 these findings may provide some understanding of the neurobiological processes that underlie the development of PTSD as well as some possible implications for therapeutic intervention (see Reference 115) to ensure that significant events are well remembered, but do not turn into pathophysiological conditions.


We sincerely appreciate Gabriel Hui’s assistance with the figures.


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