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Stress leads to increased activity of the sympathetic nervous system (SNS) and of the hypothalamic-pituitary-adrenal (HPA) axis. Stimulation of the latter induces the release of glucocorticoids (GCs) from the adrenal cortex. The multiple effects of GCs in the brain are the focus of the current chapter. Acute stress effects comprise the enhancement of long-term memory consolidation and the simultaneous impairment of memory retrieval. Moreover, a qualitative shift away from a cognitive response style toward a more stimulus-driven habitual response style occurs. The acute response to GCs is altered in major depressive disorder and posttraumatic stress disorder. Chronic stress causes structural alterations in the hippocampus and the medial prefrontal cortex in the form of dendritic atrophy. However, remaining plasticity and thus the potential to reverse these changes appears to be more common than previously thought. The advanced understanding of the central nervous system effects of GCs will ultimately lead to progress in the treatment of mental and systemic diseases characterized by HPA axis dysregulation.

Several factors modulate learning and memory in animals and humans, including age, biological sex, and even the type of information being learned. However, one of the most important modulators of learning and memory processes is steroid hormones, particularly sex and stress steroids. Over the last decade, the manipulations used to understand the mechanisms underlying steroid hormone influences on learning and memory have greatly advanced the field. This research has shown that across species, steroid hormones exert their influence on processes well beyond reproduction and stress; estradiol, progesterone, and cortisol substantially affect how information is encoded, consolidated, and subsequently, recalled.

Extensive evidence from both animal and human research indicates that adrenal stress hormones regulate memory of emotionally significant experiences. Epinephrine and glucocorticoids, released during an emotionally arousing experience, enhance the consolidation of newly acquired memories. Both stress hormone effects are integrated through noradrenergic activation within the basolateral complex of the amygdala. Recent findings indicate that glucocorticoid interactions with the noradrenergic system involve rapid actions via a membrane-associated steroid receptor and downstream endocannabinoid signaling. In contrast to their enhancing effects on consolidation, glucocorticoids impair memory retrieval and working memory during emotionally arousing situations, which also require noradrenergic and endocannabinoid signaling.

Stress can have impairing, enhancing, or no influence on memory systems and processes. The present chapter reviews, albeit selectively, the impact of stress on human memory with a particular focus on clinical populations. The consequence of stress on memory systems will be reviewed focusing on working memory, implicit and explicit memory, episodic, and autobiographical memory. This is followed by the review of the impact of stress on memory phases including encoding, consolidation, retrieval, and reconsolidation. Throughout the review, the effects of stress on memory are linked to psychiatric disorders, and clinical implications are considered.

Chronic stress is associated with a different pattern of physiological, neural, and behavioral changes depending on the sex of the subject receiving the stress. In this review, the sex-dependent effects of chronic stress on learning and memory are reviewed in adult and developing (perinatal and adolescent) rodents. While males show impairments in aspects of cognitive function following chronic stress, females show a general resilience in performance of the same cognitive tasks following the same stresses. Moreover, studies show that alcohol alleviates stress-dependent cognitive impairments in males but is associated with impaired cognition when it is administered to stressed females. The possible role of different learning and memory strategies in the sexes on the outcomes of chronic stress as well as the ability of estradiol to confer cognitive resilience to stress in females is discussed. Finally, the results presented are considered within the context of well described sex differences in mental disorders associated with stress and in relation to substance use/abuse.

Stress exerts influences on learning and memory in multiple ways. We will begin by outlining how stress and stress hormones affect episodic memory in its three stages: encoding, consolidation, and retrieval from long-term memory. Following this, different stages of conditioning processes such as acquisition, extinction, and retrieval will be examined. In particular, we will present and discuss available data on sex differences to emphasize the impact of gonadal hormones and the intake of hormonal contraceptives on these two forms of long-term memory. A better understanding of why women and men sometimes react differently to the very same stressor is important for basic research on learning and memory, but also for deeper insights into the development and maintenance of psychiatric disorders based on these processes.

During a traumatic event, mainly emotional, sensory, and perceptual information is stored in an interconnected neural network. This network can be activated by environmental stimuli and internal cues later at any given time. An activation of the entire network is thought to be a flashback, which is one of the cardinal symptoms of post-traumatic stress disorder (PTSD). Additionally, the PTSD symptom of avoidance can be seen as a consequence of the activation of the trauma network. In contrast to the extensive memory of sensory-perceptual information, memories of traumatic events are characterized by a disconnectedness from temporal and spatial information about the general event and cannot be clearly positioned in a lifetime period. Furthermore, traumatic stress and the distribution of stress hormones during a traumatic event cause strong structural and functional alterations of brain structures involved in memory processing, like the hippocampus and the amygdala.

Stress activates the hypothalamus-pituitary-adrenal axis, which causes the release of glucocorticoids, a class of adrenal steroid hormones. Stress also activates the sympathetic nervous system and thereby, the release of the transmitters adrenaline and noradrenaline. Stress has a memory-modulatory effect in humans as well as in animals. In humans, the hippocampus, prefrontal cortex, and amygdala are rich in cortisol receptors. Acute and tolerable stress may increase memory performance, while excessive levels and chronic stress may have negative effects, thereby mimicking the pattern in animals. Stress in humans seems to have different effects on the various stages of memory (the memory process: encoding, consolidation, and retrieval) and can be enhanced by emotional arousal. Animals learn to associate events in their environment. Studies of the effects of manipulation of corticosterone levels in animals have helped to disentangle the influences of stress on memory and learning, and indicated that low levels enhance spatial learning, whereas higher levels impair performance.

For a cognitive conceptualization, stress arises when environmental demands are perceived as taxing or potentially exceeding one's own capacity or resources to manage them, and there is threat to well-being if coping responses do not satisfy such demands. A cognitive vulnerability factor enhancing stress is trait anxiety, through hypervigilant processing styles involving selective orienting to threat cues, biased negative interpretation of ambiguous stimuli, and focusing attention on unfavorable thoughts. Short-term episodes of mild-intensity stress can facilitate cognitive functions, mainly encoding and memory consolidation of task-relevant stimuli, and in implicit memory or simple declarative tasks. However, exposure to high-intensity stress impairs the formation and retrieval of explicit memories and cognitive processes requiring complex or flexible reasoning. Long-term stress, particularly during childhood and adolescence, consistently undermines cognitive mechanisms. This can be due to chronic elevations of glucocorticoids inhibiting neurogenesis, which damages important functions in the hippocampus and, possibly, the prefrontal cortex.

Chronic stress evokes profound structural and molecular changes in the hippocampus, which may underlie spatial memory deficits. Corticotropin-releasing hormone (CRH) and CRH receptor 1 (CRHR1) mediate some of the rapid effects of stress on dendritic spine morphology and modulate learning and memory, thus providing a potential molecular basis for impaired synaptic plasticity and spatial memory by repeated stress exposure. Using adult male mice with CRHR1 conditionally inactivated in the forebrain regions, we investigated the role of CRH-CRHR1 signaling in the effects of chronic social defeat stress on spatial memory, the dendritic morphology of hippocampal CA3 pyramidal neurons, and the hippocampal expression of nectin-3, a synaptic cell adhesion molecule important in synaptic remodeling. In chronically stressed wild-type mice, spatial memory was disrupted, and the complexity of apical dendrites of CA3 neurons reduced. In contrast, stressed mice with forebrain CRHR1 deficiency exhibited normal dendritic morphology of CA3 neurons and mild impairments in spatial memory. Additionally, we showed that the expression of nectin-3 in the CA3 area was regulated by chronic stress in a CRHR1-dependent fashion and associated with spatial memory and dendritic complexity. Moreover, forebrain CRHR1 deficiency prevented the down-regulation of hippocampal glucocorticoid receptor expression by chronic stress but induced increased body weight gain during persistent stress exposure. These findings underscore the important role of forebrain CRH-CRHR1 signaling in modulating chronic stress-induced cognitive, structural and molecular adaptations, with implications for stress-related psychiatric disorders.

Certainly, beyond the implication of cholinergic system in memory and therapeutic applications, the muscarinic antagonist scopolamine had been a remarkable amnesic agent. In addition, therapeutic options for AD are currently limited to symptomatic treatment that only provides modest and temporary maintenance of cognitive and memory functions, without altering disease progression. Neurotransmitters like glutamate, GABA, dopamine and serotonin seem to be involved in memory and its alterations; hence some aspects and data are summarized. Importantly, 5-HT systems and neurobiological markers related to memory systems are revised. Likewise, protocols of training/testing, memory tasks and drugs used are briefly discussed. Importantly, determination if drugs, age and/or memory alone alter receptor expression and/or signal cascades is very important. Brain areas, neurotransmitters systems, drugs together with cognitive and behavioral demand of memory tasks, and protocols of training are highlighted. Molecular signaling is key field of scientific investigation; particularly, as the study of the molecular bases of memory has been become a field of the major scientific interest, hence, in the following lines some aspects are mentioned. Moreover, quest for memory enhancement is an important investigation area; considering that the global population is increasingly aging. Finally, in addition to pharmacological approaches, there are a number of behavioral manipulations that have been found to be effective in promoting memory.

Adaptively responding to acute stress has been of great importance for human and animal survival. However, for our species, stress-related disorders are putting an ever-increasing burden on healthcare systems. It is thus crucial to understand the basic processes and cognitive changes associated with acute stress. Here, we examined the effects of acute stress exposure on spatial (water maze) and memory (delayed match to sample and episodic-memory-like tasks) performance. We found striking performance deficits in stressed animals navigating in the water maze. We also found, in an episodic-like memory task, striking object-location deficits, but not in temporal-object association learning in stressed animals. Finally, no differences were apparent for any delay periods (up to 30 s) in a delayed match to sample task. Taken together, these results show a strong differential effect of acute stress on differing memory processes.

Corticosteroid hormones secreted by the adrenal cortex protect the brain against adverse events and are essential for cognitive performance. However, in recent literature, the central action of corticosteroids has mostly been portrayed as damaging and disruptive to memory formation. We argue that this paradox can be explained by appreciating the specific role of both mineralocorticoid and glucocorticoid receptors in the various stages of information processing. In addition, the context in which corticosteroid-receptor activation takes place is crucial in determining steroid-mediated effects. These effects generally favour adaptive behaviour that is most relevant to the situation. Corticosteroid effects on cognition can, however, turn from adaptive into maladaptive, when actions via the two corticosteroid-receptor types are imbalanced for a prolonged period of time.

In teleost fishes, acute stressors induce a complex stress response coordinated by the brain and mediated via catecholamines, in particular adrenalin, and the corticosteroid cortisol. Adrenalin actions provide the energy for immediate action directed at survival, which is supported by actions of cortisol directed at reallocation of energy away from growth, reproduction, and the immune system. Cortisol further promotes adaptations increasing the stress resistance and restores the disturbance of the hydromineral imbalance, a phenomenon typical for stress in fishes. During chronic stress, adrenalin hyperactivity may result in cardiovascular problems and elevated cortisol in loss of body weight, reproductive failure, and reduced disease resistance. The endocrine coordination and interactions during stress involve almost all hormones. Marked individual differences in the stress response are related to past experiences and adaptations, inherent differences in stress-coping style, and maternal effects on the offspring.

Memories are sometimes enhanced by stress and at other times diminished. A unified conceptual framework is herein developed to identify the circumstances in which these opposing effects of stress are likely to be seen. Significant contributory factors appear to be the nature of the stressor, the nature of the learning task, and the relationship between the two. Stimulation of glucocorticoid receptors and activation of the amygdala are common to both types of effect. The challenge of future research is to further characterize downstream mechanisms that determine how these neural responses to stress promote or prevent memory formation under different circumstances.

Stress alters many psychological and behavioral processes. In humans, neuroimaging studies have demonstrated that long-term exposure to stress can lead to structural changes in brain areas, which are important in cognitive and emotional functions. Animal studies have extended these observations to the cellular level, showing that neurons within discrete regions of the hippocampus, prefrontal cortex, and amygdala demonstrate significant morphological plasticity in response to chronic stress. Though stress-induced changes in brain and behavior are largely reversible, some effects may be permanent. Given the clear role of stress in psychological and behavioral dysfunctions, a greater understanding of the effects of stress on the brain is essential.

Memory and learning appear to be important factors influencing animal survival and fitness. Animals need to learn and remember numerous pieces of information about breeding sites, food sources, shelters, neighbors, etc. Hormones are well known to have strong effects on learning and memory, and the effects of glucocorticoid and gonadal hormones on memory have been studied especially well. It has been established that glucocorticoid hormones produced by the adrenal glands are necessary for the maintenance of memory. Short-term elevations in glucocorticoids are generally considered to enhance memory and learning, but these effects appear to be both concentration and time dependent. Only moderate elevations seem to enhance memory while both strong elevations and low concentrations seem to impair memory. Long-term or chronic glucocorticoid elevations are generally considered memory impairing, but such generalization is somewhat controversial as data are mixed. It seems that moderate long-term elevations may have memory-enhancing effects, while only strong chronic elevations have negative effects. More research is needed to investigate specific effects of long-term elevations in glucocorticoids in a variety of species to better understand causal and evolutionary relationships between glucocorticoids and memory. Gonadal (testosterone, estradiol) hormones also appear to modulate memory, but effects of testosterone and estradiol on memory and learning seem to be quite complex and may depend on hormone concentration, timing, sex, and age. In addition, testosterone may affect memory both as an androgen and as an estrogen when it is converted into estradiol by aromatase in the brain. Future work should consider better integration of both environmental factors causing hormonal changes, the effects of hormonal changes on memory and learning, mechanisms, and consequences of these effects for biological fitness in a variety of species.

This article summarizes the effects of stress hormones on cognitive function in humans. The stress response that is generated by the body in response to a real or implied threat (an absolute or relative stressor) leads to the secretion of stress hormones that cross the blood–brain barrier and access the brain, where they can influence learning and memory by binding to receptors in specific regions of the brain. The effects of stress hormones on cognition in humans are relative, that is, they can be positive or negative, depending on a number of factors such as time of day, dose, nature, and valence of the to-be-remembered material.

The hippocampus is intimately sensitive to stress hormones and responds to stress through changes in structure, neurochemistry, and excitability. Both acute and chronic stress can compromise the hippocampus: acute stress exacerbates hippocampal damage when combined with a metabolic challenge, while chronic stress directly produces hippocampal dendritic retraction. Neurons expressing dendritic retraction may inadvertently increase the risk for compromised hippocampal health. Factors influencing hippocampal health include genetics, stress exposure during development, gender, and coping strategies. Understanding these risks and taking steps to avoid or attenuate the impact of chronic stress can help mitigate the potential negative effects on the body and brain.

Extensive evidence from both animal and human research indicates that epinephrine and glucocorticoid hormones, released from the adrenal glands during emotionally arousing experiences, facilitate the consolidation of newly acquired memories. These adrenal stress hormone effects are integrated through noradrenergic activation within the basolateral amygdala, which regulates memory consolidation via interactions with many other brain regions. In contrast to their enhancing effects on consolidation, adrenal stress hormones impair memory retrieval and working memory. This phenomenon, which is usually highly adaptive, provides also some understanding of the neurobiological processes that might underlie the formation and persistence of very strong emotional or traumatic memories in patients with posttraumatic stress disorder, phobias and other anxiety disorders as well as some possible implications for therapeutic intervention.

The neurobiological substrate of learning process and persistent memory storage involves multiple brain areas. The neocortex and hippocampal formation are known as processing and storage sites for explicit memory, whereas the striatum, amygdala, neocortex and cerebellum support implicit memory. Synaptic plasticity, long-term changes in synaptic transmission efficacy and transient recruitment of intracellular signaling pathways in these brain areas have been proposed as possible mechanisms underlying short- and long-term memory retention. In addition to the classical neurotransmitters (glutamate, GABA), experimental evidence supports a role for neuropeptides in modulating memory processes. This review focuses on the role of the Melanin-Concentrating Hormone (MCH) and receptors on memory formation in animal studies. Possible mechanisms may involve direct MCH modulation of neural circuit activity that support memory storage and cognitive functions, as well as indirect effect on arousal.

Mood disorders, depression, and bipolar disorder are characterized by abnormal adrenal steroid concentrations and neurocognitive impairments that may persist even after full recovery and hence may relate to fundamental underlying pathophysiologies of the illnesses. It has been suggested that the alterations in the functions of the hypothalamic-pituitary-adrenal (HPA) axis in patients, leading to corticosteroid overproduction, damages brain structures, including the frontal cortex and the hippocampus, thus causing neurocognitive impairment. Specifically, episodic memory, memory for previously encountered events, has been shown to be affected in mood disorders. The hippocampus and prefrontal cortex, which are known to play an important role in episodic memory, are cortisol sensitive. Cortisol administration to healthy volunteers has been shown to impair episodic memory and to lead to qualitative changes in the activity of frontal brain regions. Recently, dehydroepiandrosterone (DHEA) and other anti-glucocorticoids have been shown to improve episodic memory in healthy subjects and may have beneficial effects in the treatment of neurocognitive impairment in patients with mood disorders.

This chapter reviews extensive evidence from both animal and human research indicating that stress hormones activated by emotional arousal modulate the consolidation of memory of recent experiences. The hormones interact with other neuromodulatory systems in influencing noradrenergic activation of the basolateral amygdala. The amygdala regulates the consolidation of different kinds of memory via its projections to other brain regions. This coordinated modulatory system serves to regulate the strength of memories in relation to their emotional significance. Stress hormones also influence memory retrieval and working memory. And, as with memory consolidation, their effects involve noradrenergic activation of the basolateral amygdala and its interactions with other brain regions.

Glucoccorticoids (GCs) are secreted in response to stress in order to enhance adaptation. With respect to memory, these hormones enhance the consolidation of emotionally relevant information. This beneficial effect comes at a certain cost, namely impaired retrieval and impaired working memory. The effects are modulated by multiple factors such as sex, time of day, GC dose, and the emotionality of the learning material. Chronically elevated GC levels appear mostly to impair memory. Simultaneously, structural alterations are observed in several brain regions. However, remaining plasticity appears to be more common than previously thought.

Traumatic stress can lead to chronic symptoms of posttraumatic stress disorder (PTSD), which are mediated by changes in brain structure and function. Brain areas involved in memory, including the hippocampus, prefrontal cortex, and amygdala, mediate symptoms of PTSD and associated memory dysfunction.

A key assumption in the study of stress-induced cognitive and neurobiological modifications is that alterations in hippocampal functioning after stress are due to an excessive activity exerted by the amygdala on the hippocampus. Research so far focused on stress-induced impairment of hippocampal plasticity and memory but an exposure to stress may simultaneously also result in strong emotional memories. In fact, under normal conditions emotionally charged events are better remembered compared with neutral ones. Results indicate that under these conditions there is an increase in activity within the amygdala that may lead to memory of a different quality. Studying the way emotionality activates the amygdala and the functional impact of this activation we found that the amygdala modulates memory-related processes in other brain areas, such as the hippocampus. However, this modulation is complex, involving both enhancing and suppressing effects, depending on the way the amygdala is activated and the hippocampal subregion examined. The current review summarizes our findings and attempts to put them in context with the impact of an exposure to a traumatic experience, in which there is a mixture of a strong memory of some aspects of the experience but impaired memory of other aspects of that experience. Toward that end, we have recently developed an animal model for the induction of predisposition to stress-related disorders, focusing on the consequences of exposure to stressors during juvenility on the ability to cope with stress in adulthood. Exposing juvenile-stressed rats to an additional stressful challenge in adulthood revealed their impairment to cope with stress and resulted in significant elevation of the amygdala. Interestingly, and similar to our electrophysiological findings, differential effects were observed between the impact of the emotional challenge on CA1 and dentate gyrus subregions of the hippocampus. Taken together, the results indicate that long-term alterations within the amygdala contribute to stress-related mnemonic symptoms and suggest that elucidating further these intra-amygdala alterations and their effects on modulating other brain regions is likely to be beneficial for the development of novel approaches to treat stress-related disorders.

Publisher Summary This chapter focuses on the impact of the stress-related adrenal hormones, epinephrine and corticosterone, and the reproduction-related ovarian hormones, estrogen and progesterone on learning and memory. Epinephrine enhances learning and memory in a wide range of tasks, including avoidance, extinction of avoidance, and spatial memory tasks. Some of the recent works indicate that adrenal steroids, particularly corticosterone, have potent effects on learning and memory. Like injections of epinephrine, injections of corticosterone enhance memory for a wide range of tasks, e.g., inhibitory avoidance, fear conditioning, and object recognition. Estrogen has potent effects on the structure and functioning of the adult brain. The direction of estrogen action on learning and memory depends on several variables: stress levels, type and duration of hormone regimen, and specific task and memory demands. Present literature validates that estradiol, the most potent naturally found estrogen in mammals, modulates memory formation and maintenance; and biases the learning strategy used to solve a task by altering the relative participation of different neural systems during task performance. There are also consistent findings present showing that progesterone has dramatic effects on brain function and behavior, particularly related to anxiety and fear. The effects of progesterone on cognition are dependent on factors such as the timing of treatments and testing paradigms. The chapter also describes evidence that both stress hormones and reproductive hormones have robust and reliable effects on learning and memory. There are several features of this finding: broad cognitive effects, timing, peripheral and central effects, and molecular and cellular bases

An organism undergoes a series of physiological changes when exposed to a stressor. In the short term, several brain centers can be activated, including, among others, the locus coeruleus in the brain stem, the paraventricular nucleus in the hypothalamus, and amygdala and hippocampus in the limbic system. The activation of these centers leads to increased sympathetic nervous system (SNS) activity and elevated hypothalamic-pituitary-adrenocortical (HPA) axis hormones. These responses are homeostatic mechanisms that allow an individual to cope with a stressor and eventually turn off the stress response through negative feedback. However, if people are exposed to a very severe or prolonged stressor, more persistent changes characteristic of posttraumatic stress disorder or a general stress reaction can become established. Animal models of stress have been used to study these and other facets of acute and chronic stress responses.

Publisher Summary This chapter proposes a translational model of the pathogenesis of post-traumatic stress disorder (PTSD), according to which a psychologically traumatic event (unconditioned stimulus, UCS) overstimulates endogenous stress hormones as part of a physiological unconditioned response (UCR). These in turn overly strengthen the consolidation of the memory of the event, leading to a powerful and persistent memory (or conditioned response, CR) that is too easily activated, with consequent anxiety and dysfunction. The model further posits that after the memory of the traumatic event has been consolidated, free or cue-induced recall of the event (conditioned stimulus, CS) causes re-releases of stress hormones that further enhance the strength of the memory trace (or CR), increasing the likelihood that it will be re-recalled with yet further stress hormone releases, thereby resulting in a positive feedback loop, or vicious cycle, that promotes the development of PTSD. The purpose of this model is to illustrate at the theoretical level the numerous, and sometimes opposing, potential influences of the HPA axis on the pathogenesis of PTSD. According to this model, CRH, adrenocorticotropin (ACTH), and arginine vasopressin (AVP), as well as epinephrine and norepinephrine, are expected to facilitate the formation of a traumatic memory after an intensely frightening event in humans, and thereby be potentially involved in the formation of PTSD.

Extensive evidence indicates that stress hormones released from the adrenal glands are critically involved in memory consolidation of emotionally arousing experiences. Epinephrine or glucocorticoids administered after exposure to emotionally arousing experiences enhance the consolidation of long-term memories of these experiences. Our findings indicate that adrenal stress hormones influence memory consolidation via interactions with arousal-induced activation of noradrenergic mechanisms within the amygdala. In turn, the amygdala regulates memory consolidation via its efferent projections to many other brain regions. In contrast to the enhancing effects on consolidation, high circulating levels of stress hormones impair memory retrieval and working memory. Such effects also require noradrenergic activation of the amygdala and interactions with other brain regions.

Normal aging is associated with mild, but significant changes in learning and memory. One brain structure that has been well-studied with regard to memory deficits that occur in advanced age is the hippocampus. The hippocampus plays an important role in memory in mammals, and is required in many species for accurate navigation and way-finding. Age-related hippocampal changes that may contribute to observed age-related spatial learning deficits are reviewed. Although cell numbers are well-preserved in the hippocampus during aging, there are specific changes that occur in connectivity and plasticity mechanisms in the hippocampus that have been correlated with spatial memory decline in rodents. These neural changes lead to alterations in hippocampal network dynamics that result in failures of information retrieval, and the behavioral appearance of older animals having a greater tendency to become lost. Understanding age-related changes in brain structure and function may ultimately lead to the development of methods that can attenuate memory loss and improve life quality of older individuals.

Publisher Summary Findings from extensive research involving both human and animal subjects converge on the view that modulation of memory storage for emotionally arousing events occurs, at least in part, by an interaction of endogenous stress hormone systems and the amygdala complex. This chapter discusses the key findings supporting this view, including new evidence from human subject studies. While many different stress hormones have been implicated in memory modulation, including adrenocortical hormones, the focus is on the catecholamines, as they have been most consistently implicated in memory. The chapter also addresses another hypothesis of amygdale function in memory— namely, that the amygdala is the place where Pavlovian fear conditioning associations are formed and permanently stored. The findings in this chapter argues strongly against the view that narrative rehearsal is a sufficient explanation of enhanced memory associated with emotional arousal, and provide additional support for amygdala modulation of memory for emotional material.

Publisher Summary This chapter provides evidence to indicate that the amygdaloid complex (AC) has a particular role in brain memory mechanisms. It interacts with stress hormones released during and after emotional events to modulate memory for those events. The effect of endogenous stress hormones on memory follows a typical pattern. The chapter suggests that memory for emotionally arousing events requires activation of β-adrenergic receptors and the AC. The effect of β-adrenergic impairment has been examined on enhanced memory associated with emotional arousal in healthy humans. It has been found that the AC is involved in long-term, emotionally influenced, declarative memory in humans. The fact that both the β-adrenergic system and the AC are implicated in memory within a single experimental paradigm further argues for an interaction between the two in storing memory for emotional events. It has been also demonstrated that selective involvement of the amygdala in enhanced long-term, emotionally influenced, declarative memory in healthy humans using positron emission tomography (PET). These PET findings indicate that the amygdala is not required for declarative memory in all circumstances; rather, it is selectively important for the formation of enhanced memory normally associated with emotional arousal. Collectively, these experiments strongly support the view that memory for emotionally arousing events is modulated by endogenous, hormonally based systems.