Stress, memory and amygdala

Department of Neuroscience, University Medical Center Groningen, University of Groningen, the Netherlands.
Nature Reviews Neuroscience (Impact Factor: 31.43). 07/2009; 10(6):423-33. DOI: 10.1038/nrn2651
Source: PubMed


Emotionally significant experiences tend to be well remembered, and the amygdala has a pivotal role in this process. But the efficient encoding of emotional memories can become maladaptive - severe stress often turns them into a source of chronic anxiety. Here, we review studies that have identified neural correlates of stress-induced modulation of amygdala structure and function - from cellular mechanisms to their behavioural consequences. The unique features of stress-induced plasticity in the amygdala, in association with changes in other brain regions, could have long-term consequences for cognitive performance and pathological anxiety exhibited in people with affective disorders.

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Available from: Benno Roozendaal,
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    • "In addition, intra-BLA infusion of drugs that boost noradrenergic activity is sufficient to enhance DLS-dependent habit memory (Packard and Wingard, 2004; Elliott and Packard, 2008; Wingard and Packard, 2008), suggesting that the BLA noradrenergic system might have a critical role in the emotional enhancement of habit memory. The BLA has also been verified as an important locus for the effects of glucocorticoid and noradrenergic interactions on memory (Roozendaal et al., 2009). Stimulation of glucocorticoid receptors in the BLA enhances memory in an inhibitory avoidance task, and this effect may be attributed to glucocorticoids' facilitation of BLA b-adrenoreceptors, which in turn stimulates the cAMPdependent protein kinase pathway (Roozendaal et al., 2002). "
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    ABSTRACT: Previous findings indicate that post-training administration of glucocorticoid stress hormones can interact with the noradrenergic system to enhance consolidation of hippocampus- or amygdala-dependent cognitive/emotional memory. The present experiments were designed to extend these findings by examining the potential interaction of glucocorticoid and noradrenergic mechanisms in enhancement of dorsolateral striatum (DLS)-dependent habit memory. In experiment 1, different groups of adult male Long-Evans rats received training in two DLS-dependent memory tasks. In a cued water maze task, rats were released from various start points and were reinforced to approach a visibly cued escape platform. In a response-learning version of the water plus-maze task, animals were released from opposite starting positions and were reinforced to make a consistent egocentric body-turn to reach a hidden escape platform. Immediately post-training, rats received peripheral injections of the glucocorticoid corticosterone (1 or 3 mg/kg) or vehicle solution. In both tasks, corticosterone (3 mg/kg) enhanced DLS-dependent habit memory. In experiment 2, a separate group of animals received training in the response learning version of the water plus-maze task and were given peripheral post-training injections of corticosterone (3 mg/kg), the β-adrenoreceptor antagonist propranolol (3 mg/kg), corticosterone and propranolol concurrently, or control vehicle solution. Corticosterone injections again enhanced DLS-dependent memory, and this effect was blocked by concurrent administration of propranolol. Propranolol administration by itself (3 mg/kg) did not influence DLS-dependent memory. Taken together, the findings indicate an interaction between glucocorticoid and noradrenergic mechanisms in DLS-dependent habit memory. Propranolol administration may be useful in treating stress-related human psychopathologies associated with a dysfunctional DLS-dependent habit memory system.
    Neuroscience 10/2015; 311:1-8. DOI:10.1016/j.neuroscience.2015.10.014 · 3.36 Impact Factor
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    • "In addition to the research on chronic stress and amygdala structure, animal studies (Roozendall et al., 2009) as well as investigations of human trauma victims (Shin et al., 2006) reveal greater amygdala reactivity among organisms in relation to chronic stress exposure and for adolescents exposed to a family history of depression and stressful life events (Swartz et al., 2015a). Moreover, these relations also appear to be sensitive to developmental timing , with earlier-relative to later-in-life stress more effective in altering amygdala functioning (Tottenham and Sheridan, 2010; Nelson and Sheridan, 2011). "
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    ABSTRACT: Considerable work indicates that early cumulative risk exposure is aversive to human development, but very little research has examined the neurological underpinnings of these robust findings. This study investigates amygdala volume and reactivity to facial stimuli among adults (mean 23.7 years of age, n = 54) as a function of cumulative risk exposure during childhood (9 and 13 years of age). In addition, we test to determine whether expected cumulative risk elevations in amygdala volume would mediate functional reactivity of the amygdala during socioemotional processing. Risks included substandard housing quality, noise, crowding, family turmoil, child separation from family, and violence. Total and left hemisphere adult amygdala volumes were positively related to cumulative risk exposure during childhood. The links between childhood cumulative risk exposure and elevated amygdala responses to emotionally neutral facial stimuli in adulthood were mediated by the corresponding amygdala volumes. Cumulative risk exposure in later adolescence (17 years of age), however, was unrelated to subsequent adult amygdala volume or function. Physical and socioemotional risk exposures early in life appear to alter amygdala development, rendering adults more reactive to ambiguous stimuli such as neutral faces. These stress-related differences in childhood amygdala development might contribute to the well-documented psychological distress as a function of early risk exposure. © 2015 Wiley Periodicals, Inc.
    Journal of Neuroscience Research 10/2015; DOI:10.1002/jnr.23681 · 2.59 Impact Factor
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    • "Other outcomes of excessively high levels of cortisol expression include decreased immunocompetence [26], increased risk of infection, osteoporosis, steroid diabetes, and destruction of hippocampal neurons leading to cell loss, depression and chronic distress [25] [27]. Relevant to the study of anxiety, hypercortisolaemia may also alter the structure and function of brain regions [28] which may contribute to the development of anxiety, depression [29] [30] [31] and other psychiatric conditions [32]. Of interest, prolonged hypercortisolaemia can also induce hypocortisolaemia via the feedback process in the hypothalamus that monitors serum cortisol and adjusts production of CRF accordingly. "
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    ABSTRACT: To identify if age influenced the relationship between one of the central symptoms of Autism Spectrum Disorder (ASD) and physiological stress, the association between stereotypic behaviour (SB) and stress-related cortisol concentrations was examined in a sample of 150 young males with an ASD. Parent-rated SB was significantly correlated with cortisol concentrations for boys aged 6years to 12years but not for adolescents aged 13years to 18years. This age-related difference in this association was not a function of cortisol concentrations but was related to differences in SB across these two age groups. IQ did not have a significant effect on this relationship, suggesting that age-related learning may have been a possible pathway for reduced SB during adolescence. The aspect of SB that was most powerfully related to cortisol was general repetitive behaviour rather than movements of specific body parts. Explanations of these findings are raised for further investigation.
    Physiology & Behavior 10/2015; DOI:10.1016/j.physbeh.2015.10.010 · 2.98 Impact Factor
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