Stress effects on memory: An update and integration

Schwabe, Lars; Joëls, Marian; Roozendaal, Benno; Wolf, Oliver T.; Oitzl, Melly S.

doi:10.1016/j.neubiorev.2011.07.002

Cited by 633 publications

(516 citation statements)

References 128 publications

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“…The effects of acute stress on cognition are complex and determined by a number of factors including the specific stressor, task, sex of the subject, and timing of the stress relative to the task [1][2][3][4][5]. Acute stress has been associated with detrimental effects on cognition, as has been demonstrated for the retrieval of declarative-like forms of memory such as spatial and recognition memory mediated by structures of the temporal lobe [2,3].…”

Section: Introductionmentioning

confidence: 99%

Stress facilitates late reversal learning using a touchscreen-based visual discrimination procedure in male Long Evans rats

Bryce

Howland

2015

Behavioural Brain Research

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The stress response is essential to the survival of all species as it maintains internal equilibrium and allows organisms to respond to threats in the environment. Most stress research has focused on the detrimental impacts of stress on cognition and behavior. Reversal learning, which requires a change in response strategy based on one dimension of the stimuli, is one type of behavioral flexibility that is facilitated following some brief stress procedures. The current study investigated a potential mechanism underlying this facilitation by blocking glucocorticoid receptors (GRs) during stress. Thirty-seven male Long Evans rats learned to discriminate between two images on a touchscreen, one of which was rewarded. Once a criterion was reached, rats received stress (30 min of restraint stress or no stress) and drug (GR antagonist RU38486 or vehicle) administration prior to each of the first 3 days of reversal learning. We expected that stress would facilitate reversal learning and RU38486 (10 mg/kg) would prevent this facilitation in both early (<50% correct in one session) and late (>50% correct in one session) stages of reversal learning. Results showed that stressed rats performed better than unstressed rats (fewer days for late reversal, fewer correction trials, and fewer errors) in the late but not early stage of reversal learning. RU38486 did not block the facilitation of RL by stress, although it dramatically increased response, but not reward, latencies. These results confirm the facilitation of late reversal by stress in a touchscreenbased operant task in rats and further our understanding of how stress affects higher level cognitive functioning and behavior.

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Section: Introductionmentioning

confidence: 99%

Stress facilitates late reversal learning using a touchscreen-based visual discrimination procedure in male Long Evans rats

Bryce

Howland

2015

Behavioural Brain Research

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“…Cognitive brain networks, including those centered on the hippocampus and prefrontal cortex regions involved in emotional processes, such as amygdala and the nucleus accumbens, as well as network involved in social behaviors, appear to be particularly vulnerable to the effects of stress (Kim and Diamond, 2002;Joëls and Baram, 2009;Lupien et al, 2009;Malter Cohen et al, 2013;Sandi and Haller, 2015). Important parameters that govern the effects of stress on brain functions include the context and nature of the stress (Zoladz and Diamond, 2008;Joëls and Baram, 2009;McEwen and Gianaros, 2011;Schwabe et al, 2011). Stress is not a unitary entity, but a spectrum of signals that vary both in severity and in duration.…”

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confidence: 99%

“…However, these same mechanisms, when activated intensely or for a prolonged period, may provoke detrimental effects (McEwen and Gianaros, 2011;Maras et al, 2014). In the mature human and rodent, chronic stress often exerts adverse effects on cognitive functions including memory (Kim and Diamond, 2002;McEwen and Gianaros, 2011;Schwabe et al, 2011).…”

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Toward Understanding How Early-Life Stress Reprograms Cognitive and Emotional Brain Networks

Chen

Baram

2015

Neuropsychopharmacol

409

327

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Vulnerability to emotional disorders including depression derives from interactions between genes and environment, especially during sensitive developmental periods. Adverse early-life experiences provoke the release and modify the expression of several stress mediators and neurotransmitters within specific brain regions. The interaction of these mediators with developing neurons and neuronal networks may lead to long-lasting structural and functional alterations associated with cognitive and emotional consequences. Although a vast body of work has linked quantitative and qualitative aspects of stress to adolescent and adult outcomes, a number of questions are unclear. What distinguishes 'normal' from pathologic or toxic stress? How are the effects of stress transformed into structural and functional changes in individual neurons and neuronal networks? Which ones are affected? We review these questions in the context of established and emerging studies. We introduce a novel concept regarding the origin of toxic early-life stress, stating that it may derive from specific patterns of environmental signals, especially those derived from the mother or caretaker. Fragmented and unpredictable patterns of maternal care behaviors induce a profound chronic stress. The aberrant patterns and rhythms of early-life sensory input might also directly and adversely influence the maturation of cognitive and emotional brain circuits, in analogy to visual and auditory brain systems. Thus, unpredictable, stress-provoking early-life experiences may influence adolescent cognitive and emotional outcomes by disrupting the maturation of the underlying brain networks. Comprehensive approaches and multiple levels of analysis are required to probe the protean consequences of early-life adversity on the developing brain. These involve integrated human and animal-model studies, and approaches ranging from in vivo imaging to novel neuroanatomical, molecular, epigenomic, and computational methodologies. Because early-life adversity is a powerful determinant of subsequent vulnerabilities to emotional and cognitive pathologies, understanding the underlying processes will have profound implications for the world's current and future children.

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“…Although most studies focused on GC effects on the acquisition and consolidation of memory, extensive evidence also indicates that acutely elevated GC levels at the time of retention testing impair the retrieval of memory of spatial and contextual training (5)(6)(7)(8)(9). Because a glucocorticoid receptor (GR) agonist infused into the hippocampus before retention induces comparable memory retrieval impairment (10,11), such findings suggest that GC effects on memory retrieval depend, at least in part, on activation of GRs in the hippocampus.…”

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confidence: 99%

Glucocorticoids interact with the hippocampal endocannabinoid system in impairing retrieval of contextual fear memory

Atsak

Hauer

Campolongo

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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123

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There is extensive evidence that glucocorticoid hormones impair the retrieval of memory of emotionally arousing experiences. Although it is known that glucocorticoid effects on memory retrieval impairment depend on rapid interactions with arousalinduced noradrenergic activity, the exact mechanism underlying this presumably nongenomically mediated glucocorticoid action remains to be elucidated. Here, we show that the hippocampal endocannabinoid system, a rapidly activated retrograde messenger system, is involved in mediating glucocorticoid effects on retrieval of contextual fear memory. Systemic administration of corticosterone (0.3-3 mg/kg) to male Sprague-Dawley rats 1 h before retention testing impaired the retrieval of contextual fear memory without impairing the retrieval of auditory fear memory or directly affecting the expression of freezing behavior. Importantly, a blockade of hippocampal CB1 receptors with AM251 prevented the impairing effect of corticosterone on retrieval of contextual fear memory, whereas the same impairing dose of corticosterone increased hippocampal levels of the endocannabinoid 2-arachidonoylglycerol. We also found that antagonism of hippocampal β-adrenoceptor activity with local infusions of propranolol blocked the memory retrieval impairment induced by the CB receptor agonist WIN55,212-2. Thus, these findings strongly suggest that the endocannabinoid system plays an intermediary role in regulating rapid glucocorticoid effects on noradrenergic activity in impairing memory retrieval of emotionally arousing experiences.cannabinoid receptor | norepinephrine | emotional arousal | fear conditioning | posttraumatic stress disorder I t is well-established that glucocorticoid (GC) hormones, released from the adrenal cortex during stressful episodes, can modulate different memory processes (1-4). Although most studies focused on GC effects on the acquisition and consolidation of memory, extensive evidence also indicates that acutely elevated GC levels at the time of retention testing impair the retrieval of memory of spatial and contextual training (5-9). Because a glucocorticoid receptor (GR) agonist infused into the hippocampus before retention induces comparable memory retrieval impairment (10, 11), such findings suggest that GC effects on memory retrieval depend, at least in part, on activation of GRs in the hippocampus. Findings of studies of human subjects are consistent with the findings of animal studies and indicate that exogenous GC administration or exposure to a psychosocial stressor shortly before retention testing impairs retrieval of declarative (mostly episodic) information (7, 12, 13) and reduces hippocampal activity (14). Moreover, previous findings indicate that emotionally arousing information is especially sensitive to the retrieval-impairing effects of GCs (8) and that emotional arousal during the test situation enables GC effects on memory retrieval (15). Findings of recent clinical studies suggest that the administration of stress doses of GCs may have therapeutic v...

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Stress effects on memory: An update and integration

Cited by 633 publications

References 128 publications

Stress facilitates late reversal learning using a touchscreen-based visual discrimination procedure in male Long Evans rats

Stress facilitates late reversal learning using a touchscreen-based visual discrimination procedure in male Long Evans rats

Toward Understanding How Early-Life Stress Reprograms Cognitive and Emotional Brain Networks

Glucocorticoids interact with the hippocampal endocannabinoid system in impairing retrieval of contextual fear memory

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