Acute stress and episodic memory retrieval: neurobiological mechanisms and behavioral consequences

Abstract

Episodic retrieval allows people to access memories from the past to guide current thoughts and decisions. In many real-world situations, retrieval occurs under conditions of acute stress, either elicited by the retrieval task or driven by other, unrelated concerns. Memory under such conditions may be hindered, as acute stress initiates a cascade of neuromodulatory changes that can impair episodic retrieval. Here, we review emerging evidence showing that dissociable stress systems interact over time, influencing neural function. In addition to the adverse effects of stress on hippocampal-dependent retrieval, we consider how stress biases attention and prefrontal cortical function, which could further affect controlled retrieval processes. Finally, we consider recent data indicating that stress at retrieval increases activity in a network of brain regions that enable reflexive, rapid responding to upcoming threats, while transiently taking offline regions supporting flexible, goal-directed thinking. Given the ubiquity of episodic memory retrieval in everyday life, it is critical to understand the theoretical and applied implications of acute stress. The present review highlights the progress that has been made, along with important open questions.

The effects of acute stress on core executive functions: A meta-analysis and comparison with cortisol

“…Although cortisol administration appears to bias cognitive processing in this way, we found that stress impaired cognitive inhibition. Second, our results provide only partial support for the perspective that stress impairs executive control and shifts cognition to a state of reactive or habitual action to facilitate adaptation to current circumstances (Gagnon and Wagner, 2016; Vogel et al, 2016). Although stress impaired almost all executive functions, stress enhanced response inhibition, which is inconsistent with the idea that stress impairs all executive control.…”

“…By impairing executive control of cognition (i.e., working memory, cognitive inhibition, and cognitive flexibility), stress contributes to a reactive cognitive state that is fine-tuned to rapidly consider highly salient (i.e., stressor-related) information (Gagnon and Wagner, 2016; Vogel et al, 2016). Our perspective is thus in agreement with models that suggests stress impairs executive control in order to force attention toward highly salient information (Vogel et al, 2016), but our perspective differs from these models by arguing that it is not all top-down control that is impaired by stress—only executive control of cognition is impaired, leaving executive control of motor actions intact.…”

“…That is, although there are clear cases in which stress disrupts some aspects of cognition there are others in which it clearly benefits cognitive processes. For example, stress generally impairs long term memory retrieval (Gagnon and Wagner, 2016), whereas it can enhance memory encoding (Wiemers et al, 2013), memory retention (Cahill et al, 2003), and decision-making (Shields et al, 2016a). Moreover, although there are many reports of stress impairing executive functions (Alexander et al, 2007; Schoofs et al, 2009), there are other cases in which stress has no effect on executive functions (Quinn and Joormann, 2015), and yet others show that stress can even improve them (Schwabe et al, 2013).…”

“…Recently, another theory of stress and cognitive function has been proposed that argues that stress shifts cognition from top-down control processes to more bottom-up automatic processes (Gagnon and Wagner, 2016; Vogel et al, 2016). Because all core executive functions are thought to be top-down processes, this model would fit with the literature discussed above that has found impairing effects of stress on cognitive inhibition, working memory, and cognitive flexibility.…”

Commentary: Retrieval practice protects memory against acute stress

“…This phenomenon has been replicated repeatedly (e.g., Buchanan et al, 2006; Smeets, 2011) even though, of course, non-significant effects and even the reversed pattern were reported (e.g., Wolf et al, 2002; Hupbach and Fieman, 2012). These non-replications may reflect a more moderate stress response and/or particularities of the learning material used in the studies (for reviews see Cadle and Zoladz, 2015; Gagnon and Wagner, 2016; Wolf, 2017). Studies in rodents revealed that this effect is caused by an interaction of a noradrenergic signal induced by the first response wave (the sympathetic nervous system) and a glucocorticoid signal induced by the second response wave (the hypothalamus-pituitary-adrenal (HPA) axis) (Roozendaal et al, 2006).…”