Stress can interfere with the functioning of memory by either augmenting the impact and persistence of the recollection of an event, or by diminishing both. A recent article by Schwabe et al. (2012) summarizes and updates the most recent findings on the effects of stress on memory. Their research concludes that the timing of the exposure to the stressor is crucial in determining whether memory is improved or impaired. Timing may explain why there are stressful situations in which we are unable to retrieve critical information that we have learned prior to the stressor, e.g. an important phone number or address. In contrast, experiencing stress at the same time as we participate in certain embarrassing, shameful, or frightening events can cause a dramatic enhancement of memory formation.
Schwabe and colleagues examine and attempt to integrate two models of how stress may alter memory processes, the “vertical” model (the mechanisms of stress on memory) and the “horizontal” model (the changes in stress effects on memory over time.)
The vertical perspective implicates principally the action of glucocorticoids (GC) and noradrenaline on the basolateral amygdala. In a typical stress reaction, the hypothalamus activates the hypothalamic-pituitary-adrenal (HPA) axis in response to input from several other brain regions and the sympathetic nervous system (SNS). Through the portal blood system, corticotrophin releasing hormone (CRH) and vasopressin flood the pituitary gland, which trigger its secretion of adrenocorticotropic hormone (ACTH). In response to ACTH release from the pituitary, the adrenal glands secrete glucocorticoids (GCs), of which cortisol is the principal component. GCs, which are lipophilic (fat-loving) steroid hormones, enter the brain relatively easily and can exert their excitatory effect in multiple regions throughout the brain. These effects are often mediated through the binding to the two receptors for the hormone: the mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR). These two receptors differ in their affinity for cortisol (with the MR having a much higher affinity) and also in their localization in the brain. In addition, GCs can exert nongenomic effects (occurring rapidly and acutely) by influencing ion channels or neurotransmitter receptors at the membrane level. It is important to note that CRH, vasopressin, and ACTH can, on their own, influence cognition. When released in concurrence with a stressor, they can have an almost instantaneous effect on memory processes.
The horizontal perspective suggests that the memory of an event or cognition is enhanced when new information is acquired during the stressful situation, whereas the memory process is impaired for information that was acquired prior to or after the stressful situation. In these situations, the flood of GCs acutely enhances memory consolidation of emotional arousing material, while significantly impairing memory retrieval. At the moment of greatest stress, the memory of a significantly stressful event is instantaneously etched into the memory banks in vivid and abundant detail. The recollection of a sometimes important and well-known piece of information is inhibited. It is as if the whole of our attention is absorbed, or mobilized, toward the assessment of the threat presented by the stressor and in the formulation of a reaction to it. The excitatory hormones cursing through the blood system rapidly arouse the nervous, cardio-circulatory, respiratory, and endocrine system. There is no time or resource available for other activities that are not related to the defense of the organism against the perceived (or real) threat of the stressor. Included in these “secondary” activities that are postponed as non-critical is memory retrieval of old information.
Other important findings highlighted in this article are the effects of stress on the striatum, a brain structure that was originally associated with motor control but that is now receiving increased attention as one of the loci of mnemonic function. Secondly, memory is affected by stress not only in terms of its quantity, but also its quality. Lastly, the authors cite important research conducted in the last decade which points to the effects of maternal stress during pregnancy or early childhood stress as harbingers of an individual’s impaired performance as an adult in high-stress environments.
The article concludes with several important questions, which provide an indication of the limits of current research in explaining important aspects of memory formation. For example, it remains difficult to understand how the same neurochemicals can exert opposite effects on the same brain structures, or how individuals in similar situations exhibit such differing recollections of the same event, and other similarly unexplored mysteries. These limitations do not detract from the thoroughness and relevance of this article.