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. There are stressful situations in which we are unable to retrieve information that we have learned and thus should be readily available for recollection. This would be the case in a situation that carries enough stress to literally drain the blood supply from those regions of the brain that handle memory retrieval.
In contrast, we are also familiar with how well we seem to remember certain embarrassing, shameful, or frightening events from the past, which is an example of how stress can enhance our memory. This is the case in situations that carry such a strong power of emotional penetration that they burrow the deepest furrows in our memory circuits, often never to be forgotten and always readily recollected.
Finally, there are situations of chronic stress or stress associated with psychiatric disorders that are characterized by persistent hypo- (lower than normal) or hyperamnesia.
When Stress Attacks
Interaction with a stressor of sufficient strength that meets and surpasses the individual’s threshold of resistance leads to a cascade of neuroendocrine stress responses, which are in fact designed to attempt an adaptation (response) to the demands of the situation.
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 the aftermath of a stressor, they can have an almost instantaneous effect on the memory of humans.
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.
When the Threat Subsides
When the threat of the real of perceived stressor recedes in the distance either because of its elimination, its significant reduction, successful coping, or simply due to the passing of time, the organism gradually returns to the previous state of normal arousal. Cortisol is reabsorbed, GCs secretion ceases, and the systems of the body return to the status quo ante. Calm returns. This can take from just a few minutes to several hours or days. In some cases, as in chronic stress, the organism can never fully regain the state of normal arousal, reabsorption of cortisol is inhibited, the nervous system remains in a state of elevated alert, and the body experiences elevated blood pressure, muscle tension, and other disturbances.
What is often left behind is a complex effect on memory. Significant and rapid increases in GCs induced by acute stress episodes enhance memory consolidation of the details of these situations, but impair memory retrieval of other valuable information of lesser emotional charge. The impairing effects of stress-induced GC secretion might hinder us in performing well in an important exam or at an important job interview. In addition, GCs also appear to reduce the amount of items that can be stored in working memory, but this is less well documented than the effects on declarative long-term memory.