Stress time-dependently influences the acquisition and retrieval of unrelated information by producing a memory of its own

Abstract

Stress induces several temporally guided "waves" of psychobiological responses that differentially influence learning and memory. One way to understand how the temporal dynamics of stress influence these cognitive processes is to consider stress, itself, as a learning experience that influences additional learning and memory. Indeed, research has shown that stress results in electrophysiological and biochemical activity that is remarkably similar to the activity observed as a result of learning. In this review, we will present the idea that when a stressful episode immediately precedes or follows learning, such learning is enhanced because the learned information becomes a part of the stress context and is tagged by the emotional memory being formed. In contrast, when a stressful episode is temporally separated from learning or is experienced prior to retrieval, such learning or memory is impaired because the learning or memory is experienced outside the context of the stress episode or subsequent to a saturation of synaptic plasticity, which renders the retrieval of information improbable. The temporal dynamics of emotional memory formation, along with the neurobiological correlates of the stress response, are discussed to support these hypotheses.

Keywords: amygdala; hippocampus; long-term potentiation (LTP); metaplasticity; stress.

FIGURE 1

Temporal dynamics of acute stress effects on hippocampus-dependent learning and memory. Shortly following onset, stress induces a rapid increase in norepinephrine (NE), glutamate (Glu) and several other neurochemical substances (e.g., CRH, acetylcholine, dopamine, etc.). Within a few minutes, corticosteroids (CORT) are also released and can exert rapid, non-genomic effects on cellular activity. Combined, this rapid stress-induced neurochemical activity results in an enhancement of hippocampal function, and learning that occurs around this time frame would be enhanced (A). However, as time and/or the stressor continues, desensitization of glutamatergic NMDA receptors and delayed, gene-dependent corticosteroid activity results in an inhibition of hippocampal function, and learning that occurs around this time frame would be impaired. The bottom figure (B) illustrates these principles. When stress (indicated by the red lightning bolts) occurs in close temporal proximity to learning, long-term memory retrieval will be enhanced. When the stressor is temporally separated from the learning or occurs prior to retrieval, long-term memory will be impaired.