Stress is widely considered to negatively impact hippocampal function, thus impairing episodic memory. However, the hippocampus is not merely the seat of episodic memory. Rather, it also (via distinct circuitry) supports statistical learning. On the basis of rodent work suggesting that stress may impair the hippocampal pathway involved in episodic memory while sparing or enhancing the pathway involved in statistical learning, we developed a behavioral experiment to investigate the effects of acute stress on both episodic memory and statistical learning in humans. Participants were randomly assigned to one of three conditions: stress (socially evaluated cold pressor) immediately before learning, stress ∼15 min before learning, or no stress. In the learning task, participants viewed a series of trial-unique scenes (allowing for episodic encoding of each image) in which certain scene categories reliably followed one another (allowing for statistical learning of associations between paired categories). Memory was assessed 24 hr later to isolate stress effects on encoding/learning rather than retrieval. We found modest support for our hypothesis that acute stress can amplify statistical learning: Only participants stressed ∼15 min in advance exhibited reliable evidence of learning across multiple measures. Furthermore, stress-induced cortisol levels predicted statistical learning retention 24 hr later. In contrast, episodic memory did not differ by stress condition, although we did find preliminary evidence that acute stress promoted memory for statistically predictable information and attenuated competition between statistical and episodic encoding. Together, these findings provide initial insights into how stress may differentially modulate learning processes within the hippocampus.

Acute stress has been shown to modulate the engagement of different memory systems, leading to preferential expression of stimulus–response (SR) rather than episodic context memory when both types of memory can be used. However, questions remain regarding the cognitive mechanism that underlies this bias in humans—specifically, how each form of memory is individually influenced by stress in order for SR memory to be dominant. Here we separately measured context and SR memory and investigated how each was influenced by acute stress after learning (Experiment 1) and before retrieval (Experiment 2). We found that postlearning stress, in tandem with increased adrenergic activity during learning, impaired consolidation of context memory and led to preferential expression of SR rather than context memory. Preretrieval stress also impaired context memory, albeit transiently. Neither postlearning nor preretrieval stress changed the expression of SR memory. However, individual differences in cortisol reactivity immediately after learning were associated with variability in initial SR learning. These results reveal novel cognitive mechanisms by which stress can modulate multiple memory systems.

Acute stress has frequently been shown to impair cognitive flexibility. Most studies have examined the effect of stress on cognitive flexibility by measuring how stress changes performance in paradigms that require participants to switch between different task demands. These processes typically implicate pFC function, a region known to be impaired by stress. However, cognitive flexibility is a multifaceted construct. Another dimension of flexibility, updating to incorporate relevant information, involves the dorsal striatum. Function in this region has been shown to be enhanced by stress. Using a within-subject design, we tested whether updating flexibility in a DMS task would be enhanced by an acute stress manipulation (cold pressor task). Participants' cortisol response to stress positively correlated with a relative increase in accuracy on updating flexibility (compared with trials with no working memory interference). In contrast, in line with earlier studies, cortisol responses correlated with worse performance when switching between trials with different task demands. These results demonstrate that stress-related increases in cortisol are associated with both increases and decreases in cognitive flexibility, depending on task demands.