Search

Although the feeling of stress is ubiquitous, the neural mechanisms underlying this affective experience remain unclear. Here, we investigate functional hippocampal connectivity throughout the brain during an acute stressor and use machine learning to demonstrate that these networks can specifically predict the subjective feeling of stress. During a stressor, hippocampal connectivity with a network including the hypothalamus (known to regulate physiological stress) predicts feeling more stressed, whereas connectivity with regions such as dorsolateral prefrontal cortex (associated with emotion regulation) predicts less stress. These networks do not predict a subjective state unrelated to stress, and a nonhippocampal network does not predict subjective stress. Hippocampal networks are consistent, specific to the construct of subjective stress, and broadly informative across measures of subjective stress. This approach provides opportunities for relating hypothesis-driven functional connectivity networks to clinically meaningful subjective states. Together, these results identify hippocampal networks that modulate the feeling of stress., Although the feeling of being stressed is ubiquitous and clinically significant, the underlying neural mechanisms are unclear. Using a novel predictive modeling approach, the authors show that functional hippocampal networks specifically and consistently predict the feeling of stress.

The COVID-19 pandemic represents a worldwide stressor. Considering the influence of stress on research participants during this time and beyond may provide new insights and benefit the broader field of human neuroscience., Considering the influence of stress on research participants during the pandemic and beyond may provide new insights and benefit the broader field of human neuroscience.

Memory for prior drinking experiences may powerfully drive later alcohol use in familiar drinking contexts, yet we know little about what patients with alcohol use disorder (AUD) remember of alcohol-related episodes. Although animal and theoretical models of addiction emphasize the importance of different memory systems for understanding maladaptive use, clinical research parsing what AUD patients remember from alcohol-related episodes is lacking. The current study applied a novel memory task in which moderate drinkers (N = 30) and treatment-seeking individuals with alcohol use disorder (AUD: N = 29) encoded associations between photographs of objects (alcoholic beverages and neutral items) and photographs of neutral scenes. At least 24 h later, two types of memory were assessed: item memory (object recognition) and associative memory (cued recognition of scenes associated with objects). To assess which memories predicted drinking, real-world behavior was assessed in patients with AUD at baseline and for 4 weeks following memory tests. Despite demographic differences, the results showed broadly impaired item memory in AUD compared with moderate drinkers (p

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.

Stress can strongly influence memory, in part by modulating the relative engagement of multiple memory systems. Over the last fifteen years, researchers have demonstrated that stress leads striatal, rather than hippocampal, memory to be dominant in both humans and non-human animals. This shift has been proposed to explain the etiology and maintenance of symptoms of stress-related psychopathology. However, it remains unclear how hippocampal and striatal memory are affected individually in order to facilitate this trade-off. Recent studies provide empirical support for (at least) three different pathways by which stress could modulate these memory systems. Evidence for these diverse effects of stress, and circumstances under which each might occur, are discussed.

Emotional stress responses, encompassing both stress reactivity and regulation, have been shown to differ between men and women, but the neural networks supporting these processes remain unclear. The current study used functional neuroimaging (fMRI) to investigate sex differences in neural responses during stress and the sex-specific relationships between these responses and emotional stress responses for men and women. A significant sex by condition interaction revealed that men showed greater stress responses in prefrontal cortex (PFC) regions, whereas women had stronger responses in limbic/striatal regions. Although men and women did not significantly differ in emotional stress reactivity or subjective reports of stress regulation, these responses were associated with distinct neural networks. Higher dorsomedial PFC responses were associated with lower stress reactivity in men, but higher stress reactivity in women. In contrast, while higher ventromedial PFC stress responses were associated with worse stress regulation in men (but better regulation in women), dynamic increases in vmPFC responses during stress were associated with lower stress reactivity in men. Finally, stress-induced hippocampal responses were more adaptive for women: for men, high and dynamically increasing responses in left hippocampus were associated with high stress reactivity, and dynamic increases in the left (but not right) hippocampus were associated with worse stress regulation. Together, these results reveal that men and women engage distinct neural networks during stress, and sex-specific neural stress responses facilitate optimal emotional stress responses. Keywords: Stress, Sex, Emotion, fMRI, Medial prefrontal cortex, Hippocampus

Emotional experiences often contain a multitude of details that may be represented in memory as individual elements or integrated into a single representation. How details associated with a negative emotional event are represented in memory can have important implications for extinction strategies designed to reduce emotional responses. For example, is extinguishing one cue associated with an aversive outcome sufficient to reduce learned behavior to other cues present at the time of learning that were not directly extinguished? Here, we used a between-subjects multi-day threat conditioning and extinction task to assess whether participants generalize extinction from one cue to unextinguished cues. On Day 1, one group of participants learned that a compound conditioned stimulus, composed of a tone and colored square, predicted an uncomfortable shock to the wrist (Compound group). A second group learned that the tone and square separately predicted shock (Separate group). On Day 2, participants in both groups were exposed to the tone in the absence of shocks (cue extinction). On Day 3, we tested whether extinction generalized from the extinguished to the unextinguished cue, as well as to a compound composed of both cues. Results showed that configural and elemental learning had unique and opposite effects on extinction generalization. Subjects who initially learned that a compound cue predicted shock successfully generalized extinction learning from the tone to the square, but exhibited threat relapse to the compound cue. In contrast, subjects who initially learned that each cue individually predicted shock did not generalize extinction learning from the tone to the square, but threat responses to the compound were low. These results highlight the importance of whether details of an aversive event are represented as integrated or separated memories, as these representations affect the success or limits of extinction generalization.

Contains fulltext : 173050.pdf (Publisher’s version ) (Open Access) 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.

The biological stress response of the body forms one of the foundations of adaptive behavior, including promoting (and impairing) different forms of memory. This response transcends stressful experiences and underlies reactions to challenges and even reinforcers such as addictive substances. Nevertheless, drug-induced stress responses are rarely incorporated into models of addiction. We propose here that drug-induced stress responses (particularly glucocorticoids) play a crucial role in addictive behavior by modulating the formation of memories for substance-use experiences. We review the contributions of amygdala-, striatum-, and hippocampus-based memory systems to addiction, and reveal common effects of addictive drugs and acute stress on these different memories. We suggest that the contributions of drug-induced stress responses to memory may provide insights into the mechanisms driving addictive behavior.

Stress can strongly influence what we learn and remember, including by making memories stronger. Experiments probing stress effects on hippocampus-dependent memory in rodents have revealed modulatory factors and physiological mechanisms by which acute stress can enhance long-term memory. However, extending these findings and mechanisms to understand when stress will enhance declarative memory in humans faces important challenges. This review synthesizes human and rodent studies of stress and memory, examining translational gaps related to measurements of declarative memory and stress responses in humans. Human studies diverge from rodent research by assessing declarative memories that may not depend on the hippocampus and by measuring peripheral rather than central stress responses. This highlights opportunities for future research across species, including assessing stress effects on hippocampal-dependent memory processes in humans and relating peripheral stress responses to stress effects on the function of memory-related brain regions in rodents. Together, these investigations will facilitate the translation of stress effects on memory function from rodents to humans and inform interventions that can harness the positive effects of stress on long-term memory.

Exposure to stress throughout life can cumulatively influence later health, even among young adults. The negative effects of high cumulative stress exposure are well-known, and a shift from episodic to stimulus–response memory has been proposed to underlie forms of psychopathology that are related to high lifetime stress. At the other extreme, effects of very low stress exposure are mixed, with some studies reporting that low stress leads to better outcomes, while others demonstrate that low stress is associated with diminished resilience and negative outcomes. However, the influence of very low lifetime stress exposure on episodic and stimulus–response memory is unknown. Here we use a lifetime stress assessment system (STRAIN) to assess cumulative lifetime stress exposure and measure memory performance in young adults reporting very low and moderate levels of lifetime stress exposure. Relative to moderate levels of stress, very low levels of lifetime stress were associated with reduced use and retention (24 h later) of stimulus–response (SR) associations, and a higher likelihood of using context memory. Further, computational modeling revealed that participants with low levels of stress exhibited worse expression of memory for SR associations than those with moderate stress. These results demonstrate that very low levels of stress exposure can have negative effects on cognition.