Effects Of Acute Psychological Stress Research Articles

Effects of acute stress on biological motion perception.

Biological motion perception is an essential part of the cognitive process. Stress can affect the cognitive process. The present study explored the intrinsic ERP features of the effects of acute psychological stress on biological motion perception. The results contributed scientific evidence for the adaptive behavior changes under acute stress. After a mental arithmetic task was used to induce stress, the paradigm of point-light displays was used to evaluate biological motion perception. Longer reaction time and lower accuracy were found in the inverted walking condition than in the upright walking condition, which was called the "inversion effect". The P2 peak amplitude and the LPP mean amplitude were significantly higher in the local inverted perception than in the local upright walking condition. Compared to the control condition, the stress condition induced lower RT, shorter P1 peak latency of biological motion perception, lower P2 peak amplitude and LPP mean amplitude, and higher N330 peak amplitude. There was an "inversion effect" in biological motion perception. This effect was related to the structural characteristics of biological motion perception but unrelated to the state of acute psychological stress. Acute psychological stress accelerated the reaction time and enhanced attention control of biological motion perception. Attention resources were used earlier, and less attentional investment was made in the early stage of biological motion perception processing. In the late stage, a continuous weakening of inhibition was shown in the parieto-occipital area.

Abstract LB135: Effects of acute psychological stress on DNA damage levels in peripheral blood mononuclear cells: An experimental study with healthy human volunteers

Abstract Increased levels of DNA damage in human peripheral blood mononuclear cells (PBMC), as indicated by classic alkaline comet and γ-H2AX assays, have been widely used in toxicology and epidemiology studies of potential environmental carcinogens. To date, however, little research has explored the possibility that exposure to acute psychological stresses in daily life may acutely increase levels of DNA damage and thus, much like repeated tobacco use, may cumulatively contribute to lifetime cancer risk. The purpose of the present experimental study was to provide a first critical test of the hypothesis that exposure of healthy humans to a brief psychological stress results in increased levels of DNA damage. We also tested preventative effects of a beta-adrenergic receptor blocker (propranolol), a mechanistic pathway for psychological stress effects on DNA supported by preclinical research. Healthy volunteers were recruited by multiple strategies including targeted outreach (telephone/email), with oversampling for age, sex, and minority status. Eligibility was confirmed by self-report, clinical testing (blood & urine), and MD review. On the experimental day, participants were randomized to receive either a single dose of propranolol (80mg) or a placebo. After a 60 min rest period with video distraction, all participants (n=123; 48.8% ≥ 40yr; 52% women; 52% minority) underwent a well-established, 15-minute stress challenge, a speech task and mental arithmetic (Trier Social Stress Test, TSST), with psychological stress confirmed by visual analog scales. Blood samples were collected (via IV line) immediately before and after the TSST. As the primary study outcome, DNA damage in PBMC was assessed (blind) with Comet IV software (% tail intensity) following single cell gel electrophoresis under alkaline conditions with and without in vitro exposure to 25uM H2O2 (comet assay). For a subset of participants with sufficient frozen PBMC samples available (n=43), levels of pan-nuclear γ-H2AX were determined with a validated, sensitive, immunoblot method that detects H2AX phosphorylation at Ser139, and expresses γ-H2AX as the ratio of p-Ser139-H2AX to total H2AX. Exploratory nonparametric analyses revealed that undergoing the TSST significantly increased levels of DNA damage in PBMC (H2O2 comet assay [p<.001] and γ-H2AX biomarker [p=.03], Wilcoxon tests) in the group of participants that was randomized to pretreatment with placebo. In the group pretreated with propranolol before the TSST, a significant increase in γ-H2AX was not found. Conclusion. Supporting the study hypothesis that acute stress can increase levels of DNA damage, the results of the present study highlight the potential importance of additional research to address the possibility that repeated exposures to acute life stresses may cumulatively contribute to increased lifetime risk of cancer. Citation Format: Dana H. Bovbjerg, John Schmitz, Kurt D. Ackerman, Scott R. Beach, Albert D. Donnenberg, Jessica Manculich, Matthew F. Muldoon, Patricia L. Opresko, Patrick M. Tarwater, Hong Wang, Frank J. Jenkins. Effects of acute psychological stress on DNA damage levels in peripheral blood mononuclear cells: An experimental study with healthy human volunteers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(7_Suppl):Abstract nr LB135.

Effect of Acute Psychological Stress on Speed Perception: An Event-Related Potential Study

The present study tested the intrinsic ERP features of the effects of acute psychological stress on speed perception. A mental arithmetic task was used to induce acute psychological stress, and the light spot task was used to evaluate speed perception. Compared with judgments in the constant speed and uniform acceleration motion, judgments in the uniform deceleration motion were made more quickly and with higher accuracy; attention control was higher and peaked later; and there was longer N2 peak latency, larger N2 peak amplitude, and lower mean amplitude of the late negative slow wave (SW). Under stress, the reaction time was significantly shorter. The N2 peak amplitude and SW mean amplitude were significantly higher, attention control was higher and appeared earlier, and there was a greater investment of cognitive resources. The type of movement and evoked stress also interacted to predict behavioral and ERP measures. Under acute stress, judgments made in the uniform deceleration motion condition elicited lower N2 peak latency, higher attention control, and later peak attention. The results suggest that judgments of the speed of decelerating motion require a lower investment of cognitive resources than judgments of other kinds of motion, especially under acute stress. These findings are best interpreted in terms of the interaction of arousal and attention.

Acute psychological stress increases paracellular permeability and modulates immune activity in rectal mucosa of healthy volunteers.

Psychological stress and increased permeability are implicated as contributing factors in the initiation and worsening of gastrointestinal diseases. A link between stress and intestinal permeability has been shown in animal models as well as in human small intestine, but stress effects on the human colorectal mucosal barrier has not been reported. To investigate the potential effects of acute psychological stress on colorectal mucosal barrier function and to explore stress-induced molecular events in the rectal mucosa under healthy conditions. Endoscopic biopsies were taken from the rectosigmoid region of healthy volunteers, who had been subjected to dichotomous listening stress and after a control session, respectively. Paracellular and transcellular permeability were assessed in modified Ussing chambers. RNA expression (microarray technology confirmed by quantitative real-time polymerase chain reaction) and biological pathway analysis were used to investigate the local mucosal response to acute stress. Dichotomous listening stress induced a subjective and objective stress response, and significantly increased paracellular but not transcellular permeability. We also identified a stress-induced reduction in RNA expression of genes related to immune cell activation and maturation (CR2, CD20, TCLA1, BANK1, CD22, FDCSP), signaling molecules of homing of immune cells to the gut (chemokines: CCL21, CXCL13, and CCL19, and receptors: CCR7, CXCR5), and innate immunity (DUOX2). Eight of the 10 top down-regulated genes are directly involved in B cell activation, signaling and migration. The systemic stress response correlated positively with paracellular permeability and negatively with DUOX2 expression. Dichotomous listening stress increases paracellular permeability and modulates immune cell activity in the rectal mucosa. Further studies are warranted to identify the primary mechanisms of stress-mediated reduction of mucosal defensive activity and barrier dysfunction, and their potential implications for gastrointestinal disorders.

Genome-Wide mRNA Expression Analysis of Acute Psychological Stress Responses.

Most previous studies have examined the effects of acute psychological stress in humans based on select gene panels. The genomic approach may help identify novel genes that underline biological mechanisms of acute psychological stress responses. This exploratory study aimed to investigate genome-wide transcriptional activity changes in response to acute psychological stress. The sample included 40 healthy women (mean age 31.4 ± 11.6 years). Twenty-two participants had a stress experience induced by the Trier Social Stress Test (experimental group) and 18 did not (control group). Psychological stress levels and hemodynamic changes were assessed before and after the Trier Social Stress Test. Peripheral blood samples obtained before and after the Trier Social Stress Test were processed for mRNA sequencing. Psychological and hemodynamic stress parameters indicated that the Trier Social Stress Test induced moderate levels of stress in the experimental group. Six genes (HCG26, HCP5, HLA-F, HLA-F-AS1, LOC1019287, and SLC22A16) were up-regulated, and fi ve genes (CA1, FBXO9, SNCA, STRADB, and TRMT12) were down-regulated among those who experienced stress induction, compared with the control group. Nine genes of eleven were linked to endocrine system disorders, neurological disease, and organismal injury and abnormalities. Of the genes identifi ed in this study, HCP5, SLC22A16, and SNCA genes have previously been proposed as therapeutic targets for cancer and Parkinson disease. Further studies are needed to examine pathological mechanisms through which these genes mediate eff ects of psychological stress on adverse health outcomes. Such studies may ultimately identify therapeutic targets that enhance biological resilience to adverse eff ects of psychological stress.

Maintaining normal sleep patterns, lifestyles and emotion during the COVID-19 pandemic: The stabilizing effect of daytime napping.

This study aimed to assess changes in sleep pattern and their influence on people's daily life and emotion during the COVID‐19 pandemic. Self‐developed questionnaires were used to measure changes in nocturnal sleep, daytime napping, lifestyles and negative emotions in individuals before and after the COVID‐19 pandemic. Nine hundred and thirty effective questionnaires were collected in this study. Repeated measures analysis of variance and hierarchical regression analysis were applied. We found that individuals' sleep rhythms were delayed, and sleep duration and sleep latency were increased during the stay‐at‐home orders. Meanwhile, their exercise levels and learning/working efficiency were decreased, and electronic device use time, annoyance levels and anxiety levels were increased. Delayed sleep patterns affected lifestyles and emotions. Moreover, sleep quality positively predicted learning/working efficiency and exercise levels, and negatively predicted use of electronic devices and negative emotions. Sleep patterns became delayed on weekdays during stay‐at‐home orders in all four daytime napping groups (no daytime napping, daytime napping as before, more daytime napping and less daytime napping), and the group taking daytime naps as before had a minimal variation, and their lifestyles and emotions were significantly better than those of the other groups. This study demonstrated that under the influence of stress caused by the pandemic, maintaining regular daytime napping was an effective way to stabilize sleep patterns and biological rhythms, keep good lifestyles and alleviate the effect of acute psychological stress, and to prevent and control mental disorders during the pandemic.

Effect of Acute Psychological Stress on Motion-in-Depth Perception: An Event-Related Potential Study.

The present study explored the intrinsic event-related potential (ERP) features of the effects of acute psychological stress on the processing of motion-in-depth perception using a dual-task paradigm. After a mental arithmetic task was used to induce acute psychological stress, a collision task was used to evaluate motion-in-depth perception. The error value and average amplitude of late slow waves (SW) were significantly larger for the earlier colliding spheres’ than for the later colliding spheres. The P1 peak latency in the left occipital region was significantly shorter than that of the right occipital region in the motion-in-depth perception task. Compared to the control condition, the estimated value of residual time-to-collision and error value were significantly reduced, and the N1 peak amplitude and the SW averaged amplitude were significantly increased in the stress condition. Longer motion-in-depth time improved discrimination accuracy and decreased the investment of cognitive resources. Acute psychological stress increased behavioral performance and enhanced attention resources on the motion-in-depth perception task together with greater investment of cognitive resources.

Abstract 12683: Genome-wide Mrna Expression Analysis of Acute Psychological Stress Responses

Introduction: Previous studies have examined effects of acute psychological stress in humans on selected panels of genes. This exploratory study aimed to investigate genome-wide transcriptional activity changes in responses to acute psychological stress. Methods: The sample included 40 healthy women who participated in a previous study (22 who had a stress induced experience (experimental group) and 18 who did not (control group)). The psychological stress was induced by the Trier Social Stress Test (TSST). Psychological stress levels (measured by the Subjective Units of Distress Scale (SUDS) and the state anxiety subscale of the Spielberger State-Trait Anxiety Inventory) and hemodynamic changes (measured by blood pressure (BP) and heart rate (HR)) were assessed before and after the TSST. The peripheral blood samples obtained before and after the TSST were processed for mRNA-sequencing. Results: The mean age of the participants was 31 years (SD 11.6). The psychological and hemodynamic stress parameters indicated that the TSST successfully induced moderate but statistically significant levels of acute psychological stress in the participants of the experimental group. Compared with the participants in the control group, six genes ( BCL2L14, FAM3B, HCG26, HLA-F-AS1, LOC101928710 , and SLC22A16 ) were up-regulated and 9 genes ( ATP2C2, CA1, CRYBG3, FBXO9, HBD, SLC39A9, SNCA, STRADB , and TRMT12 ) were down-regulated among those who experienced stress induction. The IPA analysis identified one network of cell-to-cell signaling and interaction, cellular function and maintenance, and hematological system development and function. Thirteen genes out of 15 were found in this network. Conclusions: The identified genes including FAM3B, BCL2L14, SLC22A16 , and SNCA , have been proposed as the therapeutic targets of diabetes-related CVDs, certain cancers, and Parkinson’s disease, but have not previously been reported to be associated with psychological stress. Future studies are suggested to examine the pathological mechanisms by which the identified genes may mediate the association between psychological stress and adverse health outcome.

Acute psychological stress, autonomic function, and arterial stiffness among women

This study aimed to investigate the effect of acute psychological stress on autonomic function and arterial stiffness, and to test a mediating role of changes in autonomic function between acute stress and arterial stiffness. Eighty-five healthy female adults were randomized into either an experimental or control group. The Trier Social Stress Test (TSST) was used to induce acute psychological stress. Autonomic function (measured by pre-ejection period [PEP] from cardiac impedance and high frequency [HF] of heart rate variability [HRV]) and arterial stiffness (measured by carotid and femoral pulse wave velocity [cfPWV] and augmentation index [AIx]) were assessed before and after the TSST. The mean age of the participants was 28.78 (±9.84) years old. Experimental group participants had a significant increase in cfPWV (p = .025) and AIx (p = .017) following the stressor, compared with those in the control group, after controlling for age, body mass index, and systolic blood pressure. However, no significant group differences were observed in changes in PEP (p = .181) and HF (p = .058). Changes in PEP and HF were neither associated with changes in cfPWV (p = .975 and p = .654, respectively), nor in AIx (p = .376 and p = .323, respectively). The results suggest that even a brief period of mild to moderate stress, which does not cause sustainable changes in autonomic function, may still exert significant adverse effects on arterial stiffness. The changes in arterial stiffness were not related to changes in autonomic function. Future experimental studies with several measurement points are recommended to identify distinct effects of stress on autonomic function and arterial stiffness.

48-LB: The Effect of Acute Psychosocial Stress in Adults with Type 1 Diabetes

The effects of acute psychological stress, heart rate variability (HRV), an indicator of autonomic function and glycemic variability (GV) have not been extensively researched in type 1 diabetes (T1D). The aim of this study is to explore the effect of acute psychosocial stress on HRV and GV in people with T1D. Methods: Eleven participants with T1D (33.00 ± 11.25 years) participated in the study. To assess acute mental stress, the subjects 1) participated in the Trier Social Stress Test (TSST); and 2) played competitive video games (Nintendo Switch™). The TSST followed standardized procedures whereby stress was induced asking participants to provide a job talk and arithmetic in front of two judges. Participants played the Mario Kart to go-kart races (10 minutes) and rotated their controllers to untangle the Treasure Chest (10 minutes). Resting HRV and GV were obtained. The subjects wore a continuous glucose monitor and a Zephyr Bioharness™ to record GV and HRV, respectively. Nonparametric, paired samples T-tests were conducted using SPSS 24. Results: During TSST, there were significant differences between the resting and TSST testing period in the sympathetic nervous sympathetic nervous system index (.57 ± 1.33 vs. 1.36 ± 1.40; z = -2.845, respectively; p <.01; and stress index (8.17 ± 3.69 vs. 10.27 ± 5.69; z = -2.578, respectively; p <.05). When subjects were playing video games, there were significant differences in the parasympathetic nervous sympathetic nervous system index (-.09 ± 1.75 vs. -.87 ± 1.05; z = -2.134, respectively; p <.05) compared to a resting period. However, there were no significant differences in GV compared to a resting period in during TSST and playing video game. Conclusion: This study suggests that the TSST induced stress in people with T1D, increased sympathetic activity; however, the TSST did not change glycemic variability. Playing competitive video game did not appear to neither induces stress nor affected glycemic variability. The competitive video game did not cause stress compared to TSST. Disclosure M. Park: None. Y. Song: None. M. Chu: None. M. Sevil: None. N. Hobbs: None. L. Sharp: None. A. Cinar: Research Support; Self; Dexcom, Inc., JDRF. Stock/Shareholder; Self; Dexcom, Inc., Eli Lilly and Company, Insulet Corporation, Medtronic, Novo Nordisk A/S, Tandem Diabetes Care. L.T. Quinn: None. Funding JDRF

Effects of acute psychological stress on athletic performance in elite male swimmers.

While physical activity has been shown to affect psychological as well as physiological stress responses, less research has explored the effects of acute stress on athletic performance. The current study hence aimed to investigate the effect of an acute psychological stress (APS) provocation on performance and plasma lactate concentration during a following 200-m swim race among elite male swimmers. Furthermore, associations between physiological stress responses (salivary cortisol and testosterone), and outcome measures (speed and lactate) were explored. Twenty-three elite male swimmers participated in an experimental counterbalanced within-group repeated measures design consisting of an APS provocation followed by a 200-m race and, on a separate day, a control race without prior stress exposure. Salivary cortisol and testosterone were collected prior to each race. Race time was recorded, and serum lactate was collected immediately following, and five min after completed race. Race speed was significantly slower (1.53 [95% CI: 0.08-2.79] seconds) following the APS provocation than under control conditions. Prerace cortisol levels were positively associated with lactate response when preceding stress exposure was present (rho =0.483 immediately, and rho=0.429 five minutes post race, P<0.05). Under control conditions however, both increased testosterone (rho =-657, P=0.001) and cortisol (rho =-0.491, P=0.020) levels were associated with faster race times. The results indicated a negative impact of APS exposure on athletic performance. Further, potential beneficial effects on performance from physiological stress responses (as reflected by salivary cortisol and testosterone) may be diminished during performance following an APS provocation, compared with a regular non-provoked performance situation.

Effects of acute psychological stress on placebo and nocebo responses in a clinically relevant model of visceroception.

There is evidence to suggest a role of emotions in placebo and nocebo effects, but whether acute psychological stress changes the magnitude of placebo or nocebo responses has not been tested. In a clinically relevant model of visceroception, we assessed effects of acute psychological stress on changes in urgency and pain in response to positive or negative treatment suggestions. In 120 healthy volunteers, perceived urge-to-defecate and pain in response to individually calibrated rectal distensions were measured with visual analogue scales during a BASELINE. Participants then underwent the Trier Social Stress Test (N = 60) or a simple cognitive task (control, N = 60) and were randomized to positive (placebo), negative (nocebo), or neutral treatment information regarding intravenous administration of saline. The series of distensions was repeated, and changes in visual analogue scales from BASELINE to TEST were compared between groups using analysis of covariance and planned post hoc tests. Treatment information emerged as a main factor (P <0.001), supporting treatment information effects for both urgency and pain. Effects for urgency were modulated by stress (interaction effect: P <0.05): Positive information reduced urgency (P = 0.025), while negative information increased urgency (P = 0.026) only in stressed groups. For pain, effects of stress emerged for nocebo responses, which were only evident in stressed groups (P = 0.009). This is the first experimental study supporting effects of acute psychological stress on placebo and nocebo responses in visceroception. Results call for mechanistic as well as patient studies to assess how psychological stress shapes patients' treatment expectations and thereby affects health outcomes.

Effect of acute psychological stress on response inhibition: An event-related potential study

This study aimed to investigate the effect of acute psychological stress on response inhibition and its electrophysiological correlates using a dual-task paradigm. Acute stress was induced by a primary task (mental arithmetic task), which consisted of a stress block and a control block. Response inhibition was measured using a secondary task (Go/NoGo task). In each trial, a Go/NoGo stimulus was presented immediately after the mental arithmetic task. The results revealed increased subjective stress and negative affect for the stress relative to control block, suggesting that the mental arithmetic task triggered a reliable stress response. ERPs locked to the Go/NoGo stimuli revealed that decreased P2 and increased N2 components were evoked for the stress block compared to the control block. These results demonstrated that acute psychological stress alters the response inhibition process by reducing the early selective attention process and enhancing the cognitive control process.

The effects of acute psychological stress on circulating and stimulated inflammatory markers: A systematic review and meta-analysis

Inflammatory reactivity to acute laboratory stress is thought to reflect individual differences in responsivity to environmental stressors and may confer future health risk. To characterize this response, we conducted a meta-analysis of 34 studies that measured circulating inflammatory markers and 15 studies that measured stimulated production of inflammatory markers before and after exposure to laboratory challenge. Results showed significant stress-related increases in circulating interleukin (IL)-1β (d=0.66, p<0.001), IL-6 (d=0.35, p<0.001), IL-10 (d=0.69, p<0.001), and tumor necrosis factor(TNF)-α (d=0.28, p<0.001), but not IL-1ra, IL-2, interferon-γ, or C-reactive protein. There were sufficient data to assess the time course of IL-6, IL-1β, and TNF-α reactivity. IL-6 increased from baseline to measures taken 40–50, 60–75, 90, and 120min following stress, with the largest effect at 90min post-stress (d=0.70, p<0.001). IL-1β increased from baseline to 20–30, 40–50, and 60–70min following stress, with the largest effect between 40 and 50min post-stress (d=0.73, p=0.02). For TNF-α, there was a significant increase from baseline to 31–50min post stress (d=0.44, p=0.01), but not at later times. There was no difference in magnitude of IL-6 reactivity as a function of type of stress (social-evaluative versus other). For stimulated inflammatory markers, results showed stress-related increases in IL-1β when measured 20–120min post-stress (d=1.09, p<0.001), and in IL-4 and interferon-γ when measured 0–10min post stressor (d=−0.42, p<0.001 and d=0.47, p<0.001). These results extend findings from a prior meta-analysis (Steptoe et al., 2007) to show reliable increases in circulating IL-6, IL-1β, IL-10 and TNF-α and stimulated IL-1β, IL-4 and interferon-γ in response to acute stress. It is possible that these responses contribute to associations between exposure to life challenges and vulnerability to inflammatory disease.

Abstract # 1807 Systematic review of studies examining the effects of acute psychological stress on circulating inflammatory markers

Inflammatory reactivity to acute laboratory stress is thought to reflect individual differences in responsivity to environmental stressors and may confer future health risk. To characterize this response, we conducted a meta-analysis of 34 studies that measured circulating inflammatory markers before and after exposure to laboratory challenge. Results showed significant stress-related increases in interleukin(IL)-1 β (d = 0.66, CI [0.21, 1.12], p α (d = 0.28, CI [0.05, 0.51], p α . For IL-6, there was a significant increase from baseline to post-stress measures at 40–50 min, 60–75 min, 90 min, and 120 min, with the largest effect at 90 min post-stress (d = 0.70, CI [0.45, 0.95], p α , there was a significant increase from baseline to post-stress measurement at 31–50 min (d = 0.17, CI [0.10, 0.78], Z = 2.51, p = .01). There was no significant difference in magnitude of IL-6 reactivity as a function of type of stress (social-evaluative versus other). These results extend findings from a prior meta-analysis (Steptoe et al., 2007), showing reliable increases in IL-6, IL-1 β , IL-10 and TNF- α in response to acute stress. It is possible that these responses provide a pathway mediating relationships between exposure to life challenges and vulnerability to inflammatory disease.

Progenitor cells are mobilized by acute psychological stress but not beta-adrenergic receptor agonist infusion.

Stimuli that activate the sympathetic nervous system, such as acute psychological stress, rapidly invoke a robust mobilization of lymphocytes into the circulation. Experimental animal studies suggest that bone marrow-derived progenitor cells (PCs) also mobilize in response to sympathetic stimulation. Here we tested the effects of acute psychological stress and brief pharmacological β-adrenergic (βAR) stimulation on peripheral PC numbers in humans. In two studies, we investigated PC mobilization in response to an acute speech task (n=26) and βAR-agonist (isoproterenol) infusion (n=20). A subset of 8 participants also underwent the infusion protocol with concomitant administration of the βAR-antagonist propranolol. Flow cytometry was used to enumerate lymphocyte subsets, total progenitor cells, total haematopoietic stem cells (HSC), early HSC (multi-lineage potential), late HSC (lineage committed), and endothelial PCs (EPCs). Both psychological stress and βAR-agonist infusion caused the expected mobilization of total monocytes and lymphocytes and CD8(+) T lymphocytes. Psychological stress also induced a modest, but significant, increase in total PCs, HSCs, and EPC numbers in peripheral blood. However, infusion of a βAR-agonist did not result in a significant change in circulating PCs. PCs are rapidly mobilized by psychological stress via mechanisms independent of βAR-stimulation, although the findings do not exclude βAR-stimulation as a possible cofactor. Considering the clinical and physiological relevance, further research into the mechanisms involved in stress-induced PC mobilization seems warranted.

Effect of Acute Psychological Stress on Blood Pressure

Effect of Acute Psychological Stress on Blood Pressure

Dynamic Proteomics of Nucleus Accumbens in Response to Acute Psychological Stress in Environmentally Enriched and Isolated Rats

Our prior research has shown that environmental enrichment (i.e. rats reared in an environment with novel objects, social contact with conspecifics) produces a protective antidepressant-like phenotype in rats and decreases neurobiological effects of acute psychological stress. Although CREB activity has been identified as a major player, the downstream molecular mechanisms remain largely unexplored. Thus, the current study investigates proteomic differences in the accumbens of rats raised in an enriched condition (EC) versus those raised in an isolated control condition (IC) under basal conditions and after 30 min of acute restraint stress. Results showed that under basal conditions, EC rats generally expressed less mitochondria-related proteins, particularly those involved in TCA cycle and electron transport compared to IC rats. After 30 min of acute stress, EC rats displayed increased expression of energy metabolism enzymes (among others) while IC rats exhibited decreased expression of similar proteins. Further, network and pathway analyses also identified links to AKT signaling proteins, 14-3-3 family proteins, heat-shock proteins, and ubiquitin-interacting proteins. The protein ENO1 showed marked differential expression and regulation; EC rats expressed higher levels under basal conditions that increased subsequent to stress, while the basal IC expression was lower and decreased further still after stress. The results of this study define differential protein expression in a protective rat model for major depression and additionally identify a dynamic and coordinated differential response to acute stress between the two groups. These results provide new avenues for exploration of the molecular determinants of depression and the response to acute stress.

Acute Psychological Stress Accelerates Reverse Cholesterol Transport via Corticosterone-Dependent Inhibition of Intestinal Cholesterol Absorption

Psychological stress is associated with an increased risk of cardiovascular diseases. However, the connecting mechanisms of the stress-inducing activation of the hypothalamic-pituitary-adrenal axis with atherosclerosis are not well-understood. To study the effect of acute psychological stress on reverse cholesterol transport (RCT), which transfers peripheral cholesterol to the liver for its ultimate fecal excretion. C57Bl/6J mice were exposed to restraint stress for 3 hours to induce acute psychological stress. RCT in vivo was quantified by measuring the transfer of [(3)H]cholesterol from intraperitoneally injected mouse macrophages to the lumen of the small intestine within the stress period. Surprisingly, stress markedly increased the contents of macrophage-derived [(3)H]cholesterol in the intestinal lumen. In the stressed mice, intestinal absorption of [(14)C]cholesterol was significantly impaired, the intestinal mRNA expression level of peroxisome proliferator-activated receptor-α increased, and that of the sterol influx transporter Niemann-Pick C1-like 1 decreased. The stress-dependent effects on RCT rate and peroxisome proliferator-activated receptor-α gene expression were fully mimicked by administration of the stress hormone corticosterone (CORT) to nonstressed mice, and they were blocked by the inhibition of CORT synthesis in stressed mice. Moreover, the intestinal expression of Niemann-Pick C1-like 1 protein decreased when circulating levels of CORT increased. Of note, when either peroxisome proliferator-activated receptor α or liver X receptor α knockout mice were exposed to stress, the RCT rate remained unchanged, although plasma CORT increased. This indicates that activities of both transcription factors were required for the RCT-accelerating effect of stress. Acute psychological stress accelerated RCT by compromising intestinal cholesterol absorption. The present results uncover a novel functional connection between the hypothalamic-pituitary-adrenal axis and RCT that can be triggered by a stress-induced increase in circulating CORT.

Effect of Acute Psychological Stress on Prefrontal GABA Concentration Determined by Proton Magnetic Resonance Spectroscopy

Effect of Acute Psychological Stress on Prefrontal GABA Concentration Determined by Proton Magnetic Resonance Spectroscopy