Strength through adversity: Moderate lifetime stress exposure is associated with psychological resilience in breast cancer survivors

PubMed Central

Dooley, Larissa N.; Slavich, George M.; Moreno, Patricia I.; Bower, Julienne E.

2017-01-01

Stress research typically emphasizes the toxic effects of stress, but recent evidence has suggested that stress exposure, in moderation, can facilitate resilience. To test whether moderate stress exposure promotes psychological resilience to cancer, we examined the relationship between lifetime stress exposure prior to cancer diagnosis and postdiagnosis psychological functioning among 122 breast cancer survivors. Lifetime acute and chronic stress was assessed using an interview-based measure, and psychological functioning was assessed using measures of cancer-related intrusive thoughts and positive and negative affect. Results indicated that acute stress exposure was associated with cancer-related intrusive thoughts in a quadratic fashion (p = .016), such that participants with moderate acute stress reported fewer intrusive thoughts compared to those with low or high acute stress. Similarly, a quadratic relationship emerged between acute stress exposure and positive affect (p = .009), such that individuals with moderate acute stress reported the highest levels of positive affect. In contrast, acute and chronic stress were related to negative affect in a positive, linear fashion (ps < .05). In conclusion, moderate stress exposure was associated with indicators of psychological resilience among breast cancer survivors, supporting stress exposure as a key factor influencing adjustment to breast cancer and providing evidence for stress-induced resilience in a novel population. PMID:28052491

Adulthood stress responses in rats are variably altered as a factor of adolescent stress exposure.

PubMed

Moore, Nicole L T; Altman, Daniel E; Gauchan, Sangeeta; Genovese, Raymond F

2016-05-01

Stress exposure during development may influence adulthood stress response severity. The present study investigates persisting effects of two adolescent stressors upon adulthood response to predator exposure (PE). Rats were exposed to underwater trauma (UWT) or PE during adolescence, then to PE after reaching adulthood. Rats were then exposed to predator odor (PO) to test responses to predator cues alone. Behavioral and neuroendocrine assessments were conducted to determine acute effects of each stress experience. Adolescent stress altered behavioral response to adulthood PE. Acoustic startle response was blunted. Bidirectional changes in plus maze exploration were revealed as a factor of adolescent stress type. Neuroendocrine response magnitude did not predict severity of adolescent or adult stress response, suggesting that different adolescent stress events may differentially alter developmental outcomes regardless of acute behavioral or neuroendocrine response. We report that exposure to two different stressors in adolescence may differentially affect stress response outcomes in adulthood. Acute response to an adolescent stressor may not be consistent across all stressors or all dependent measures, and may not predict alterations in developmental outcomes pertaining to adulthood stress exposure. Further studies are needed to characterize factors underlying long-term effects of a developmental stressor.

Comparison of the effects of acute and chronic psychological stress on metabolic features in rats*

PubMed Central

Rostamkhani, Fatemeh; Zardooz, Homeira; Zahediasl, Saleh; Farrokhi, Babak

2012-01-01

This study was aimed to compare the effects of acute and chronic psychological stress on metabolic factors. Forty-two male Wistar rats were divided into control and stressed groups. Stress was applied by a communication box acutely (1 d) and chronically (15 and 30 d). Blood sampling was carried out by retro-orbital-puncture method. The plasma levels of glucose, cholesterol, triglyceride, insulin, and corticosterone were measured. In addition, feed and water intake, latency to eat and drink, adrenal and body weights were determined. Acute and chronic psychological stress did not significantly change basal plasma corticosterone levels. However, immediately (1 min) after acute exposure to stress, plasma corticosterone level increased compared to that before stress exposure. Acute stress increased plasma insulin levels significantly. Fifteen days of stress exposure resulted in plasma glucose increase. Chronic stress significantly increased feed intake, latency to eat, and adrenal weight compared to acute stress. The body weights of both control and stressed groups increased markedly during the experiment. Homeostasis model assessment of insulin resistance (HOMA-IR) index did not change significantly in the stressed group. In conclusion, application of acute and chronic psychological stress leads to different metabolic and/or behavioral changes but the metabolic changes resulting from acute exposure to stress seem to be more pronounced. PMID:23125083

Strength through adversity: Moderate lifetime stress exposure is associated with psychological resilience in breast cancer survivors.

PubMed

Dooley, Larissa N; Slavich, George M; Moreno, Patricia I; Bower, Julienne E

2017-12-01

Stress research typically emphasizes the toxic effects of stress, but recent evidence has suggested that stress exposure, in moderation, can facilitate resilience. To test whether moderate stress exposure promotes psychological resilience to cancer, we examined the relationship between lifetime stress exposure prior to cancer diagnosis and postdiagnosis psychological functioning among 122 breast cancer survivors. Lifetime acute and chronic stress was assessed using an interview-based measure, and psychological functioning was assessed using measures of cancer-related intrusive thoughts and positive and negative affect. Results indicated that acute stress exposure was associated with cancer-related intrusive thoughts in a quadratic fashion (p = .016), such that participants with moderate acute stress reported fewer intrusive thoughts compared to those with low or high acute stress. Similarly, a quadratic relationship emerged between acute stress exposure and positive affect (p = .009), such that individuals with moderate acute stress reported the highest levels of positive affect. In contrast, acute and chronic stress were related to negative affect in a positive, linear fashion (ps < .05). In conclusion, moderate stress exposure was associated with indicators of psychological resilience among breast cancer survivors, supporting stress exposure as a key factor influencing adjustment to breast cancer and providing evidence for stress-induced resilience in a novel population. Copyright © 2017 John Wiley & Sons, Ltd.

Acute stress reactions after submarine accidents.

PubMed

Eid, Jarle; Johnsen, Bjørn Helge

2002-05-01

The aim of the present study was to explore contextual and individual factors associated with acute stress reactions in three Norwegian submarine crews exposed to different significant peacetime maneuver accidents. Approximately 2 to 3 weeks after the accidents, crew members completed the Coping Style Questionnaire, the General Health Questionnaire, the Impact of Event Scale, and the Post-Traumatic Symptom Scale. Although exposed subjects (N = 47) revealed more posttraumatic stress symptoms than nonexposed crew members on shore leave (N = 7), they showed less acute stress reactions than survivors from a surface ship accident in the Norwegian Navy. Inspection of individual cases revealed that 4% of the exposed submariners showed high loads of acute stress symptoms. Unit cohesion and habitual coping styles emerged as resilience factors, whereas previous exposure to critical incidents and personal experience of not coping in the accident situation emerged as vulnerability factors, explaining 32% of the acute stress reactions reported by submarine crew members.

El Salvador earthquakes: relationships among acute stress disorder symptoms, depression, traumatic event exposure, and resource loss.

PubMed

Sattler, David N; de Alvarado, Ana Maria Glower; de Castro, Norma Blandon; Male, Robert Van; Zetino, A M; Vega, Raphael

2006-12-01

Four and seven weeks after powerful earthquakes in El Salvador, the authors examined the relationships among demographics, traumatic event exposure, social support, resource loss, acute stress disorder (ASD) symptoms, depression, and posttraumatic growth. Participants were 253 college students (Study 1) and 83 people in the community (Study 2). In Study 1, female gender, traumatic event exposure, low social support, and loss of personal characteristic, condition, and energy resources contributed to ASD symptoms and depression. In Study 2, damage to home and loss of personal characteristic and object resources contributed to ASD symptoms and depression. Posttraumatic growth was not associated with ASD symptoms or depression. Findings support the conservation of resources stress theory (Hobfoll, 1998). Resource loss spirals, excessive demands on coping, and exposure to multiple disasters are discussed.

Differential Effects of 5-HTTLPR Genotypes on Inhibition of Negative Emotional Information Following Acute Stress Exposure and Tryptophan Challenge

PubMed Central

Markus, C Rob; De Raedt, Rudi

2011-01-01

Previous data suggest that a polymorphism at the serotonin (5-HT) transporter gene (5-HTTLPR) may influence stress resilience and stress-related depression symptoms due to interactions between brain 5-HT dysfunction and stress exposure. Although attentional bias for emotional information has been reliably observed in depression, the interaction between 5-HT transporter-linked promoter region (5-HTTLPR), brain 5-HT vulnerability, and acute stress on affective information processing has not yet been investigated. This study examines the effects of tryptophan (TRP) augmentation (indicating 5-HT manipulation) on inhibition of negative emotional information under stress in mainly female S′/S′- vs L′/L′-allele carriers. A total of 15 female homozygotic short-allele 5-HTTLPR (S′/S′=S/S, S/LG, LG/LG) and 13 female homozygotic long-allele 5-HTTLPR (L′/L′=LA/LA) subjects were tested for mood and inhibition of emotional information in a double-blind, placebo-controlled design before and after stress exposure following TRP manipulation. Stress exposure significantly impaired inhibition of negative affective information only in S′/S′ carriers, whereas L′/L′ carriers even showed increased inhibition of negative information. The S′/S′ allele 5-HTTLPR genotype increases cognitive-attentional bias for negative emotional information under acute stress. As this bias is an important component of depression, this may be a mediating mechanism making S′/S′-allele carriers more vulnerability for stress-induced depression symptoms. Moreover, current data suggest that L′/L′-allele genotypes are more resilient, even increasing cognitive emotional (inhibitory) control after stress. PMID:21150915

Differential effects of 5-HTTLPR genotypes on inhibition of negative emotional information following acute stress exposure and tryptophan challenge.

PubMed

Markus, C Rob; De Raedt, Rudi

2011-03-01

Previous data suggest that a polymorphism at the serotonin (5-HT) transporter gene (5-HTTLPR) may influence stress resilience and stress-related depression symptoms due to interactions between brain 5-HT dysfunction and stress exposure. Although attentional bias for emotional information has been reliably observed in depression, the interaction between 5-HT transporter-linked promoter region (5-HTTLPR), brain 5-HT vulnerability, and acute stress on affective information processing has not yet been investigated. This study examines the effects of tryptophan (TRP) augmentation (indicating 5-HT manipulation) on inhibition of negative emotional information under stress in mainly female S'/S'- vs L'/L'-allele carriers. A total of 15 female homozygotic short-allele 5-HTTLPR (S'/S'=S/S, S/L(G), L(G)/L(G)) and 13 female homozygotic long-allele 5-HTTLPR (L'/L'=L(A)/L(A)) subjects were tested for mood and inhibition of emotional information in a double-blind, placebo-controlled design before and after stress exposure following TRP manipulation. Stress exposure significantly impaired inhibition of negative affective information only in S'/S' carriers, whereas L'/L' carriers even showed increased inhibition of negative information. The S'/S' allele 5-HTTLPR genotype increases cognitive-attentional bias for negative emotional information under acute stress. As this bias is an important component of depression, this may be a mediating mechanism making S'/S'-allele carriers more vulnerability for stress-induced depression symptoms. Moreover, current data suggest that L'/L'-allele genotypes are more resilient, even increasing cognitive emotional (inhibitory) control after stress.

Stress integration after acute and chronic predator stress: differential activation of central stress circuitry and sensitization of the hypothalamo-pituitary-adrenocortical axis.

PubMed

Figueiredo, Helmer F; Bodie, Bryan L; Tauchi, Miyuki; Dolgas, C Mark; Herman, James P

2003-12-01

Predator exposure is a naturalistic stressor of high ethological relevance. In the current study, our group examined central and peripheral integration of stress responses in rats after acute or repeated exposure to a natural predator (cat). Acute cat exposure rapidly induced hypothalamo-pituitary-adrenocortical (HPA) axis activation and paraventricular nucleus (PVN) CRH mRNA production. Repeated daily cat exposure (7 and 14 d) also up-regulated PVN mRNA CRH expression, but did not result in frank adrenocortical hyperactivity. Unlike other chronic homotypic stress regimens, repeated cat exposure facilitated corticosterone secretion after the 6th or 13th day of exposure. Notably, ACTH secretion and central amygdaloid nucleus CRH mRNA expression were enhanced in animals that were preexposed to the holding chamber relative to chamber-naive rats, suggesting that contextual cues can sensitize subsequent responses to a fearful stimulus. Analysis of c-fos activation was then used to identify brain circuits activated by acute predator stress. Cat exposure elicited a pattern of central c-fos activation that differed substantially from that after either restraint or hypoxia. Predator-specific c-fos mRNA induction was observed in several brain regions comprising the hypothetical brain defense circuit (bed nucleus of the stria terminalis, medial region of the ventromedial nucleus, and dorsal premammillary nucleus). Surprisingly, acute cat exposure did not induce c-fos expression in the PVN. In summary, the data indicate that 1) predation stress invokes a unique stress circuitry that promotes homotypic sensitization of the HPA axis, and 2) familiarization of animals to testing environments can prime central stress pathways to respond robustly to novel threats.

Stress response in rat brain after different durations of noise exposure.

PubMed

Samson, James; Sheeladevi, Rathinasamy; Ravindran, Rajan; Senthilvelan, Manohar

2007-01-01

The alteration in the levels of plasma corticosterone, brain norepinephrine (NE), and expression of brain heat shock proteins (Hsp70) after different durations of noise exposure (acute, 1 day; sub-acute, 15 days; chronic, 30 days) has been studied to analyze their role in combating time-dependent stress effects of noise. Broadband white noise (100dB) exposure to male Wistar albino rats significantly increased the levels of plasma corticosterone and NE in all three durations of noise exposure. The sustained increase observed in their levels in the chronic group suggests that animals are not getting adapted to noise even after 30 days of exposure. The important role of Hsp70 in combating noise induced stress is evident from the significant increase in its expression after chronic exposure, while there was a reciprocal decrease in the NE and corticosterone when compared with their levels after acute and sub-acute noise exposure. This clearly indicates that the time-dependent stress response to noise exposure is a complex mechanism involving highly interconnected systems such as hypothalamo-pituitary-adrenal (HPA) axis, heat shock proteins and may have serious implications in vital organs, particularly in the brain when there is a prolonged noise exposure.

Effects of acute tryptophan depletion on affective processing in first-degree relatives of depressive patients and controls after exposure to uncontrollable stress.

PubMed

Firk, Christine; Markus, C Rob

2008-08-01

Individuals with a family history of depression may be more likely to develop depression due to an innate vulnerability of their serotonergic system. However, even though serotonergic vulnerability may constitute a risk factor in the development of depression, it does not seem to be sufficient to cause a depressive episode. Based on previous data, it is suggested that stress may be a mediating factor. This study examined the role of serotonin (5-HT) in stress coping in individuals with or without a family history of depression. Nineteen healthy first-degree relatives of depressive patients (FH+) and 19 healthy controls without a family history of depression (FH-) were tested in a double-blind placebo-controlled design for affective processing under acute stress exposure, following acute tryptophan depletion (ATD) or placebo. Significant negative effects were found of stress on affective processing in FH- and FH+. In addition, FH- responded slower to positive words after stress only following ATD, whereas FH+ responded marginally slower under stress already after placebo and before stress following ATD. Acute stress exposure reduces positive affective bias; supporting the role of stress as an important predecessor in the development of depression. Furthermore, FH+ may be more susceptible than FH- to the negative effects of stress as well as to the negative effects of ATD. The results support the assumption that the 5-HT system is involved in stress resilience and may be more vulnerable in first-degree relatives of depression.

Acute Exposure to Stress Improves Performance in Trace Eyeblink Conditioning and Spatial Learning Tasks in Healthy Men

ERIC Educational Resources Information Center

Duncko, Roman; Cornwell, Brian; Cui, Lihong; Merikangas, Kathleen R.; Grillon, Christian

2007-01-01

The present study investigated the effects of acute stress exposure on learning performance in humans using analogs of two paradigms frequently used in animals. Healthy male participants were exposed to the cold pressor test (CPT) procedure, i.e., insertion of the dominant hand into ice water for 60 sec. Following the CPT or the control procedure,…

Time course of systemic oxidative stress and inflammatory response induced by an acute exposure to Residual Oil Fly Ash

DOE Office of Scientific and Technical Information (OSTI.GOV)

Marchini, T.; Magnani, N.D.; Paz, M.L.

2014-01-15

It is suggested that systemic oxidative stress and inflammation play a central role in the onset and progression of cardiovascular diseases associated with the exposure to particulate matter (PM). The aim of this work was to evaluate the time changes of systemic markers of oxidative stress and inflammation, after an acute exposure to Residual Oil Fly Ash (ROFA). Female Swiss mice were intranasally instilled with a ROFA suspension (1.0 mg/kg body weight) or saline solution, and plasma levels of oxidative damage markers [thiobarbituric acid reactive substances (TBARSs) and protein carbonyls], antioxidant status [reduced (GSH) and oxidized (GSSG) glutathione, ascorbic acidmore » levels, and superoxide dismutase (SOD) activity], cytokines levels, and intravascular leukocyte activation were evaluated after 1, 3 or 5 h of exposure. Oxidative damage to lipids and decreased GSH/GSSG ratio were observed in ROFA-exposed mice as early as 1 h. Afterwards, increased protein oxidation, decreased ascorbic acid content and SOD activity were found in this group at 3 h. The onset of an adaptive response was observed at 5 h after the ROFA exposure, as indicated by decreased TBARS plasma content and increased SOD activity. The observed increase in oxidative damage to plasma macromolecules, together with systemic antioxidants depletion, may be a consequence of a systemic inflammatory response triggered by the ROFA exposure, since increased TNF-α and IL-6 plasma levels and polymorphonuclear leukocytes activation was found at every evaluated time point. These findings contribute to the understanding of the increase in cardiovascular morbidity and mortality, in association with environmental PM inhalation. - Highlights: • An acute exposure to ROFA triggers the occurrence of systemic oxidative stress. • Changes in plasmatic oxidative stress markers appear as early as 1 h after exposure. • ROFA induces proinflammatory cytokines release and intravascular leukocyte activation. �

Hypnotizability in acute stress disorder.

PubMed

Bryant, R A; Guthrie, R M; Moulds, M L

2001-04-01

This study investigated the relationship between acute dissociative reactions to trauma and hypnotizability. Acutely traumatized patients (N=61) with acute stress disorder, subclinical acute stress disorder (no dissociative symptoms), and no acute stress disorder were administered the Stanford Hypnotic Clinical Scale within 4 weeks of their trauma. Although patients with acute stress disorder and patients with subclinical acute stress disorder displayed comparable levels of nondissociative psychopathology, acute stress disorder patients had higher levels of hypnotizability and were more likely to display reversible posthypnotic amnesia than both patients with subclinical acute stress disorder and patients with no acute stress disorder. The findings may be interpreted in light of a diathesis-stress process mediating trauma-related dissociation. People who develop acute stress disorder in response to traumatic experience may have a stronger ability to experience dissociative phenomena than people who develop subclinical acute stress disorder or no acute stress disorder.

Acute Assessment of Traumatic Brain Injury and Post-Traumatic Stress After Exposure to a Deployment-Related Explosive Blast.

PubMed

Baker, Monty T; Moring, John C; Hale, Willie J; Mintz, Jim; Young-McCaughan, Stacey; Bryant, Richard A; Broshek, Donna K; Barth, Jeffrey T; Villarreal, Robert; Lancaster, Cynthia L; Malach, Steffany L; Lara-Ruiz, Jose M; Isler, William; Peterson, Alan L

2018-05-18

Traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD) are two of the signature injuries in military service members who have been exposed to explosive blasts during deployments to Iraq and Afghanistan. Acute stress disorder (ASD), which occurs within 2-30 d after trauma exposure, is a more immediate psychological reaction predictive of the later development of PTSD. Most previous studies have evaluated service members after their return from deployment, which is often months or years after the initial blast exposure. The current study is the first large study to collect psychological and neuropsychological data from active duty service members within a few days after blast exposure. Recruitment for blast-injured TBI patients occurred at the Air Force Theater Hospital, 332nd Air Expeditionary Wing, Joint Base Balad, Iraq. Patients were referred from across the combat theater and evaluated as part of routine clinical assessment of psychiatric and neuropsychological symptoms after exposure to an explosive blast. Four measures of neuropsychological functioning were used: the Military Acute Concussion Evaluation (MACE); the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS); the Headminder Cognitive Stability Index (CSI); and the Automated Neuropsychological Assessment Metrics, Version 4.0 (ANAM4). Three measures of combat exposure and psychological functioning were used: the Combat Experiences Scale (CES); the PTSD Checklist-Military Version (PCL-M); and the Acute Stress Disorder Scale (ASDS). Assessments were completed by a deployed clinical psychologist, clinical social worker, or mental health technician. A total of 894 patients were evaluated. Data from 93 patients were removed from the data set for analysis because they experienced a head injury due to an event that was not an explosive blast (n = 84) or they were only assessed for psychiatric symptoms (n = 9). This resulted in a total of 801 blast-exposed patients for data

Chronic mitochondrial uncoupling treatment prevents acute cold-induced oxidative stress in birds.

PubMed

Stier, Antoine; Massemin, Sylvie; Criscuolo, François

2014-12-01

Endotherms have evolved two major types of thermogenesis that allow them to actively produce heat in response to cold exposure, either through muscular activity (i.e. shivering thermogenesis) or through futile electro-chemical cycles (i.e. non-shivering thermogenesis). Amongst the latter, mitochondrial uncoupling is of key importance because it is suggested to drive heat production at a low cost in terms of oxidative stress. While this has been experimentally shown in mammals, the oxidative stress consequences of cold exposure and mitochondrial uncoupling are clearly less understood in the other class of endotherms, the birds. We compared metabolic and oxidative stress responses of zebra finches chronically treated with or without a chemical mitochondrial uncoupler (2,4-dinitrophenol: DNP), undergoing an acute (24 h) and a chronic (4 weeks) cold exposure (12 °C). We predicted that control birds should present at least a transient elevation of oxidative stress levels in response to cold exposure. This oxidative stress cost should be more pronounced in control birds than in DNP-treated birds, due to their lower basal uncoupling state. Despite similar increase in metabolism, control birds presented elevated levels of DNA oxidative damage in response to acute (but not chronic) cold exposure, while DNP-treated birds did not. Plasma antioxidant capacity decreased overall in response to chronic cold exposure. These results show that acute cold exposure increases oxidative stress in birds. However, uncoupling mitochondrial functioning appears as a putative compensatory mechanism preventing cold-induced oxidative stress. This result confirms previous observations in mice and underlines non-shivering thermogenesis as a putative key mechanism for endotherms in mounting a response to cold at a low oxidative cost.

Occupational role stress is associated with higher cortisol reactivity to acute stress.

PubMed

Wirtz, Petra H; Ehlert, Ulrike; Kottwitz, Maria U; La Marca, Roberto; Semmer, Norbert K

2013-04-01

We investigated whether occupational role stress is associated with differential levels of the stress hormone cortisol in response to acute psychosocial stress. Forty-three medication-free nonsmoking men aged between 22 and 65 years (mean ± SEM: 44.5 ± 2) underwent an acute standardized psychosocial stress task combining public speaking and mental arithmetic in front of an audience. We assessed occupational role stress in terms of role conflict and role ambiguity (combined into a measure of role uncertainty) as well as further work characteristics and psychological control variables including time pressure, overcommitment, perfectionism, and stress appraisal. Moreover, we repeatedly measured salivary cortisol and blood pressure levels before and after stress exposure, and several times up to 60 min thereafter. Higher role uncertainty was associated with a more pronounced cortisol stress reactivity (p = .016), even when controlling for the full set of potential confounders (p < .001). Blood pressure stress reactivity was not associated with role uncertainty. Our findings suggest that occupational role stress in terms of role uncertainty acts as a background stressor that is associated with increased HPA-axis reactivity to acute stress. This finding may represent a potential mechanism regarding how occupational role stress may precipitate adverse health outcomes.

Low-Grade Inflammation and Ambulatory Cortisol in Adolescents: Interaction Between Interviewer-Rated Versus Self-Rated Acute Stress and Chronic Stress.

PubMed

Schreier, Hannah M C; Chen, Edith

To determine whether the association between self-rated or interviewer-rated recent acute stress exposures and low-grade inflammation and daily cortisol production in adolescents is moderated by chronic stress ratings. Acute and chronic stress exposures were assessed in 261 adolescents aged 13 to 16 years using a semistructured life stress interview. The negative impact of acute stressors was independently rated by both adolescents (self-rated) and interviewers (interviewer-rated). Markers of inflammation (interleukin (IL)-6, IL-1ra, C-reactive protein) were measured from peripheral blood samples obtained via antecubital venipuncture. Participants collected 4 saliva samples at home on each of 6 consecutive days for the analysis of diurnal salivary cortisol profiles. There were no main effects of acute stressors (self- and interviewer-rated) and chronic family or peer stress on adolescent inflammation markers and cortisol (p values > .10). However, the interaction between interviewer-rated acute stress and chronic family stress was significantly associated with adolescent inflammation markers (IL-6, IL-1ra). Specifically, as chronic family stress increased, the association between acute stressor impact (interviewer-rated) and inflammation markers became more positive (IL-6 (B = .054, SE = .023, p = .022); IL-1ra (B = .030, SE = .014, p = .034)). Interactions between self-rated acute stress and chronic family stress were not associated with any biological measures (p values > .10). Interactions between acute stressor impact (both self- and interviewer-rated) and chronic peer stress were also not significantly associated with any biological measures (p values > .05). Among adolescents, interviewer-based ratings of acute stressor impact may allow for better prediction of health-relevant inflammation markers than adolescents' own ratings.

Low-Grade Inflammation and Ambulatory Cortisol in Adolescents: Interaction between Interviewer-rated versus Self-rated Acute Stress and Chronic Stress

PubMed Central

Schreier, Hannah M. C.; Chen, Edith

2016-01-01

Objective To determine whether the association between self-rated or interviewer-rated recent acute stress exposures and low-grade inflammation and daily cortisol production in adolescents is moderated by chronic stress ratings. Methods Acute and chronic stress exposures were assessed in 261 adolescents aged 13-16 using a semi-structured life stress interview. The negative impact of acute stressors was independently rated by both adolescents (self-rated) and interviewers (interviewer-rated). Markers of inflammation (IL-6, IL-1ra, CRP) were measured from peripheral blood samples obtained via antecubital venipuncture. Participants collected 4 saliva samples at home on each of six consecutive days for the analysis of diurnal salivary cortisol profiles. Results There were no main effects of acute stressors (self- and interviewer-rated) and chronic family or peer stress on adolescent inflammation markers and cortisol (ps > .10). However, the interaction between interviewer-rated acute stress and chronic family stress was significantly associated with adolescent inflammation markers (IL-6, IL-1ra). Specifically, as chronic family stress increased, the association between acute stressor impact (interviewer-rated) and inflammation markers became more positive (IL-6 (B = .054, SE = .023, p = .022); IL-1ra (B = .030, SE = .014, p = .034)). Interactions between self-rated acute stress and chronic family stress were not associated with any biological measures (ps > .10). Interactions between acute stressor impact (both self- and interviewer-rated) and chronic peer stress were also not significantly associated with any biological measures (ps > .05). Conclusions Among adolescents, interviewer-based ratings of acute stressor impact may allow for better prediction of health-relevant inflammation markers than adolescents’ own ratings. PMID:27490853

Skin temperature reveals the intensity of acute stress

PubMed Central

Herborn, Katherine A.; Graves, James L.; Jerem, Paul; Evans, Neil P.; Nager, Ruedi; McCafferty, Dominic J.; McKeegan, Dorothy E.F.

2015-01-01

Acute stress triggers peripheral vasoconstriction, causing a rapid, short-term drop in skin temperature in homeotherms. We tested, for the first time, whether this response has the potential to quantify stress, by exhibiting proportionality with stressor intensity. We used established behavioural and hormonal markers: activity level and corticosterone level, to validate a mild and more severe form of an acute restraint stressor in hens (Gallus gallus domesticus). We then used infrared thermography (IRT) to non-invasively collect continuous temperature measurements following exposure to these two intensities of acute handling stress. In the comb and wattle, two skin regions with a known thermoregulatory role, stressor intensity predicted the extent of initial skin cooling, and also the occurrence of a more delayed skin warming, providing two opportunities to quantify stress. With the present, cost-effective availability of IRT technology, this non-invasive and continuous method of stress assessment in unrestrained animals has the potential to become common practice in pure and applied research. PMID:26434785

Executive functioning performance predicts subjective and physiological acute stress reactivity: preliminary results.

PubMed

Hendrawan, Donny; Yamakawa, Kaori; Kimura, Motohiro; Murakami, Hiroki; Ohira, Hideki

2012-06-01

Individual differences in baseline executive functioning (EF) capacities have been shown to predict state anxiety during acute stressor exposure. However, no previous studies have clearly demonstrated the relationship between EF and physiological measures of stress. The present study investigated the efficacy of several well-known EF tests (letter fluency, Stroop test, and Wisconsin Card Sorting Test) in predicting both subjective and physiological stress reactivity during acute psychosocial stress exposure. Our results show that letter fluency served as the best predictor for both types of reactivity. Specifically, the higher the letter fluency score, the lower the acute stress reactivity after controlling for the baseline stress response, as indicated by lower levels of state anxiety, negative mood, salivary cortisol, and skin conductance. Moreover, the predictive power of the letter fluency test remained significant for state anxiety and cortisol indices even after further adjustments for covariates by adding the body mass index (BMI) as a covariate. Thus, good EF performance, as reflected by high letter fluency scores, may dampen acute stress responses, which suggests that EF processes are directly associated with aspects of stress regulation. Copyright © 2012 Elsevier B.V. All rights reserved.

Dynamic changes in saliva after acute mental stress

PubMed Central

Naumova, Ella A.; Sandulescu, Tudor; Bochnig, Clemens; Khatib, Philipp Al; Lee, Wing-Kee; Zimmer, Stefan; Arnold, Wolfgang H.

2014-01-01

Stress-related variations of fluoride concentration in supernatant saliva and salivary sediment, salivary cortisol, total protein and pH after acute mental stress were assessed. The hypothesis was that stress reactions have no influence on these parameters. Thirty-four male students were distributed into two groups: first received the stress exposure followed by the same protocol two weeks later but without stress exposure, second underwent the protocol without stress exposure followed by the stress exposure two weeks later. The stressor was a public speech followed by tooth brushing. Saliva was collected before, immediately after stress induction and immediately, at 10, 30 and 120 min. after tooth brushing. Cortisol concentrations, total protein, intraoral pH, and fluoride content in saliva were measured. The data were analyzed statistically. Salivary sediment was ca 4.33% by weight of whole unstimulated saliva. Fluoride bioavailability was higher in salivary sediment than in supernatant saliva. The weight and fluoride concentration was not altered during 2 hours after stress exposure. After a public speech, the salivary cortisol concentration significantly increased after 20 minutes compared to the baseline. The salivary protein concentration and pH also increased. Public speaking influences protein concentration and salivary pH but does not alter the fluoride concentration of saliva. PMID:24811301

Utilizing Telehealth to Support Treatment of Acute Stress Disorder in a Theater of War: Prolonged Exposure via Clinical Videoconferencing.

PubMed

Pelton, Dan; Wangelin, Bethany; Tuerk, Peter

2015-05-01

Posttraumatic stress disorder (PTSD) and acute stress disorder are prevalent mental health diagnoses associated with the military operations in Iraq and Afghanistan and are especially significant in service members returning from combat. Prolonged exposure (PE) therapy is a highly effective behavioral treatment for these symptoms, and providing this treatment as soon as possible, even in the midst of a soldier's combat deployment, has strong potential benefits. In the current case study, telehealth technology was used to support the delivery of PE therapy to treat a service member diagnosed with acute stress disorder in a war zone. PE was conducted face-to-face on the relatively secure Forward Operating Base for the first half of therapy and via clinical videoconferencing (CV) to the service member's remote combat outpost during the later stages of therapy. The service member exhibited marked improvements in symptoms over 10 sessions. Results are consistent with previous empirical findings and highlight the potential benefits of using telehealth to deliver evidenced-based treatment for traumatic stress disorders in a war zone. This case study provides a preliminary working model for delivering PE in a combat environment using multiple delivery systems. Benefits and clinical utility of CV-delivered exposure therapy are discussed, particularly for providers pending future operational deployments (e.g., including members of the military, independent government agencies, and first responders) and for those treating patients in remote locations.

Comparison of Acute Health Effects From Exposures to Diesel and Biodiesel Fuel Emissions.

PubMed

Mehus, Aaron A; Reed, Rustin J; Lee, Vivien S T; Littau, Sally R; Hu, Chengcheng; Lutz, Eric A; Burgess, Jefferey L

2015-07-01

To investigate the comparative acute health effects associated with exposures to diesel and 75% biodiesel/25% diesel (B75) blend fuel emissions. We analyzed multiple health endpoints in 48 healthy adults before and after exposures to diesel and B75 emissions in an underground mine setting-lung function, lung and systemic inflammation, novel biomarkers of exposure, and oxidative stress were assessed. B75 reduced respirable diesel particulate matter by 20%. Lung function declined significantly more after exposure to diesel emissions. Lung inflammatory cells along with sputum and plasma inflammatory mediators increased significantly to similar levels with both exposures. Urinary 8-hydroxydeoxyguanosine, a marker of oxidative stress, was not significantly changed after either exposure. Use of B75 lowered respirable diesel particulate matter exposure and some associated acute health effects, although lung and systemic inflammation were not reduced compared with diesel use.

Characterising multi-level effects of acute pressure exposure on a shallow-water invertebrate: insights into the kinetics and hierarchy of the stress response.

PubMed

Morris, James P; Thatje, Sven; Ravaux, Juliette; Shillito, Bruce; Hauton, Chris

2015-08-01

Hydrostatic pressure is an important, ubiquitous, environmental variable of particular relevance in the marine environment. However, it is widely overlooked despite recent evidence that some marine ectotherms may be demonstrating climate-driven bathymetric range shifts. Wide-ranging effects of increased hydrostatic pressure have been observed from the molecular through to the behavioural level. Still, no study has simultaneously examined these multiple levels of organisation in a single experiment in order to understand the kinetics, hierarchy and interconnected nature of such responses during an acute exposure, and over a subsequent recovery period. Here, we quantify the transcription of a set of previously characterised genes during and after acute pressure exposure in adults of the shrimp Palaemonetes varians. Further, we perform respiratory rate and behavioural analysis over the same period. Increases in expression of genes associated with stress and metabolism were observed during and after high-pressure exposure. Respiratory rate increased during exposure and into the recovery period. Finally, differential behaviour was observed under elevated hydrostatic pressure in comparison to ambient pressure. Characterising generalised responses to acute elevated pressure is a vital precursor to longer-term, acclimation-based pressure studies. Results provide a novel insight into what we term the overall stress response (OSR) to elevated pressure; a concept that we suggest to be applicable to other environmental stressors. We highlight the importance of considering more than a single component of the stress response in physiological studies, particularly in an era where environmental multi-stressor studies are proliferating. © 2015. Published by The Company of Biologists Ltd.

OXIDATIVE STRESS PARTICIPATES IN ACUTE LUNG INJURY AND ACTIVATION OF MITOGEN ACTIVATED PROTEIN KINASES (MAPK) FOLLOWING AIR POLLUTION PARTICLE EXPOSURE (PM)

EPA Science Inventory

OXIDATIVE STRESS PARTICIPATES IN ACUTE LUNG INJURY AND ACTIVATION OF MITOGEN ACTIVATED PROTEIN KINASES (MAPK) FOLLOWING AIR POLLUTION PARTICLE EXPOSURE (PM). E S Roberts1, R Jaskot2, J Richards2, and K L Dreher2. 1College of Veterinary Medicine, NC State University, Raleigh, NC a...

Dorsal CA1 interneurons contribute to acute stress-induced spatial memory deficits.

PubMed

Yu, Jing-Ying; Fang, Ping; Wang, Chi; Wang, Xing-Xing; Li, Kun; Gong, Qian; Luo, Ben-Yan; Wang, Xiao-Dong

2018-06-01

Exposure to severely stressful experiences disrupts the activity of neuronal circuits and impairs declarative memory. GABAergic interneurons coordinate neuronal network activity, but their involvement in stress-evoked memory loss remains to be elucidated. Here, we provide evidence that interneurons in area CA1 of the dorsal hippocampus partially modulate acute stress-induced memory deficits. In adult male mice, both acute forced swim stress and restraint stress impaired hippocampus-dependent spatial memory and increased the density of c-fos-positive interneurons in the dorsal CA1. Selective activation of dorsal CA1 interneurons by chemogenetics disrupted memory performance in the spatial object recognition task. In comparison, anxiety-related behavior, spatial working memory and novel object recognition memory remained intact when dorsal CA1 interneurons were overactivated. Moreover, chemogenetic activation of dorsal CA1 interneurons suppressed the activity of adjacent pyramidal neurons, whereas a single exposure to forced swim stress but not restraint stress increased the activity of CA1 pyramidal neurons. However, chemogenetic inhibition of dorsal CA1 interneurons led to spatial memory impairments and failed to attenuate acute stress-induced memory loss. These findings suggest that acute stress may overactivate interneurons in the dorsal CA1, which reduces the activity of pyramidal neurons and in turn disrupts long-term memory. Copyright © 2018 Elsevier Ltd. All rights reserved.

Perceived stress at work is associated with attenuated DHEA-S response during acute psychosocial stress.

PubMed

Lennartsson, Anna-Karin; Theorell, Töres; Kushnir, Mark M; Bergquist, Jonas; Jonsdottir, Ingibjörg H

2013-09-01

Dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) have been suggested to play a protective role during acute psychosocial stress, because they act as antagonists to the effects of the stress hormone cortisol. This study aims to investigate whether prolonged psychosocial stress, measured as perceived stress at work during the past week, is related to the capacity to produce DHEA and DHEA-S during acute psychosocial stress. It also aims to investigate whether prolonged perceived stress affects the balance between production of cortisol and DHEA-S during acute psychosocial stress. Thirty-six healthy subjects (19 men and 17 women, mean age 37 years, SD 5 years), were included. Perceived stress at work during the past week was measured by using the Stress-Energy (SE) Questionnaire. The participants were divided into three groups based on their mean scores; Low stress, Medium stress and High stress. The participants underwent the Trier Social Stress Test (TSST) and blood samples were collected before, directly after the stress test, and after 30 min of recovery. General Linear Models were used to investigate if the Medium stress group and the High stress group differ regarding stress response compared to the Low stress group. Higher perceived stress at work was associated with attenuated DHEA-S response during acute psychosocial stress. Furthermore, the ratio between the cortisol production and the DHEA-S production during the acute stress test were higher in individuals reporting higher perceived stress at work compared to individuals reporting low perceived stress at work. There was no statistical difference in DHEA response between the groups. This study shows that prolonged stress, measured as perceived stress at work during the past week, seems to negatively affect the capacity to produce DHEA-S during acute stress. Given the protective functions of DHEA-S, attenuated DHEA-S production during acute stress may lead to higher risk for adverse

Skin temperature reveals the intensity of acute stress.

PubMed

Herborn, Katherine A; Graves, James L; Jerem, Paul; Evans, Neil P; Nager, Ruedi; McCafferty, Dominic J; McKeegan, Dorothy E F

2015-12-01

Acute stress triggers peripheral vasoconstriction, causing a rapid, short-term drop in skin temperature in homeotherms. We tested, for the first time, whether this response has the potential to quantify stress, by exhibiting proportionality with stressor intensity. We used established behavioural and hormonal markers: activity level and corticosterone level, to validate a mild and more severe form of an acute restraint stressor in hens (Gallus gallus domesticus). We then used infrared thermography (IRT) to non-invasively collect continuous temperature measurements following exposure to these two intensities of acute handling stress. In the comb and wattle, two skin regions with a known thermoregulatory role, stressor intensity predicted the extent of initial skin cooling, and also the occurrence of a more delayed skin warming, providing two opportunities to quantify stress. With the present, cost-effective availability of IRT technology, this non-invasive and continuous method of stress assessment in unrestrained animals has the potential to become common practice in pure and applied research. Copyright © 2015 Elsevier Inc. All rights reserved.

Comparison of Acute Health Effects From Exposures to Diesel and Biodiesel Fuel Emissions

PubMed Central

Mehus, Aaron A.; Reed, Rustin J.; Lee, Vivien S. T.; Littau, Sally R.; Hu, Chengcheng; Lutz, Eric A.

2015-01-01

Objective: To investigate the comparative acute health effects associated with exposures to diesel and 75% biodiesel/25% diesel (B75) blend fuel emissions. Methods: We analyzed multiple health endpoints in 48 healthy adults before and after exposures to diesel and B75 emissions in an underground mine setting—lung function, lung and systemic inflammation, novel biomarkers of exposure, and oxidative stress were assessed. Results: B75 reduced respirable diesel particulate matter by 20%. Lung function declined significantly more after exposure to diesel emissions. Lung inflammatory cells along with sputum and plasma inflammatory mediators increased significantly to similar levels with both exposures. Urinary 8-hydroxydeoxyguanosine, a marker of oxidative stress, was not significantly changed after either exposure. Conclusions: Use of B75 lowered respirable diesel particulate matter exposure and some associated acute health effects, although lung and systemic inflammation were not reduced compared with diesel use. PMID:26147538

Acute posttraumatic stress symptoms and depression after exposure to the 2005 Saskatchewan Centennial Air Show disaster: prevalence and predictors.

PubMed

Taylor, Steven; Asmundson, Gordon J G; Carleton, R Nicholas; Brundin, Peter

2007-01-01

The purpose of this study was to determine the prevalence of acute distress-that is, clinically significant posttraumatic stress symptoms (PTSS) and depression-and to identify predictors of each in a sample of people who witnessed a fatal aircraft collision at the 2005 Saskatchewan Centennial Air Show. Air Show attendees (N = 157) were recruited by advertisements in the local media and completed an Internet-administered battery of questionnaires. Based on previously established cut-offs, 22 percent respondents had clinically significant PTSS and 24 percent had clinically significant depressive symptoms. Clinically significant symptoms were associated with posttrauma impairment in social and occupational functioning. Acute distress was associated with several variables, including aspects of Air Show trauma exposure, severity of prior trauma exposure, low posttrauma social support (ie, negative responses by others), indices of poor coping (eg, intolerance of uncertainty, rumination about the trauma), and elevated scores on anxiety sensitivity, the personality trait of absorption, and dissociative tendencies. Results suggest that clinically significant acute distress is common in the aftermath of witnessed trauma. The statistical predictors (correlates) of acute distress were generally consistent with the results of studies of other forms of trauma. People with elevated scores on theoretical vulnerability factors (eg, elevated anxiety sensitivity) were particularly likely to develop acute distress.

Early growth rates and their relationships to mortalities of five breeds of chickens following exposure to acute gamma radiation stress

DOE Office of Scientific and Technical Information (OSTI.GOV)

Latimer, B.E.; Brisbin, I.L. Jr.

Growth and mortality responses were recorded for 541 chicks, representing five different breeds of chickens, following acute exposures to gamma radiation stress at two days of age. Although there were no statistically significant differences in the LD50/30 of the five breeds studied, Cobb broilers showed the highest (1580R) and White Leghorn bantams the lowest (980R) levels, respectively. Other breeds studied included the standard White Leghorn, Athens Randombreds and a strain of feral bantam. Growth rates of body weights were proportionately more depressed by radiation stress than were body sizes, as measured by the lengths of the culmen, tarsus, middle toemore » and longest primary wing feather of all 32 day-old survivors. Among these structures, the length of the culmen seemed to be the least affected by radiation stress in all of the breeds studied. Feral bantams were able to tolerate the greatest depression in weight gain before exhibiting mortality at exposures below their LD50/30' while Cobb broilers tolerated the greatest depression of weight gain at higher exposure levels. There was a suggestion that those characteristics which were strongly selected for in the course of a particular breed's development were those which experienced the greatest proportional depressions following exposure to gamma radiation stress.« less

How Do Stress Exposure and Stress Regulation Relate to Borderline Personality Disorder?

PubMed Central

Bourvis, Nadège; Aouidad, Aveline; Cabelguen, Clémence; Cohen, David; Xavier, Jean

2017-01-01

Borderline personality disorder (BPD) is a severe and frequent disorder characterized by a pervasive pattern of instability affecting impulse control, emotional regulation, cognitive processing, self-image and interpersonal relationships. Patients’ personal histories are often marked by stressful or traumatic experiences, either unique or repeated. Moreover, while clinical signs of the disorder include both chronic and acute features, acute features are mostly triggered by acute stressful situations. Such features include transient cognitive distortion, intense anger, uncontrollable impulsivity, and self-harm behavior – including suicide – and contribute to the burden of the disease. In this paper, we review the various aspects (epidemiological, clinical, and physiological) contributing to the relationship between BDP and stress. In particular, we explore the statistical association between stress exposure and the emergence of BPD while taking into account other psychopathologies, such as post-traumatic stress disorder. Then, the different aspects of stress responses (namely, the phenomenological, behavioral, hormonal, neuro-vegetative and neural responses) are reviewed in BPD patients. Pathophysiological hypotheses are formulated to explain the differences in responses between BPD patients and healthy subjects and their relation to BPD symptoms. Although the pathogenesis remains uncertain, our conclusions seem to reflect a specific biological and neural pattern of altered stress perception and regulation in BPD. PMID:29250007

How Do Stress Exposure and Stress Regulation Relate to Borderline Personality Disorder?

PubMed

Bourvis, Nadège; Aouidad, Aveline; Cabelguen, Clémence; Cohen, David; Xavier, Jean

2017-01-01

Borderline personality disorder (BPD) is a severe and frequent disorder characterized by a pervasive pattern of instability affecting impulse control, emotional regulation, cognitive processing, self-image and interpersonal relationships. Patients' personal histories are often marked by stressful or traumatic experiences, either unique or repeated. Moreover, while clinical signs of the disorder include both chronic and acute features, acute features are mostly triggered by acute stressful situations. Such features include transient cognitive distortion, intense anger, uncontrollable impulsivity, and self-harm behavior - including suicide - and contribute to the burden of the disease. In this paper, we review the various aspects (epidemiological, clinical, and physiological) contributing to the relationship between BDP and stress. In particular, we explore the statistical association between stress exposure and the emergence of BPD while taking into account other psychopathologies, such as post-traumatic stress disorder. Then, the different aspects of stress responses (namely, the phenomenological, behavioral, hormonal, neuro-vegetative and neural responses) are reviewed in BPD patients. Pathophysiological hypotheses are formulated to explain the differences in responses between BPD patients and healthy subjects and their relation to BPD symptoms. Although the pathogenesis remains uncertain, our conclusions seem to reflect a specific biological and neural pattern of altered stress perception and regulation in BPD.

Exposure to Acute Stress is Associated with Attenuated Sweet Taste

PubMed Central

al’Absi, Mustafa; Nakajima, Motohiro; Hooker, Stephanie; Wittmers, Larry; Cragin, Tiffany

2011-01-01

This study examined the effects of stress on taste perception. Participants (N = 38; 21 women) completed two laboratory sessions: one stress (public speaking, math, and cold pressor) and one control rest session. The taste perception test was conducted at the end of each session and included rating the intensity and pleasantness of sweet, salty, sour, and savory solutions at suprathreshold concentrations. Cardiovascular, hormonal, and mood measures were collected throughout the sessions. Participants showed the expected changes in cardiovascular, hormonal, and mood measures in response to stress. Reported intensity of the sweet solution was significantly lower on the stress day than on the rest day. Cortisol level post stress predicted reduced intensity of salt and sour, suggesting that stress-related changes in adrenocortical activity were related to reduced taste intensity. Results indicate that acute stress may alter taste perception, and ongoing research investigates the extent to which these changes mediate effects of stress on appetite. PMID:22091733

Acute and sub-lethal exposure to copper oxide nanoparticles causes oxidative stress and teratogenicity in zebrafish embryos.

PubMed

Ganesan, Santhanamari; Anaimalai Thirumurthi, Naveenkumar; Raghunath, Azhwar; Vijayakumar, Savitha; Perumal, Ekambaram

2016-04-01

Nano-copper oxides are a versatile inorganic material. As a result of their versatility, the immense applications and usage end up in the environment causing a concern for the lifespan of various beings. The ambiguities surround globally on the toxic effects of copper oxide nanoparticles (CuO-NPs). Hence, the present study endeavored to study the sub-lethal acute exposure effects on the developing zebrafish embryos. The 48 hpf LC50 value was about 64 ppm. Therefore, we have chosen the sub-lethal dose of 40 and 60 ppm for the study. Accumulation of CuO-NPs was evidenced from the SEM-EDS and AAS analyzes. The alterations in the AChE and Na(+)/K(+)-ATPase activities disrupted the development process. An increment in the levels of oxidants with a concomitant decrease in the antioxidant enzymes confirmed the induction of oxidative stress. Oxidative stress triggered apoptosis in the exposed embryos. Developmental anomalies were observed with CuO-NPs exposure in addition to oxidative stress in the developing embryos. Decreased heart rate and hatching delay hindered the normal developmental processes. Our work has offered valuable data on the connection between oxidative stress and teratogenicity leading to lethality caused by CuO-NPs. A further molecular mechanism unraveling the uncharted connection between oxidative stress and teratogenicity will aid in the safe use of CuO-NPs. Copyright © 2015 John Wiley & Sons, Ltd.

Childhood poverty and health: cumulative risk exposure and stress dysregulation.

PubMed

Evans, Gary W; Kim, Pilyoung

2007-11-01

A massive literature documents the inverse association between poverty or low socioeconomic status and health, but little is known about the mechanisms underlying this robust relation. We examined longitudinal relations between duration of poverty exposure since birth, cumulative risk exposure, and physiological stress in two hundred seven 13-year-olds. Chronic stress was assessed by basal blood pressure and overnight cortisol levels; stress regulation was assessed by cardiovascular reactivity to a standard acute stressor and recovery after exposure to this stressor. Cumulative risk exposure was measured by multiple physical (e.g., substandard housing) and social (e.g., family turmoil) risk factors. The greater the number of years spent living in poverty, the more elevated was overnight cortisol and the more dysregulated was the cardiovascular response (i.e., muted reactivity). Cardiovascular recovery was not affected by duration of poverty exposure. Unlike the duration of poverty exposure, concurrent poverty (i.e., during adolescence) did not affect these physiological stress outcomes. The effects of childhood poverty on stress dysregulation are largely explained by cumulative risk exposure accompanying childhood poverty.

Chronic but not acute foot-shock stress leads to temporary suppression of cell proliferation in rat hippocampus.

PubMed

Dagyte, G; Van der Zee, E A; Postema, F; Luiten, P G M; Den Boer, J A; Trentani, A; Meerlo, P

2009-09-15

Stressful experiences, especially when prolonged and severe are associated with psychopathology and impaired neuronal plasticity. Among other effects on the brain, stress has been shown to negatively regulate hippocampal neurogenesis, and this effect is considered to be exerted via glucocorticoids. Here, we sought to determine the temporal dynamics of changes in hippocampal neurogenesis after acute and chronic exposure to foot-shock stress. Rats subjected to a foot-shock procedure showed strong activation of the hypothalamic-pituitary-adrenal (HPA) axis, even after exposure to daily stress for 3 weeks. Despite a robust release of corticosterone, acute foot-shock stress did not affect the rate of hippocampal cell proliferation. In contrast, exposure to foot-shock stress daily for 3 weeks led to reduced cell proliferation 2 hours after the stress procedure. Interestingly, this stress-induced effect did not persist and was no longer detected 24 hours later. Also, while chronic foot-shock stress had no impact on survival of hippocampal cells that were born before the stress procedure, it led to a decreased number of doublecortin-positive granule neurons that were born during the chronic stress period. Thus, whereas a strong activation of the HPA axis during acute foot-shock stress is not sufficient to reduce hippocampal cell proliferation, repeated exposure to stressful stimuli for prolonged period of time ultimately results in dysregulated neurogenesis. In sum, this study supports the notion that chronic stress may lead to cumulative changes in the brain that are not seen after acute stress. Such changes may indicate compromised brain plasticity and increased vulnerability to neuropathology.

Exposure to acute stress is associated with attenuated sweet taste.

PubMed

Al'Absi, Mustafa; Nakajima, Motohiro; Hooker, Stephanie; Wittmers, Larry; Cragin, Tiffany

2012-01-01

This study examined the effects of stress on taste perception. Participants (N = 38; 21 women) completed two laboratory sessions: one stress (public speaking, math, and cold pressor) and one control rest session. The taste perception test was conducted at the end of each session and included rating the intensity and pleasantness of sweet, salty, sour, and savory solutions at suprathreshold concentrations. Cardiovascular, hormonal, and mood measures were collected throughout the sessions. Participants showed the expected changes in cardiovascular, hormonal, and mood measures in response to stress. Reported intensity of the sweet solution was significantly lower on the stress day than on the rest day. Cortisol level poststress predicted reduced intensity of salt and sour, suggesting that stress-related changes in adrenocortical activity were related to reduced taste intensity. Results indicate that acute stress may alter taste perception, and ongoing research investigates the extent to which these changes mediate effects of stress on appetite. Copyright © 2011 Society for Psychophysiological Research.

Exposure to Discrimination and Heart Rate Variability Reactivity to Acute Stress among Women with Diabetes.

PubMed

Wagner, Julie; Lampert, Rachel; Tennen, Howard; Feinn, Richard

2015-08-01

Exposure to racial discrimination has been linked to physiological reactivity. This study investigated self-reported exposure to racial discrimination and parasympathetic [high-frequency heart rate variability (HF-HRV)] and sympathetic (norepinephrine and cortisol) activity at baseline and then again after acute laboratory stress. Lifetime exposure to racial discrimination was measured with the Schedule of Racist Events scale. Thirty-two women (16 Black and 16 White) with type 2 diabetes performed a public speaking stressor. Beat-to-beat intervals were recorded on electrocardiograph recorders, and HF-HRV was calculated using spectral analysis and natural log transformed. Norepinephrine and cortisol were measured in blood. Higher discrimination predicted lower stressor HF-HRV, even after controlling for baseline HF-HRV. When race, age, A1c and baseline systolic blood pressure were also controlled, racial discrimination remained a significant independent predictor of stressor HF-HRV. There was no association between lifetime discrimination and sympathetic markers. In conclusion, preliminary data suggest that among women with type 2 diabetes mellitus (T2DM), exposure to racial discrimination is adversely associated with parasympathetic, but not sympathetic, reactivity. Copyright © 2013 John Wiley & Sons, Ltd.

Critical disease windows shaped by stress exposure alter allocation trade-offs between development and immunity.

PubMed

Kirschman, Lucas J; Crespi, Erica J; Warne, Robin W

2018-01-01

Ubiquitous environmental stressors are often thought to alter animal susceptibility to pathogens and contribute to disease emergence. However, duration of exposure to a stressor is likely critical, because while chronic stress is often immunosuppressive, acute stress can temporarily enhance immune function. Furthermore, host susceptibility to stress and disease often varies with ontogeny; increasing during critical developmental windows. How the duration and timing of exposure to stressors interact to shape critical windows and influence disease processes is not well tested. We used ranavirus and larval amphibians as a model system to investigate how physiological stress and pathogenic infection shape development and disease dynamics in vertebrates. Based on a resource allocation model, we designed experiments to test how exposure to stressors may induce resource trade-offs that shape critical windows and disease processes because the neuroendocrine stress axis coordinates developmental remodelling, immune function and energy allocation in larval amphibians. We used wood frog larvae (Lithobates sylvaticus) to investigate how chronic and acute exposure to corticosterone, the dominant amphibian glucocorticoid hormone, mediates development and immune function via splenocyte immunohistochemistry analysis in association with ranavirus infection. Corticosterone treatments affected immune function, as both chronic and acute exposure suppressed splenocyte proliferation, although viral replication rate increased only in the chronic corticosterone treatment. Time to metamorphosis and survival depended on both corticosterone treatment and infection status. In the control and chronic corticosterone treatments, ranavirus infection decreased survival and delayed metamorphosis, although chronic corticosterone exposure accelerated rate of metamorphosis in uninfected larvae. Acute corticosterone exposure accelerated metamorphosis increased survival in infected larvae. Interactions

Acute psychosocial stress reduces pain modulation capabilities in healthy men.

PubMed

Geva, Nirit; Pruessner, Jens; Defrin, Ruth

2014-11-01

Anecdotes on the ability of individuals to continue to function under stressful conditions despite injuries causing excruciating pain suggest that acute stress may induce analgesia. However, studies exploring the effect of acute experimental stress on pain perception show inconsistent results, possibly due to methodological differences. Our aim was to systematically study the effect of acute stress on pain perception using static and dynamic, state-of-the-art pain measurements. Participants were 29 healthy men who underwent the measurement of heat-pain threshold, heat-pain intolerance, temporal summation of pain, and conditioned pain modulation (CPM). Testing was conducted before and during exposure to the Montreal Imaging Stress Task (MIST), inducing acute psychosocial stress. Stress levels were evaluated using perceived ratings of stress and anxiety, autonomic variables, and salivary cortisol. The MIST induced a significant stress reaction. Although pain threshold and pain intolerance were unaffected by stress, an increase in temporal summation of pain and a decrease in CPM were observed. These changes were significantly more robust among individuals with stronger reaction to stress ("high responders"), with a significant correlation between the perception of stress and the performance in the pain measurements. We conclude that acute psychosocial stress seems not to affect the sensitivity to pain, however, it significantly reduces the ability to modulate pain in a dose-response manner. Considering the diverse effects of stress in this and other studies, it appears that the type of stress and the magnitude of its appraisal determine its interactions with the pain system. Copyright © 2014 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

Glucocorticoid exposure alters the pathogenesis of Theiler’s murine encephalomyelitis virus during acute infection

PubMed Central

Young, Erin E.; Prentice, Thomas W.; Satterlee, Danielle; McCullough, Heath; Sieve, Amy N.; Johnson, Robin R.; Welsh, Thomas H.; Welsh, C. Jane R.; Meagher, Mary W.

2008-01-01

Previous research has shown that chronic restraint stress exacerbates Theiler’s virus infection, a murine model for CNS inflammation and multiple sclerosis. The current set of experiments was designed to evaluate the potential role of glucocorticoids in the deleterious effects of restraint stress on acute CNS inflammatory disease. Exposure to chronic restraint stress resulted in elevated levels of corticosterone as well as increased clinical scores and weight loss (Experiment 1). In addition, corticosterone administration alone exacerbated behavioral signs of TMEV-induced sickness (i.e. decreased body weight, increased symptoms of encephalitis, and increased mortality) and reduced inflammation in the CNS (Experiment 2). Infected subjects receiving exogenous corticosterone showed exacerbation of acute phase measures of sickness and severe mortality as well as decreased viral clearance from CNS (Experiment 3). These findings indicate that corticosterone exposure alone is sufficient to exacerbate acute CNS inflammatory disease. PMID:18538803

U.S. EPA'S ACUTE REFERENCE EXPOSURE METHODOLOGY FOR ACUTE INHALATION EXPOSURES

EPA Science Inventory

The US EPA National Center for Environmental Assessment has developed a methodology to derive acute inhalation toxicity benchmarks, called acute reference exposures (AREs), for noncancer effects. The methodology provides guidance for the derivation of chemical-specific benchmark...

The role of dehydroepiandrosterone on functional innate immune responses to acute stress.

PubMed

Prall, Sean P; Larson, Emilee E; Muehlenbein, Michael P

2017-12-01

The androgen dehydroepiandrosterone (DHEA) responds to stress activation, exhibits anti-glucocorticoid properties, and modulates immunity in diverse ways, yet little is known of its role in acute stress responses. In this study, the effects of DHEA and its sulfate ester DHEA-S on human male immune function during exposure to an acute stressor is explored. Variation in DHEA, DHEA-S, testosterone, and cortisol, along with bacterial killing assays, was measured in response to a modified Trier Social Stress test in 27 young adult males. Cortisol was positively related to salivary innate immunity but only for participants who also exhibited high DHEA responses. Additionally, DHEA positively and DHEA-S negatively predicted salivary immunity, but the opposite was observed for serum-based innate immunity. The DHEA response to acute stress appears to be an important factor in stress-mediated immunological responses, with differential effects on immunity dependent upon the presence of other hormones, primarily cortisol and DHEA-S. These results suggest that DHEA plays an important role, alongside other hormones, in modulating immunological shifts during acute stress. Copyright © 2017 John Wiley & Sons, Ltd.

Effects of acute and chronic psychological stress on platelet aggregation in mice.

PubMed

Matsuhisa, Fumikazu; Kitamura, Nobuo; Satoh, Eiki

2014-03-01

Although psychological stress has long been known to alter cardiovascular function, there have been few studies on the effect of psychological stress on platelets, which play a pivotal role in cardiovascular disease. In the present study, we investigated the effects of acute and chronic psychological stress on the aggregation of platelets and platelet cytosolic free calcium concentration ([Ca(2+)]i). Mice were subjected to both transportation stress (exposure to novel environment, psychological stress) and restraint stress (psychological stress) for 2 h (acute stress) or 3 weeks (2 h/day) (chronic stress). In addition, adrenalectomized mice were subjected to similar chronic stress (both transportation and restraint stress for 3 weeks). The aggregation of platelets from mice and [Ca(2+)]i was determined by light transmission assay and fura-2 fluorescence assay, respectively. Although acute stress had no effect on agonist-induced platelet aggregation, chronic stress enhanced the ability of the platelet agonists thrombin and ADP to stimulate platelet aggregation. However, chronic stress failed to enhance agonist-induced increase in [Ca(2+)]i. Adrenalectomy blocked chronic stress-induced enhancement of platelet aggregation. These results suggest that chronic, but not acute, psychological stress enhances agonist-stimulated platelet aggregation independently of [Ca(2+)]i increase, and the enhancement may be mediated by stress hormones secreted from the adrenal glands.

Effect of acute and repeated restraint stress on glucose oxidation to CO2 in hippocampal and cerebral cortex slices.

PubMed

Torres, I L; Gamaro, G D; Silveira-Cucco, S N; Michalowski, M B; Corrêa, J B; Perry, M L; Dalmaz, C

2001-01-01

It has been suggested that glucocorticoids released during stress might impair neuronal function by decreasing glucose uptake by hippocampal neurons. Previous work has demonstrated that glucose uptake is reduced in hippocampal and cerebral cortex slices 24 h after exposure to acute stress, while no effect was observed after repeated stress. Here, we report the effect of acute and repeated restraint stress on glucose oxidation to CO2 in hippocampal and cerebral cortex slices and on plasma glucose and corticosterone levels. Male adult Wistar rats were exposed to restraint 1 h/day for 50 days in the chronic model. In the acute model there was a single exposure. Immediately or 24 h after stress, the animals were sacrificed and the hippocampus and cerebral cortex were dissected, sliced, and incubated with Krebs buffer, pH 7.4, containing 5 mM glucose and 0.2 microCi D-[U-14C] glucose. CO2 production from glucose was estimated. Trunk blood was also collected, and both corticosterone and glucose were measured. The results showed that corticosterone levels after exposure to acute restraint were increased, but the increase was smaller when the animals were submitted to repeated stress. Blood glucose levels increased after both acute and repeated stress. However, glucose utilization, measured as CO2 production in hippocampal and cerebral cortex slices, was the same in stressed and control groups under conditions of both acute and chronic stress. We conclude that, although stress may induce a decrease in glucose uptake, this effect is not sufficient to affect the energy metabolism of these cells.

Human Physiological Responses to Acute and Chronic Cold Exposure

NASA Technical Reports Server (NTRS)

Stocks, Jodie M.; Taylor, Nigel A. S.; Tipton, Michael J.; Greenleaf, John E.

2001-01-01

When inadequately protected humans are exposed to acute cold, excessive body heat is lost to the environment and unless heat production is increased and heat loss attenuated, body temperature will decrease. The primary physiological responses to counter the reduction in body temperature include marked cutaneous vasoconstriction and increased metabolism. These responses, and the hazards associated with such exposure, are mediated by a number of factors which contribute to heat production and loss. These include the severity and duration of the cold stimulus; exercise intensity; the magnitude of the metabolic response; and individual characteristics such as body composition, age, and gender. Chronic exposure to a cold environment, both natural and artificial, results in physiological alterations leading to adaptation. Three quite different, but not necessarily exclusive, patterns of human cold adaptation have been reported: metabolic, hypothermic, and insulative. Cold adaptation has also been associated with an habituation response, in which there is a desensitization, or damping, of the normal response to a cold stress. This review provides a comprehensive analysis of the human physiological and pathological responses to cold exposure. Particular attention is directed to the factors contributing to heat production and heat loss during acute cold stress, and the ability of humans to adapt to cold environments.

Sex and genetic differences in the effects of acute diesel exhaust exposure on inflammation and oxidative stress in mouse brain

PubMed Central

Cole, Toby B.; Coburn, Jacki; Dao, Khoi; Roqué, Pam; Chang, Yu-Chi; Kalia, Vrinda; Guilarte, Tomas R.; Dziedzic, Jennifer; Costa, Lucio G.

2016-01-01

In addition to increased morbidity and mortality caused by respiratory and cardiovascular diseases, air pollution may also contribute to central nervous system (CNS) diseases. Traffic-related air pollution is a major contributor to global air pollution, and diesel exhaust (DE) is its most important component. DE contains more than 40 toxic air pollutants and is a major constituent of ambient particulate matter (PM), particularly of ultrafine-PM. Limited information suggest that exposure to DE may cause oxidative stress and neuroinflammation in the CNS. We hypothesized that males may be more susceptible than females to DE neurotoxicity, because of a lower level of expression of paraoxonase 2 (PON2), an intracellular anti-oxidant and anti-inflammatory enzyme. Acute exposure of C57BL/6 mice to DE (250–300 µg/m3 for 6h) caused significant increases in lipid peroxidation and of pro-inflammatory cytokines (IL-1α, IL-1β, IL-3, IL-6, TNF-α) in various brain regions (particularly olfactory bulb and hippocampus). In a number of cases the observed effects were more pronounced in male than in female mice. DE exposure also caused microglia activation, as measured by increased Iba1 (ionized calcium-binding adapter molecule 1) expression, and of TSPO (translocator protein) binding. Mice heterozygotes for the modifier subunit of glutamate cysteine ligase (the limiting enzyme in glutathione biosynthesis; Gclm+/− mice) appeared to be significantly more susceptible to DE-induced neuroinflammation than wild type mice. These findings indicate that acute exposure to DE causes neuroinflammation and oxidative stress in brain, and suggests that sex and genetic background may play important roles in modulating susceptibility to DE neurotoxicity. PMID:27865893

PTSD, Acute Stress, Performance and Decision-Making in Emergency Service Workers.

PubMed

Regehr, Cheryl; LeBlanc, Vicki R

2017-06-01

Despite research identifying high levels of stress and traumatic stress symptoms among those in the emergency services, the impact of these symptoms on performance and hence public safety remains uncertain. This review paper discusses a program of research that has examined the effects of prior critical incident exposure, acute stress, and current post-traumatic symptoms on the performance and decision-making during an acutely stressful event among police officers, police communicators, paramedics and child protection workers. Four studies, using simulation methods involving video simulators, human-patient simulators, and/or standardized patients, examined the performance of emergency workers in typical workplace situations related to their individual profession. Results varied according to level of acuity of stress and the nature of performance and decision-making. There was no evidence that PTSD had a direct impact on global performance on tasks for which emergency responders are highly trained. However, PTSD was associated with assessment of risk in situations that required professional judgement. Further, individuals experiencing PTSD symptoms reported higher levels of acute stress when faced with high acuity situations. Acute stress in these studies was associated with performance deficits on complex cognitive tasks, verbal memory impairment and heightened assessment of risk. © 2017 American Academy of Psychiatry and the Law.

History of chronic stress modifies acute stress-evoked fear memory and acoustic startle in male rats.

PubMed

Schmeltzer, Sarah N; Vollmer, Lauren L; Rush, Jennifer E; Weinert, Mychal; Dolgas, Charles M; Sah, Renu

2015-01-01

Chronicity of trauma exposure plays an important role in the pathophysiology of posttraumatic stress disorder (PTSD). Thus, exposure to multiple traumas on a chronic scale leads to worse outcomes than acute events. The rationale for the current study was to investigate the effects of a single adverse event versus the same event on a background of chronic stress. We hypothesized that a history of chronic stress would lead to worse behavioral outcomes than a single event alone. Male rats (n = 14/group) were exposed to either a single traumatic event in the form of electric foot shocks (acute shock, AS), or to footshocks on a background of chronic stress (chronic variable stress-shock, CVS-S). PTSD-relevant behaviors (fear memory and acoustic startle responses) were measured following 7 d recovery. In line with our hypothesis, CVS-S elicited significant increases in fear acquisition and conditioning versus the AS group. Unexpectedly, CVS-S elicited reduced startle reactivity to an acoustic stimulus in comparison with the AS group. Significant increase in FosB/ΔFosB-like immunostaining was observed in the dentate gyrus, basolateral amygdala and medial prefrontal cortex of CVS-S rats. Assessments of neuropeptide Y (NPY), a stress-regulatory transmitter associated with chronic PTSD, revealed selective reduction in the hippocampus of CVS-S rats. Collectively, our data show that cumulative stress potentiates delayed fear memory and impacts defensive responding. Altered neuronal activation in forebrain limbic regions and reduced NPY may contribute to these phenomena. Our preclinical studies support clinical findings reporting worse PTSD outcomes stemming from cumulative traumatization in contrast to acute trauma.

The Effects of Acute Waterborne Exposure to Sublethal Concentrations of Molybdenum on the Stress Response in Rainbow Trout, Oncorhynchus mykiss

PubMed Central

Ricketts, Chelsea D.; Bates, William R.; Reid, Scott D.

2015-01-01

To determine if molybdenum (Mo) is a chemical stressor, fingerling and juvenile rainbow trout (Oncorhynchus mykiss) were exposed to waterborne sodium molybdate (0, 2, 20, or 1,000 mg l-1 of Mo) and components of the physiological (plasma cortisol, blood glucose, and hematocrit) and cellular (heat shock protein [hsp] 72, hsp73, and hsp90 in the liver, gills, heart, and erythrocytes and metallothionein [MT] in the liver and gills) stress responses were measured prior to initiation of exposure and at 8, 24, and 96 h. During the acute exposure, plasma cortisol, blood glucose, and hematocrit levels remained unchanged in all treatments. Heat shock protein 72 was not induced as a result of exposure and there were no detectable changes in total hsp70 (72 and 73), hsp90, and MT levels in any of the tissues relative to controls. Both fingerling and juvenile fish responded with similar lack of apparent sensitivity to Mo exposure. These experiments demonstrate that exposure to waterborne Mo of up to 1,000 mg l-1 did not activate a physiological or cellular stress response in fish. Information from this study suggests that Mo water quality guidelines for the protection of aquatic life are highly protective of freshwater fish, namely rainbow trout. PMID:25629693

Prolonged Effects of Acute Stress on Decision-Making under Risk: A Human Psychophysiological Study

PubMed Central

Yamakawa, Kaori; Ohira, Hideki; Matsunaga, Masahiro; Isowa, Tokiko

2016-01-01

This study investigates the prolonged effects of physiological responses induced by acute stress on risk-taking in decision-making. Participants were divided into a Stress group (N = 14) and a Control group (N = 12). The Trier Social Stress Test was administered as an acute stressor, and reading was administered as a control task; thereafter, participants performed a decision-making task in which they needed to choose a sure option or a gamble option in Gain and Loss frame trials 2 h after (non-) exposure to the stressor. Increased cortisol, adrenaline, heart rate (HR), and subjective stress levels validated acute stress manipulation. Stressed participants made fewer risky choices only in the Gain domain, whereas no effect of stress was shown in the Loss domain. Deceleration of HR reflecting attention was greater for Gains compared with Losses only in the Stress group. Risk avoidance was determined by increased levels of cortisol caused by acute stress. These results suggest that processes regarding glucocorticoid might be involved in the prolonged effects of acute stress on the evaluation of risks and the monitoring of outcomes in decision-making. PMID:27679566

Systemic response of the stony coral Pocillopora damicornis against acute cadmium stress.

PubMed

Zhou, Zhi; Yu, Xiaopeng; Tang, Jia; Wu, Yibo; Wang, Lingui; Huang, Bo

2018-01-01

Heavy metals have become one of the main pollutants in the marine environment and a major threat to the growth and reproduction of stony corals. In the present study, the density of symbiotic zooxanthellae, levels of crucial physiological activities and the transcriptome were investigated in the stony coral Pocillopora damicornis after the acute exposure to elevated cadmium concentration. The density of symbiotic zooxanthellae decreased significantly during 12-24h period, and reached lowest at 24h after acute cadmium stress. No significant changes were observed in the activity of glutathione S-transferase during the entire stress exposure. The activities of superoxide dismutase and catalase, and the concentration of glutathione decreased significantly, but the activation level of caspase3 increased significantly after cadmium exposure. Furthermore, transcriptome sequencing and bioinformatics analysis revealed 3538 significantly upregulated genes and 8048 significantly downregulated genes at 12h after the treatment. There were 12 overrepresented GO terms for significantly upregulated genes, mostly related to unfolded protein response, endoplasmic reticulum stress and apoptosis. In addition, a total of 32 GO terms were overrepresented for significantly downregulated genes, and mainly correlated with macromolecular metabolic processes. These results collectively suggest that acute cadmium stress could induce apoptosis by repressing the production of the antioxidants, elevating oxidative stress and activating the unfolded protein response. This cascade of reactions would result to the collapse of the coral-zooxanthella symbiosis and the expulsion of symbiotic zooxanthellae in the stony coral P. damicornis, ultimately leading to coral bleaching. Copyright © 2017 Elsevier B.V. All rights reserved.

Acute stress promotes post-injury brain regeneration in fish.

PubMed

Sinyakov, Michael S; Haimovich, Amihai; Avtalion, Ramy R

2017-12-01

The central nervous system and the immune system, the two major players in homeostasis, operate in the ongoing bidirectional interaction. Stress is the third player that exerts strong effect on these two 'supersystems'; yet, its impact is studied much less. In this work employing carp model, we studied the influence of preliminary stress on neural and immune networks involved in post-injury brain regeneration. The relevant in vivo models of air-exposure stress and precisely directed cerebellum injury have been developed. Neuronal regeneration was evaluated by using specific tracers of cell proliferation and differentiation. Involvement of immune networks was accessed by monitoring the expression of selected T cells markers. Contrast difference between acute and chronic stress manifested in the fact that chronically stressed fish did not survive the brain injury. Neuronal regeneration appeared as a biphasic process whereas involvement of immune system proceeded as a monophasic route. In stressed fish, immune response was fast and accompanied or even preceded neuronal regeneration. In unstressed subjects, immune response took place on the second phase of neuronal regeneration. These findings imply an intrinsic regulatory impact of acute stress on neuronal and immune factors involved in post-injury brain regeneration. Stress activates both neuronal and immune defense mechanisms and thus contributes to faster regeneration. In this context, paradoxically, acute preliminary stress might be considered a distinct asset in speeding up the following post-injury brain regeneration. Copyright © 2017 Elsevier B.V. All rights reserved.

Acute hydrogen peroxide (H2O2) exposure does not cause oxidative stress in late-copepodite stage of Calanus finmarchicus.

PubMed

Hansen, Bjørn Henrik; Hallmann, Anna; Altin, Dag; Jenssen, Bjørn Munro; Ciesielski, Tomasz M

2017-01-01

Use of hydrogen peroxide (H 2 O 2 ) for removal of salmon lice in the aquaculture industry has created concern that non-target organisms might be affected during treatment scenarios. The aim of the present study was to examine the potential for H 2 O 2 to produce oxidative stress and reduce survival in one of the most abundant zooplankton species in Norwegian coastal areas, the copepod Calanus finmarchicus. Copepods were subjected to two 96-hr tests: (1) acute toxicity test where mortality was determined and (2) treated copepods were exposed to concentrations below the No Observed Effect Concentration (0.75 mg/L) H 2 O 2 and analyzed for antioxidant enzyme activities, as well as levels of glutathione (GSH) and malondialdehyde (MDA). Compared to available and comparable LC 50 values from the literature, our results suggest that C. finmarchicus is highly sensitive to H 2 O 2 . However, 96-hr exposure of C. finmarchicus to 0.75 mg H 2 O 2 /L did not significantly affect the antioxidant systems even though the concentration is just below the level where mortality is expected. Data suggest that aqueous H 2 O 2 exposure did not cause cellular accumulation with associated oxidative stress, but rather produced acute effects on copepod surface (carapace). Further investigation is required to ensure that aqueous exposure during H 2 O 2 treatment in salmon fish farms does not exert adverse effects on local non-target crustacean species and populations. In particular, studies on copepod developmental stages with a more permeable carapace are warranted.

Having your cake and eating it too: a habit of comfort food may link chronic social stress exposure and acute stress-induced cortisol hyporesponsiveness.

PubMed

Tryon, M S; DeCant, Rashel; Laugero, K D

2013-04-10

Stress has been tied to changes in eating behavior and food choice. Previous studies in rodents have shown that chronic stress increases palatable food intake which, in turn, increases visceral fat and inhibits acute stress-induced hypothalamic-pituitary-adrenal (HPA) axis activity. The effect of chronic stress on eating behavior in humans is less understood, but it may be linked to HPA responsivity. The purpose of this study was to investigate the influence of chronic social stress and acute stress reactivity on food choice and food intake. Forty-one women (BMI=25.9±5.1 kg/m(2), age range=41 to 52 years) were subjected to the Trier Social Stress Test or a control task (nature movie) to examine HPA responses to an acute laboratory stressor and then invited to eat from a buffet containing low- and high-calorie snacks. Women were also categorized as high chronic stress or low chronic stress based on Wheaton Chronic Stress Inventory scores. Women reporting higher chronic stress and exhibiting low cortisol reactivity to the acute stress task consumed significantly more calories from chocolate cake on both stress and control visits. Chronic stress in the low cortisol reactor group was also positively related to total fat mass, body fat percentage, and stress-induced negative mood. Further, women reporting high chronic stress consumed significantly less vegetables, but only in those aged 45 years and older. Chronic stress in women within the higher age category was positively related to total calories consumed at the buffet, stress-induced negative mood and food craving. Our results suggest an increased risk for stress eating in persons with a specific chronic stress signature and imply that a habit of comfort food may link chronic social stress and acute stress-induced cortisol hyporesponsiveness. Published by Elsevier Inc.

Sex and genetic differences in the effects of acute diesel exhaust exposure on inflammation and oxidative stress in mouse brain.

PubMed

Cole, Toby B; Coburn, Jacki; Dao, Khoi; Roqué, Pam; Chang, Yu-Chi; Kalia, Vrinda; Guilarte, Tomas R; Dziedzic, Jennifer; Costa, Lucio G

2016-12-30

In addition to increased morbidity and mortality caused by respiratory and cardiovascular diseases, air pollution may also contribute to central nervous system (CNS) diseases. Traffic-related air pollution is a major contributor to global air pollution, and diesel exhaust (DE) is its most important component. DE contains more than 40 toxic air pollutants and is a major constituent of ambient particulate matter (PM), particularly of ultrafine-PM. Limited information suggests that exposure to DE may cause oxidative stress and neuroinflammation in the CNS. We hypothesized that males may be more susceptible than females to DE neurotoxicity, because of a lower level of expression of paraoxonase 2 (PON2), an intracellular anti-oxidant and anti-inflammatory enzyme. Acute exposure of C57BL/6 mice to DE (250-300μg/m 3 for 6h) caused significant increases in lipid peroxidation and of pro-inflammatory cytokines (IL-1α, IL-1β, IL-3, IL-6, TNF-α) in various brain regions (particularly olfactory bulb and hippocampus). In a number of cases the observed effects were more pronounced in male than in female mice. DE exposure also caused microglia activation, as measured by increased Iba1 (ionized calcium-binding adapter molecule 1) expression, and of TSPO (translocator protein) binding. Mice heterozygotes for the modifier subunit of glutamate cysteine ligase (the limiting enzyme in glutathione biosynthesis; Gclm +/- mice) appeared to be significantly more susceptible to DE-induced neuroinflammation than wild type mice. These findings indicate that acute exposure to DE causes neuroinflammation and oxidative stress in brain, and suggest that sex and genetic background may play important roles in modulating susceptibility to DE neurotoxicity. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

Effect of acute heat stress on rat adrenal glands: a morphological and stereological study.

PubMed

Koko, Vesna; Djordjeviae, Jelena; Cvijiae, Gordana; Davidoviae, Vukosava

2004-11-01

The morphological and stereological structure of rat adrenal gland was analysed by light microscopy after an acute (60 min) exposure to high ambient temperature (38 degrees C). A significant increase in plasma corticotrophin (ACTH) and serum corticosterone (CORT) concentrations was observed, confirming that acute heat exposure has a strong stressful effect. Under these conditions the adrenal gland mass and volume were decreased, probably as the consequence of adrenal cortex reduction, especially that of the zona fasciculata (ZF). Histological examination revealed that many ZF cells were deprived of lipid droplets. Fibrosis was observed in all parts of the adrenal gland, both cortex and medulla, of heat stressed animals. Mitotic figures were absent in cortical cells after heat exposure, but there were no differences in ZF and zona reticularis (ZR) small blood vessels compared to nonstressed controls.

Young Children's Acute Stress After a Burn Injury: Disentangling the Role of Injury Severity and Parental Acute Stress.

PubMed

Haag, Ann-Christin; Landolt, Markus A

2017-09-01

Although injury severity and parental stress are strong predictors of posttraumatic adjustment in young children after burns, little is known about the interplay of these variables. This study aimed at clarifying mediation processes between injury severity and mother's, father's, and young child's acute stress. Structural equation modeling was used to examine the relationships between injury severity and parental and child acute stress. Parents of 138 burn-injured children (ages 1-4 years) completed standardized questionnaires on average 19 days postinjury. Sixteen children (11.7%) met Diagnostic and Statistical Manual of Mental Disorders, 5th edition, preschool criteria for posttraumatic stress disorder (excluding time criterion). The model revealed a significant mediation of maternal acute stress, with the effect of injury severity on a child's acute stress mediated by maternal acute stress. Paternal acute stress failed to serve as a mediating variable. Our findings confirm mothers' crucial role in the posttraumatic adjustment of young children. Clinically, mothers' acute stress should be monitored. © The Author 2017. Published by Oxford University Press on behalf of the Society of Pediatric Psychology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com

Effects of chronic plus acute prolonged stress on measures of coping style, anxiety, and evoked HPA-axis reactivity.

PubMed

Roth, Megan K; Bingham, Brian; Shah, Aparna; Joshi, Ankur; Frazer, Alan; Strong, Randy; Morilak, David A

2012-11-01

Exposure to psychological trauma is the precipitating factor for PTSD. In addition, a history of chronic or traumatic stress exposure is a predisposing risk factor. We have developed a Chronic plus Acute Prolonged Stress (CAPS) treatment for rats that models some of the characteristics of stressful events that can lead to PTSD in humans. We have previously shown that CAPS enhances acute fear responses and impairs extinction of conditioned fear. Further, CAPS reduced the expression of glucocorticoid receptors in the medial prefrontal cortex. In this study we examined the effects of CAPS exposure on behavioral stress coping style, anxiety-like behaviors, and acute stress reactivity of the hypothalamic-pituitary-adrenal (HPA) axis. Male Sprague-Dawley rats were exposed to CAPS treatment, consisting of chronic intermittent cold stress (4 °C, 6 h/day, 14 days) followed on day 15 by a single 1-h session of sequential acute stressors (social defeat, immobilization, swim). After CAPS or control treatment, different groups were tested for shock probe defensive burying, novelty suppressed feeding, or evoked activation of adrenocorticotropic hormone (ACTH) and corticosterone release by an acute immobilization stress. CAPS resulted in a decrease in active burying behavior and an increase in immobility in the shock probe test. Further, CAPS-treated rats displayed increases in the latency to feed in the novelty suppressed feeding test, despite an increase in food intake in the home cage. CAPS treatment also reduced the HPA response to a subsequent acute immobilization stress. These results further validate CAPS treatment as a rat model of relevance to PTSD, and together with results reported previously, suggest that CAPS impairs fear extinction, shifts coping behavior from an active to a more passive strategy, increases anxiety, and alters HPA reactivity, resembling many aspects of human PTSD. Copyright © 2012 Elsevier Ltd. All rights reserved.

Timing matters: the interval between acute stressors within chronic mild stress modifies behavioral and physiologic stress responses in male rats.

PubMed

Cavigelli, Sonia A; Bao, Alexander D; Bourne, Rebecca A; Caruso, Michael J; Caulfield, Jasmine I; Chen, Mary; Smyth, Joshua M

2018-04-12

Chronic mild stress can lead to negative health outcomes. Frequency, duration, and intensity of acute stressors can affect health-related processes. We tested whether the temporal pattern of daily acute stressors (clustered or dispersed across the day) affects depression-related physiology. We used a rodent model to keep stressor frequency, duration, and intensity constant, and experimentally manipulated the temporal pattern of acute stressors delivered during the active phase of the day. Adult male Sprague-Dawley rats were exposed to one of three chronic mild stress groups: Clustered: stressors that occurred within 1 hour of each other (n = 21), Dispersed: stressors that were spread out across the active phase (n = 21), and Control: no stressors presented (n = 21). Acute mild stressors included noise, strobe lights, novel cage, cage tilt, wet bedding, and water immersion. Depression-related outcomes included: sucrose preference, body weight, circulating glucocorticoid (corticosterone) concentration after a novel acute stressor and during basal morning and evening times, and endotoxin-induced circulating interleukin-6 concentrations. Compared to control rats, those in the Clustered group gained less weight, consumed less sucrose, had a blunted acute corticosterone response, and an accentuated acute interleukin-6 response. Rats in the Dispersed group had an attenuated corticosterone decline during the active period and after an acute stressor compared to the Control group. During a chronic mild stress experience, the temporal distribution of daily acute stressors affected health-related physiologic processes. Regular exposure to daily stressors in rapid succession may predict more depression-related symptoms, whereas exposure to stressors dispersed throughout the day may predict diminished glucocorticoid negative feedback.

Neural Mechanisms Underlying 5-HTTLPR Related Sensitivity to Acute Stress

PubMed Central

Drabant, Emily M; Ramel, Wiveka; Edge, Michael D; Hyde, Luke W; Kuo, Janice R; Goldin, Philippe R; Hariri, Ahmad R; Gross, James J

2013-01-01

Objective Many studies have shown that 5-HTTLPR genotype interacts with exposure to stress in conferring risk for psychopathology. However, the specific neural mechanisms through which this gene-by-environment interaction confers risk remain largely unknown, and no study to date has directly examined the modulatory effects of the 5-HTTLPR on corticolimbic circuit responses during exposure to acute stress. Methods An acute laboratory stressor was administered to 51 healthy women during BOLD fMRI scanning. In this task, electric shocks of uncertain intensity were threatened and unpredictably delivered to the wrist after a long anticipatory cue period of unpredictable duration. Results Relative to those carrying the L allele, SS homozygotes showed enhanced activation during threat anticipation in a network of regions including amygdala, hippocampus, anterior insula, thalamus, pulvinar, caudate, precuneus, anterior cingulate cortex, and medial prefrontal cortex. SS homozygotes also displayed enhanced positive coupling between medial prefrontal cortex activation and anxiety experience, whereas individuals carrying the L allele displayed enhanced negative coupling between insula activation and perceived success at regulating anxiety. Conclusions The present findings suggest that, when exposed to stress, SS homozygotes may preferentially engage neural systems which enhance fear and arousal, modulate attention toward threat, and perseverate on emotional salience of the threat. This may be one mechanism underlying risk for psychopathology conferred by the S allele upon exposure to life stressors. PMID:22362395

Better executive function under stress mitigates the effects of recent life stress exposure on health in young adults

PubMed Central

Shields, Grant S.; Moons, Wesley G.; Slavich, George M.

2017-01-01

Executive function is a neuropsychological construct that enables controlled cognitive processing, which has been hypothesized to enhance individuals’ resilience to stress. However, little empirical work has directly examined how executive function under different conditions mitigates the negative effects of stress exposure on health. To address this issue, we recruited 110 healthy young adults and assessed their recent life stress exposure, executive function in either a stressful or non-stressful context, and current health complaints. Based on existing research, we hypothesized that individuals exhibiting better executive function following a laboratory-based stressor (but not a control task) would demonstrate weaker associations between recent stress exposure and health because they perceived recent life stressors as being less severe. Consistent with this hypothesis, better executive function during acute stress, but not in the absence of stress, was associated with an attenuated link between participants’ recent life stress exposure and their current health complaints. Moreover, this attenuating effect was mediated by lesser perceptions of stressor severity. Based on these data, we conclude that better executive function under stress is associated with fewer health complaints and that these effects may occur by reducing individuals’ perceptions of stressor severity. The data thus suggest the possibility of reducing stress-related health problems by enhancing executive function. PMID:28114849

Better executive function under stress mitigates the effects of recent life stress exposure on health in young adults.

PubMed

Shields, Grant S; Moons, Wesley G; Slavich, George M

2017-01-01

Executive function is a neuropsychological construct that enables controlled cognitive processing, which has been hypothesized to enhance individuals' resilience to stress. However, little empirical work has directly examined how executive function under different conditions mitigates the negative effects of stress exposure on health. To address this issue, we recruited 110 healthy young adults and assessed their recent life stress exposure, executive function in either a stressful or non-stressful context, and current health complaints. Based on existing research, we hypothesized that individuals exhibiting better executive function following a laboratory-based stressor (but not a control task) would demonstrate weaker associations between recent stress exposure and health because they perceived recent life stressors as being less severe. Consistent with this hypothesis, better executive function during acute stress, but not in the absence of stress, was associated with an attenuated link between participants' recent life stress exposure and their current health complaints. Moreover, this attenuating effect was mediated by lesser perceptions of stressor severity. Based on these data, we conclude that better executive function under stress is associated with fewer health complaints and that these effects may occur by reducing individuals' perceptions of stressor severity. The data thus suggest the possibility of reducing stress-related health problems by enhancing executive function.

Ozone Exposure Increases Circulating Stress Hormones and Lipid Metabolites in Humans

EPA Science Inventory

RATIONALE: Air pollution has been associated with increased prevalence of type 2 diabetes; however, the mechanisms remain unknown. We have shown that acute ozone exposure in rats induces release of stress hormones, hyperglycemia, leptinemia, and gluoose intolerance that are assoc...

Paternal preconception ethanol exposure blunts hypothalamic-pituitary-adrenal axis responsivity and stress-induced excessive fluid intake in male mice.

PubMed

Rompala, Gregory R; Finegersh, Andrey; Homanics, Gregg E

2016-06-01

A growing number of environmental insults have been shown to induce epigenetic effects that persist across generations. For instance, paternal preconception exposures to ethanol or stress have independently been shown to exert such intergenerational effects. Since ethanol exposure is a physiological stressor that activates the hypothalamic-pituitary-adrenal (HPA) axis, we hypothesized that paternal ethanol exposure would impact stress responsivity of offspring. Adult male mice were exposed to chronic intermittent vapor ethanol or control conditions for 5 weeks before being mated with ethanol-naïve females to produce ethanol (E)- and control (C)-sired offspring. Adult male and female offspring were tested for plasma corticosterone (CORT) levels following acute restraint stress and the male offspring were further examined for stress-evoked 2-bottle choice ethanol-drinking. Paternal ethanol exposure blunted plasma CORT levels following acute restraint stress selectively in male offspring; females were unaffected. In a stress-evoked ethanol-drinking assay, there was no effect of stress on ethanol consumption. However, C-sired males exhibited increased total fluid intake (polydipsia) in response to stress while E-sired males were resistant to this stress-induced phenotype. Taken together, these data suggest that paternal ethanol exposure imparts stress hyporesponsivity to male offspring. Copyright © 2016 Elsevier Inc. All rights reserved.

Paternal preconception ethanol exposure blunts hypothalamic-pituitary-adrenal axis responsivity and stress-induced excessive fluid intake in male mice

PubMed Central

Rompala, Gregory R.; Finegersh, Andrey; Homanics, Gregg E.

2016-01-01

A growing number of environmental insults have been shown to induce epigenetic effects that persist across generations. For instance, paternal preconception exposures to ethanol or stress have independently been shown to exert such intergenerational effects. Since ethanol exposure is a physiological stressor that activates the hypothalamic-pituitary-adrenal (HPA) axis, we hypothesized that paternal ethanol exposure would impact stress responsivity of offspring. Adult male mice were exposed to chronic intermittent vapor ethanol or control conditions for 5 weeks before being mated with ethanol-naïve females to produce ethanol (E)- and control (C)-sired offspring. Adult male and female offspring were tested for plasma corticosterone (CORT) levels following acute restraint stress and the male offspring were further examined for stress-evoked 2-bottle choice ethanol drinking. Paternal ethanol exposure blunted plasma CORT levels following acute restraint stress selectively in male offspring; females were unaffected. In a stress-evoked ethanol-drinking assay, there was no effect of stress on ethanol consumption. However, C-sired males exhibited increased total fluid intake (polydipsia) in response to stress while E-sired males were resistant to this stress-induced phenotype. Taken together, these data suggest that paternal ethanol exposure imparts stress hyporesponsivity to male offspring. PMID:27286933

Mimicking acute and chronic stress exposure in naive beef steers alters the acute phase response (APR) associated with vaccination

USDA-ARS?s Scientific Manuscript database

This study was designed to determine the effect of an acute versus chronic stress model on the APR associated with vaccination in naïve beef steers. Steers (n=32; 209 +/- 8 kg) were blocked by body weight and assigned to 1 of 3 treatments: 1) Chronic stress (CHR), 0.5 mg/kg body weight dexamethasone...

Predictors of Treatment Response to Fluoxetine in PTSD Following a Recent History of War Zone Stress Exposure

DTIC Science & Technology

2010-07-01

routinely prescribed for acute stress disorder and early PTSD and recommended in the VA-DoD best practice guidelines, the efficacy of SSRIs as an early...selective serotonin reuptake inhibitors (SSRIs) are routinely prescribed for acute stress disorder and early PTSD and recommended in the VA-DoD best practice...1-0283 TITLE: Predictors of Treatment Response to Fluoxetine in PTSD Following a Recent History of War Zone Stress Exposure

Sex-specific hippocampal 5-hydroxymethylcytosine is disrupted in response to acute stress

PubMed Central

Papale, Ligia A.; Li, Sisi; Madrid, Andy; Zhang, Qi; Chen, Li; Chopra, Pankaj; Jin, Peng; Keleş, Sündüz; Alisch, Reid S.

2016-01-01

Environmental stress is among the most important contributors to increased susceptibility to develop psychiatric disorders. While it is well known that acute environmental stress alters gene expression, the molecular mechanisms underlying these changes remain largely unknown. 5-hydroxymethylcytosine (5hmC) is a novel environmentally sensitive epigenetic modification that is highly enriched in neurons and is associated with active neuronal transcription. Recently, we reported a genome-wide disruption of hippocampal 5hmC in male mice following acute stress that was correlated to altered transcript levels of genes in known stress related pathways. Since sex-specific endocrine mechanisms respond to environmental stimulus by altering the neuronal epigenome, we examined the genome-wide profile of hippocampal 5hmC in female mice following exposure to acute stress and identified 363 differentially hydroxymethylated regions (DhMRs) linked to known (e.g., Nr3c1 and Ntrk2) and potentially novel genes associated with stress response and psychiatric disorders. Integration of hippocampal expression data from the same female mice found stress-related hydroxymethylation correlated to altered transcript levels. Finally, characterization of stress-induced sex-specific 5hmC profiles in the hippocampus revealed 778 sex-specific acute stress-induced DhMRs some of which were correlated to altered transcript levels that produce sex-specific isoforms in response to stress. Together, the alterations in 5hmC presented here provide a possible molecular mechanism for the adaptive sex-specific response to stress that may augment the design of novel therapeutic agents that will have optimal effectiveness in each sex. PMID:27576189

Stress responding in cannabis smokers as a function of trauma exposure, sex, and relapse in the human laboratory.

PubMed

Chao, Thomas; Radoncic, Vanya; Hien, Denise; Bedi, Gillinder; Haney, Margaret

2018-04-01

Stress responding is linked to drug use, but little is known about stress responses in cannabis smokers. We investigated acute stress responding in cannabis smokers as a function of trauma exposure and sex, and relationships between stress responses and cannabis relapse. 125 healthy, non-treatment-seeking daily cannabis smokers (23F, 102 M) completed the Trier Social Stress Task (TSST), a standardized laboratory stressor; subsets also completed a trauma questionnaire (n = 106) and a laboratory cannabis relapse measure (n = 54). Stress responding was assessed with heart rate (HR), salivary cortisol (CORT), and self-rated mood. Cannabis smokers reporting at least one trauma exposure had higher CORT and anxiety overall compared to those reporting no trauma. Stress responding did not differ as a function of binary trauma exposure, although total number of exposures correlated positively with CORT and anxiety during stress. Females reported increased nervousness after stress relative to males matched to the females for cannabis and cigarette use. An interactive effect of sex and trauma on HR suggested that females with trauma exposure have increased cardiovascular stress responding relative to those without such exposure, with no differential effect in males. Stress responding did not predict laboratory cannabis relapse. We report differences in acute stress responding as a function of trauma, sex, and their interaction in a large sample of relatively homogenous cannabis smokers. Further investigation of how trauma impacts stress responding in male and female cannabis smokers, and how this relates to different aspects of cannabis use, is warranted. Copyright © 2018 Elsevier B.V. All rights reserved.

Evaluating the Impact of a Brief Artistic Intervention on Cardiovascular Recovery from Acute Stress

ERIC Educational Resources Information Center

Keogh, Katharina; Creaven, Ann-Marie

2017-01-01

In this study we tested whether drawing and coloring influence cardiovascular recovery and perceived stress following exposure to a stressor. In a mixed experimental design, participants (N = 62) completed an acute stress task before being randomly assigned to one of three brief activities: free-form drawing (full creative control), coloring…

Ozone Exposure Increases Circulating Stress Hormones and Lipid Metabolites in Humans

PubMed Central

Miller, Desinia B.; Ghio, Andrew J.; Karoly, Edward D.; Bell, Lauren N.; Snow, Samantha J.; Madden, Michael C.; Soukup, Joleen; Cascio, Wayne E.; Gilmour, M. Ian

2016-01-01

Rationale: Air pollution has been associated with increased prevalence of type 2 diabetes; however, the mechanisms remain unknown. We have shown that acute ozone exposure in rats induces release of stress hormones, hyperglycemia, leptinemia, and glucose intolerance that are associated with global changes in peripheral glucose, lipid, and amino acid metabolism. Objectives: To examine ozone-induced metabolic derangement in humans using serum metabolomic assessment, establish human-to-rodent coherence, and identify novel nonprotein biomarkers. Methods: Serum samples were obtained from a crossover clinical study that included two clinic visits (n = 24 each) where each subject was blindly exposed in the morning to either filtered air or 0.3 parts per million ozone for 2 hours during 15-minute on-off exercise. Serum samples collected within 1 hour after exposure were assessed for changes in metabolites using a metabolomic approach. Measurements and Main Results: Metabolomic analysis revealed that ozone exposure markedly increased serum cortisol and corticosterone together with increases in monoacylglycerol, glycerol, and medium- and long-chain free fatty acids, reflective of lipid mobilization and catabolism. Additionally, ozone exposure increased serum lysolipids, potentially originating from membrane lipid breakdown. Ozone exposure also increased circulating mitochondrial β-oxidation–derived metabolites, such as acylcarnitines, together with increases in the ketone body 3-hydroxybutyrate. These changes suggested saturation of β-oxidation by ozone in exercising humans. Conclusions: As in rodents, acute ozone exposure increased stress hormones and globally altered peripheral lipid metabolism in humans, likely through activation of a neurohormonally mediated stress response pathway. The metabolomic assessment revealed new biomarkers and allowed for establishment of rodent-to-human coherence. Clinical trial registered with www.clinicaltrials.gov (NCT 01492517

Salivary Markers of Inflammation in Response to Acute Stress

PubMed Central

Slavish, Danica C.; Graham-Engeland, Jennifer E.; Smyth, Joshua M.; Engeland, Christopher G.

2014-01-01

There is burgeoning interest in the ability to detect inflammatory markers in response to stress within naturally occurring social contexts and/or across multiple time points per day within individuals. Salivary collection is a less invasive process than current methods of blood collection and enables intensive naturalistic methodologies, such as those involving extensive repeated measures per day over time. Yet the reliability and validity of saliva-based to blood-based inflammatory biomarkers in response to stress remains unclear. We review and synthesize the published studies that have examined salivary markers of inflammation following exposure to an acute laboratory stressor. Results from each study are reviewed by analyte (IL-1β, TNF-α, IL-6, IL-2, IL-4, IL-10, IL-12, CRP) and stress type (social-cognitive and exercise-physical), after which methodological issues and limitations are addressed. Although the literature is limited, several inflammatory markers (including IL-1β, TNF-α, and IL-6) have been reliably determined from saliva and have increased significantly in response to stress across multiple studies, with effect sizes ranging from very small to very large. Although CRP from saliva has been associated with CRP in circulating blood more consistently than other biomarkers have been associated with their counterparts in blood, evidence demonstrating it reliably responds to acute stress is absent. Although the current literature is presently too limited to allow broad assertion that inflammatory biomarkers determined from saliva are valuable for examining acute stress responses, this review suggests that specific targets may be valid and highlights specific areas of need for future research. PMID:25205395

Critical features of acute stress-induced cross-sensitization identified through the hypothalamic-pituitary-adrenal axis output.

PubMed

Belda, Xavier; Nadal, Roser; Armario, Antonio

2016-08-11

Stress-induced sensitization represents a process whereby prior exposure to severe stressors leaves animals or humans in a hyper-responsive state to further stressors. Indeed, this phenomenon is assumed to be the basis of certain stress-associated pathologies, including post-traumatic stress disorder and psychosis. One biological system particularly prone to sensitization is the hypothalamic-pituitary-adrenal (HPA) axis, the prototypic stress system. It is well established that under certain conditions, prior exposure of animals to acute and chronic (triggering) stressors enhances HPA responses to novel (heterotypic) stressors on subsequent days (e.g. raised plasma ACTH and corticosterone levels). However, such changes remain somewhat controversial and thus, the present study aimed to identify the critical characteristics of the triggering and challenging stressors that affect acute stress-induced HPA cross-sensitization in adult rats. We found that HPA cross-sensitization is markedly influenced by the intensity of the triggering stressor, whereas the length of exposure mainly affects its persistence. Importantly, HPA sensitization is more evident with mild than strong challenging stressors, and it may remain unnoticed if exposure to the challenging stressor is prolonged beyond 15 min. We speculate that heterotypic HPA sensitization might have developed to optimize biologically adaptive responses to further brief stressors.

Critical features of acute stress-induced cross-sensitization identified through the hypothalamic-pituitary-adrenal axis output

PubMed Central

Belda, Xavier; Nadal, Roser; Armario, Antonio

2016-01-01

Stress-induced sensitization represents a process whereby prior exposure to severe stressors leaves animals or humans in a hyper-responsive state to further stressors. Indeed, this phenomenon is assumed to be the basis of certain stress-associated pathologies, including post-traumatic stress disorder and psychosis. One biological system particularly prone to sensitization is the hypothalamic-pituitary-adrenal (HPA) axis, the prototypic stress system. It is well established that under certain conditions, prior exposure of animals to acute and chronic (triggering) stressors enhances HPA responses to novel (heterotypic) stressors on subsequent days (e.g. raised plasma ACTH and corticosterone levels). However, such changes remain somewhat controversial and thus, the present study aimed to identify the critical characteristics of the triggering and challenging stressors that affect acute stress-induced HPA cross-sensitization in adult rats. We found that HPA cross-sensitization is markedly influenced by the intensity of the triggering stressor, whereas the length of exposure mainly affects its persistence. Importantly, HPA sensitization is more evident with mild than strong challenging stressors, and it may remain unnoticed if exposure to the challenging stressor is prolonged beyond 15 min. We speculate that heterotypic HPA sensitization might have developed to optimize biologically adaptive responses to further brief stressors. PMID:27511270

Acute stress impairs the retrieval of extinction memory in humans

PubMed Central

Raio, Candace M.; Brignoni-Perez, Edith; Goldman, Rachel; Phelps, Elizabeth A.

2014-01-01

Extinction training is a form of inhibitory learning that allows an organism to associate a previously aversive cue with a new, safe outcome. Extinction does not erase a fear association, but instead creates a competing association that may or may not be retrieved when a cue is subsequently encountered. Characterizing the conditions under which extinction learning is expressed is important to enhancing the treatment of anxiety disorders that rely on extinction-based exposure therapy as a primary treatment technique. The ventromedial prefrontal cortex, which plays an important role in the expression of extinction memory, has been shown to be functionally impaired after stress exposure. Further, recent research in rodents found that exposure to stress led to deficits in extinction retrieval, although this has yet to be tested in humans. To explore how stress might influence extinction retrieval in humans, participants underwent a differential aversive learning paradigm, in which one image was probabilistically paired with an aversive shock while the other image denoted safety. Extinction training directly followed, at which point reinforcement was omitted. A day later, participants returned to the lab and either completed an acute stress manipulation (i.e., cold pressor), or a control task, before undergoing an extinction retrieval test. Skin conductance responses and salivary cortisol concentrations were measured throughout each session as indices of fear arousal and neuroendocrine stress responses, respectively. The efficacy of our stress induction was established by observing significant increases in cortisol for the stress condition only. We examined extinction retrieval by comparing conditioned responses during the last trial of extinction (day 1) with that of the first trial of re-extinction (day 2). Groups did not differ on initial fear acquisition or extinction, however, one day later participants in the stress group (n = 27) demonstrated significantly less

OSO paradigm--A rapid behavioral screening method for acute psychosocial stress reactivity in mice.

PubMed

Brzózka, M M; Unterbarnscheidt, T; Schwab, M H; Rossner, M J

2016-02-09

Chronic psychosocial stress is an important environmental risk factor for the development of psychiatric diseases. However, studying the impact of chronic psychosocial stress in mice is time consuming and thus not optimally suited to 'screen' increasing numbers of genetically manipulated mouse models for psychiatric endophenotypes. Moreover, many studies focus on restraint stress, a strong physical stressor with limited relevance for psychiatric disorders. Here, we describe a simple and a rapid method based on the resident-intruder paradigm to examine acute effects of mild psychosocial stress in mice. The OSO paradigm (open field--social defeat--open field) compares behavioral consequences on locomotor activity, anxiety and curiosity before and after exposure to acute social defeat stress. We first evaluated OSO in male C57Bl/6 wildtype mice where a single episode of social defeat reduced locomotor activity, increased anxiety and diminished exploratory behavior. Subsequently, we applied the OSO paradigm to mouse models of two schizophrenia (SZ) risk genes. Transgenic mice with neuronal overexpression of Neuregulin-1 (Nrg1) type III showed increased risk-taking behavior after acute stress exposure suggesting that NRG1 dysfunction is associated with altered affective behavior. In contrast, Tcf4 transgenic mice displayed a normal stress response which is in line with the postulated predominant contribution of TCF4 to cognitive deficits of SZ. In conclusion, the OSO paradigm allows for rapid screening of selected psychosocial stress-induced behavioral endophenotypes in mouse models of psychiatric diseases. Copyright © 2015 IBRO. Published by Elsevier Ltd. All rights reserved.

Glucoregulatory responses of adult and aged rats after exposure to chronic stress.

PubMed

Odio, M R; Brodish, A

1990-01-01

Stress has been implicated as an environmental factor that may accelerate the process of biological aging. However, this proposal has remained largely anecdotal due to relatively few studies that directly tested this hypothesis. In the present experiments groups of 6-month-old and 20-month-old male F-344 rats were chronically stressed for a six-month period. After the last stress session, when the animals were 12 months of age (adult) and 26 months of age (old), control and chronically stressed rats were tested for their ability to: (a) elicit glucose and insulin responses to an acute, novel stressor; (b) remove a circulatory glucose load elicited either by acute stress exposure or by injection of d-glucose; and (c) raise insulin levels after a glucose challenge. In control rats, we observed a deficit in each of these parameters in old compared to adult rats. Exposure to chronic stress did not exacerbate deterioration of these response mechanisms in either adult or old rats. In fact, the data showed a modest improvement in glucose tolerance in chronically stressed compared to age-matched control rats. We conclude that chronic stress did not exacerbate age-dependent decline of glucoregulatory capacity. From these results and from our earlier work, we speculate that the decline during aging of the functional integrity of systems involved in the response to stress may be sustained by periodic challenges from the organism's external environment.

Sex-specific hippocampal 5-hydroxymethylcytosine is disrupted in response to acute stress.

PubMed

Papale, Ligia A; Li, Sisi; Madrid, Andy; Zhang, Qi; Chen, Li; Chopra, Pankaj; Jin, Peng; Keleş, Sündüz; Alisch, Reid S

2016-12-01

Environmental stress is among the most important contributors to increased susceptibility to develop psychiatric disorders. While it is well known that acute environmental stress alters gene expression, the molecular mechanisms underlying these changes remain largely unknown. 5-hydroxymethylcytosine (5hmC) is a novel environmentally sensitive epigenetic modification that is highly enriched in neurons and is associated with active neuronal transcription. Recently, we reported a genome-wide disruption of hippocampal 5hmC in male mice following acute stress that was correlated to altered transcript levels of genes in known stress related pathways. Since sex-specific endocrine mechanisms respond to environmental stimulus by altering the neuronal epigenome, we examined the genome-wide profile of hippocampal 5hmC in female mice following exposure to acute stress and identified 363 differentially hydroxymethylated regions (DhMRs) linked to known (e.g., Nr3c1 and Ntrk2) and potentially novel genes associated with stress response and psychiatric disorders. Integration of hippocampal expression data from the same female mice found stress-related hydroxymethylation correlated to altered transcript levels. Finally, characterization of stress-induced sex-specific 5hmC profiles in the hippocampus revealed 778 sex-specific acute stress-induced DhMRs some of which were correlated to altered transcript levels that produce sex-specific isoforms in response to stress. Together, the alterations in 5hmC presented here provide a possible molecular mechanism for the adaptive sex-specific response to stress that may augment the design of novel therapeutic agents that will have optimal effectiveness in each sex. Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.

Repeated, but Not Acute, Stress Suppresses Inflammatory Plasma Extravasation

NASA Astrophysics Data System (ADS)

Strausbaugh, Holly J.; Dallman, Mary F.; Levine, Jon D.

1999-12-01

Clinical findings suggest that inflammatory disease symptoms are aggravated by ongoing, repeated stress, but not by acute stress. We hypothesized that, compared with single acute stressors, chronic repeated stress may engage different physiological mechanisms that exert qualitatively different effects on the inflammatory response. Because inhibition of plasma extravasation, a critical component of the inflammatory response, has been associated with increased disease severity in experimental arthritis, we tested for a potential repeated stress-induced inhibition of plasma extravasation. Repeated, but not single, exposures to restraint stress produced a profound inhibition of bradykinin-induced synovial plasma extravasation in the rat. Experiments examining the mechanism of inhibition showed that the effect of repeated stress was blocked by adrenalectomy, but not by adrenal medullae denervation, suggesting that the adrenal cortex mediates this effect. Consistent with known effects of stress and with mediation by the adrenal cortex, restraint stress evoked repeated transient elevations of plasma corticosterone levels. This elevated corticosterone was necessary and sufficient to produce inhibition of plasma extravasation because the stress-induced inhibition was blocked by preventing corticosterone synthesis and, conversely, induction of repeated transient elevations in plasma corticosterone levels mimicked the effects of repeated stress. These data suggest that repetition of a mild stressor can induce changes in the physiological state of the animal that enable a previously innocuous stressor to inhibit the inflammatory response. These findings provide a potential explanation for the clinical association between repeated stress and aggravation of inflammatory disease symptoms and provide a model for study of the biological mechanisms underlying the stress-induced aggravation of chronic inflammatory diseases.

Mental- and physical-health effects of acute exposure to media images of the September 11, 2001, attacks and the Iraq War.

PubMed

Silver, Roxane Cohen; Holman, E Alison; Andersen, Judith Pizarro; Poulin, Michael; McIntosh, Daniel N; Gil-Rivas, Virginia

2013-09-01

Millions of people witnessed early, repeated television coverage of the September 11 (9/11), 2001, terrorist attacks and were subsequently exposed to graphic media images of the Iraq War. In the present study, we examined psychological- and physical-health impacts of exposure to these collective traumas. A U.S. national sample (N = 2,189) completed Web-based surveys 1 to 3 weeks after 9/11; a subsample (n = 1,322) also completed surveys at the initiation of the Iraq War. These surveys measured media exposure and acute stress responses. Posttraumatic stress symptoms related to 9/11 and physician-diagnosed health ailments were assessed annually for 3 years. Early 9/11- and Iraq War-related television exposure and frequency of exposure to war images predicted increased posttraumatic stress symptoms 2 to 3 years after 9/11. Exposure to 4 or more hr daily of early 9/11-related television and cumulative acute stress predicted increased incidence of health ailments 2 to 3 years later. These findings suggest that exposure to graphic media images may result in physical and psychological effects previously assumed to require direct trauma exposure.

Prenatal exposure to escitalopram and/or stress in rats produces limited effects on endocrine, behavioral, or gene expression measures in adult male rats

PubMed Central

Bourke, Chase H.; Stowe, Zachary N.; Neigh, Gretchen N.; Olson, Darin E.; Owens, Michael J.

2013-01-01

Stress and/or antidepressants during pregnancy have been implicated in a wide range of long-term effects in the offspring. We investigated the long-term effects of prenatal stress and/or clinically relevant antidepressant exposure on male adult offspring in a model of the pharmacotherapy of maternal depression. Female Sprague-Dawley rats were implanted with osmotic minipumps that delivered clinically relevant exposure to the antidepressant escitalopram throughout gestation. Subsequently, pregnant females were exposed on gestational days 10–20 to a chronic unpredictable mild stress paradigm. The male offspring were analyzed in adulthood. Baseline physiological measurements were largely unaltered by prenatal manipulations. Behavioral characterization of the male offspring, with or without pre-exposure to an acute stressor, did not reveal any group differences. Prenatal stress exposure resulted in a faster return towards baseline following the peak response to an acute restraint stressor, but not an airpuff startle stressor, in adulthood. Microarray analysis of the hippocampus and hypothalamus comparing all treatment groups revealed no significantly-altered transcripts. Real time PCR of the hippocampus confirmed that several transcripts in the CRFergic, serotonergic, and neural plasticity pathways were unaffected by prenatal exposures. This stress model of maternal depression and its treatment indicate that escitalopram use and/or stress during pregnancy produced no alterations in our measures of male adult behavior or the transcriptome, however prenatal stress exposure resulted in some evidence for increased glucocorticoid negative feedback following an acute restraint stress. Study design should be carefully considered before implications for human health are ascribed to prenatal exposure to stress or antidepressant medication. PMID:23906943

Stress Exposure and Depression in Disadvantaged Women: The Protective Effects of Optimism and Perceived Control

ERIC Educational Resources Information Center

Grote, Nancy K.; Bledsoe, Sarah E.; Larkin, Jill; Lemay, Edward P., Jr.; Brown, Charlotte

2007-01-01

In the present study, the authors predicted that the individual protective factors of optimism and perceived control over acute and chronic stressors would buffer the relations between acute and chronic stress exposure and severity of depression, controlling for household income, in a sample of financially disadvantaged women. Ninety-seven African…

Acute psychosocial stress and everyday moral decision-making in young healthy men: The impact of cortisol.

PubMed

Singer, Nina; Sommer, Monika; Döhnel, Katrin; Zänkert, Sandra; Wüst, Stefan; Kudielka, Brigitte M

2017-07-01

In everyday life, moral decisions must frequently be made under acute stress. Although there is increasing evidence that both stress and cortisol affect moral judgment and behavior as well as decision-making in various domains unrelated to morality, surprisingly few attempts have been made to explore the effects of stress on everyday moral decision-making. Therefore, in the present study, we exposed 50 young healthy men to the Trier Social Stress Test (TSST) or its non-stressful placebo version (PTSST). We investigated the impact of acute stress exposure and stress-related cortisol levels on decision-making, decision certainty, and emotions in 28 everyday moral conflict situations with altruistic versus egoistic response alternatives. Results showed that the TSST-exposed group made more altruistic decisions than the non-stress control group, while groups did not differ in decision certainty and emotion ratings. Moreover, in correlational as well as regression analyses, additionally controlling for confounding variables, we observed significant positive associations between cortisol levels and altruistic decision-making. Further analyses revealed that altruistic decisions came along with significantly higher decision certainty and significantly more positive emotion ratings than egoistic decisions. Notably, our data also raise the idea that the personality trait agreeableness plays an important role in everyday moral decision-making. In sum, our findings provide initial evidence that both acute stress exposure and cortisol levels have prosocial effects on everyday moral decision-making in young healthy men. Copyright © 2017 Elsevier Inc. All rights reserved.

Acute psychosocial stress differentially influences salivary endocrine and immune measures in undergraduate students.

PubMed

Campisi, Jay; Bravo, Yesika; Cole, Jennifer; Gobeil, Kyle

2012-10-10

Undergraduate students routinely experience acute psychosocial stress when interviewing for post-collegiate employment. While numerous studies have demonstrated that acute stress can increase release of immune-relevant molecules in blood, fewer studies have examined if acute stress also increases immune-relevant molecules into saliva. Saliva, and the biomolecules found in saliva often serve important immune defense roles and can be used to non-invasively screen for many systemic diseases. Therefore, the current study examined saliva concentrations of endocrine and immune molecules following exposure to an acute psychosocial stressor (mock job interview) in undergraduates. Heart rate, blood pressure, salivary cortisol, salivary immunoglobulin-A (S-IgA), and salivary C-reactive protein (S-CRP) were compared in healthy college undergraduates (n=15) before and after completion of the Trier Social Stress Test (TSST). The TSST induced significant increases in heart rate, systolic blood pressure, and salivary cortisol. Additional analyses revealed a non-significant (p=0.1) increase in the level of S-IgA following the TSST. A significant decrease in S-IgA was observed during the recovery period. No change in S-CRP was observed following the TSST. These results suggest that acute stress experienced by undergraduates when interviewing for a job activates the sympathetic nervous system and hypothalamic-pituitary-adrenal axis and that cortisol levels increase in saliva. Stress-induced elevations in cortisol might be responsible for the decreased S-IgA observed following the recovery period. Collectively, these data provide further insight into the interaction between psychosocial stress, endocrine, and immune functioning. Copyright © 2012 Elsevier Inc. All rights reserved.

Carbon monoxide exposure enhances arrhythmia after cardiac stress: involvement of oxidative stress.

PubMed

André, Lucas; Gouzi, Fares; Thireau, Jérôme; Meyer, Gregory; Boissiere, Julien; Delage, Martine; Abdellaoui, Aldja; Feillet-Coudray, Christine; Fouret, Gilles; Cristol, Jean-Paul; Lacampagne, Alain; Obert, Philippe; Reboul, Cyril; Fauconnier, Jérémy; Hayot, Maurice; Richard, Sylvain; Cazorla, Olivier

2011-11-01

Arrhythmias following cardiac stress are a key predictor of death in healthy population. Carbon monoxide (CO) is a ubiquitous pollutant promoting oxidative stress and associated with hospitalization for cardiovascular disease and cardiac mortality. We investigated the effect of chronic CO exposure on the occurrence of arrhythmic events after a cardiac stress test and the possible involvement of related oxidative stress. Wistar rats exposed chronically (4 weeks) to sustained urban CO pollution presented more arrhythmic events than controls during recovery after cardiac challenge with isoprenaline in vivo. Sudden death occurred in 22% of CO-exposed rats versus 0% for controls. Malondialdehyde (MDA), an end-product of lipid peroxidation, was increased in left ventricular tissue of CO-exposed rats. Cardiomyocytes isolated from CO-exposed rats showed higher reactive oxygen species (ROS) production (measured with MitoSox Red dye), higher diastolic Ca(2+) resulting from SR calcium leak and an higher occurrence of irregular Ca(2+) transients (measured with Indo-1) in comparison to control cells after a high pacing sequence. Acute treatment with a ROS scavenger (N-acetylcysteine, 20 mmol/L, 1 h) prevented this sequence of alterations and decreased the number of arrhythmic cells following high pacing. Chronic CO exposure promotes oxidative stress that alters Ca(2+) homeostasis (through RYR2 and SERCA defects) and thereby mediates the triggering of ventricular arrhythmia after cardiac stress that can lead to sudden death.

Aged rats are hypo-responsive to acute restraint: implications for psychosocial stress in aging

PubMed Central

Buechel, Heather M.; Popovic, Jelena; Staggs, Kendra; Anderson, Katie L.; Thibault, Olivier; Blalock, Eric M.

2013-01-01

Cognitive processes associated with prefrontal cortex and hippocampus decline with age and are vulnerable to disruption by stress. The stress/stress hormone/allostatic load hypotheses of brain aging posit that brain aging, at least in part, is the manifestation of life-long stress exposure. In addition, as humans age, there is a profound increase in the incidence of new onset stressors, many of which are psychosocial (e.g., loss of job, death of spouse, social isolation), and aged humans are well-understood to be more vulnerable to the negative consequences of such new-onset chronic psychosocial stress events. However, the mechanistic underpinnings of this age-related shift in chronic psychosocial stress response, or the initial acute phase of that chronic response, have been less well-studied. Here, we separated young (3 month) and aged (21 month) male F344 rats into control and acute restraint (an animal model of psychosocial stress) groups (n = 9–12/group). We then assessed hippocampus-associated behavioral, electrophysiological, and transcriptional outcomes, as well as blood glucocorticoid and sleep architecture changes. Aged rats showed characteristic water maze, deep sleep, transcriptome, and synaptic sensitivity changes compared to young. Young and aged rats showed similar levels of distress during the 3 h restraint, as well as highly significant increases in blood glucocorticoid levels 21 h after restraint. However, young, but not aged, animals responded to stress exposure with water maze deficits, loss of deep sleep and hyperthermia. These results demonstrate that aged subjects are hypo-responsive to new-onset acute psychosocial stress, which may have negative consequences for long-term stress adaptation and suggest that age itself may act as a stressor occluding the influence of new onset stressors. PMID:24575039

Acute, but not Chronic, Exposure to Arsenic Provokes Glucose Intolerance in Rats: Possible Roles for Oxidative Stress and the Adrenergic Pathway.

PubMed

Rezaei, Mohsen; Khodayar, Mohammd Javad; Seydi, Enayatollah; Soheila, Alboghobeish; Parsi, Isa Kazemzadeh

2017-06-01

Health problems due to heavy metals have become a worldwide concern. Along with its carcinogenicity, arsenic exposure results in impairment of glucose metabolism and insulin secretion as well as altered gene expression and signal transduction. However, the exact mechanism behind the behaviour of arsenic on glucose homeostasis and insulin secretion has not yet been fully understood. Fasting blood sugar and glucose tolerance tests were evaluated. In this study, we demonstrated that arsenic, when acutely administered, induced glucose intolerance in rats, although its chronic oral exposure did not provoke any glucose intolerance or hyperglycemia in rats. The protective activity of N-acetylcysteine, carvedilol and propranolol in male rats exposed to arsenic were also assessed, and N-acetylcysteine, particularly at 40 and 80 mg/kg, prevented the glucose intolerance induced in rats by arsenic. The present study showed that acute, but not chronic, contact with arsenic generates significant changes in the normal glucose tolerance pattern that may be due fundamentally to overproduction of reactive oxygen species and oxidative stress and is preventable by using N-acetylcysteine, a thiol-containing antioxidant. Copyright © 2017 Diabetes Canada. Published by Elsevier Inc. All rights reserved.

Acute high-level exposure to WTC particles alters expression of genes associated with oxidative stress and immune function in the lung

PubMed Central

Cohen, Mitchell D.; Vaughan, Joshua M.; Garrett, Brittany; Prophete, Colette; Horton, Lori; Sisco, Maureen; Kodavanti, Urmila P.; Ward, William O.; Peltier, Richard E.; Zelikoff, Judith; Chen, Lung-chi

2015-01-01

First responders (FR) present at Ground Zero in the first 72 h after the World Trade Center (WTC) collapsed have progressively exhibited significant respiratory injuries. The few toxicology studies performed to date evaluated effects from just fine (<2.5 µm) WTC dusts; none examined health effects/toxicities from atmospheres bearing larger particle sizes, despite the fact the majority (496%) of dusts were >10µm and most FR likely entrained dusts by mouth breathing. Using a system that generated/delivered supercoarse (10–53 µm) WTC dusts to F344 rats (in a manner that mimicked FR exposures), this study sought to examine potential toxicities in the lungs. In this exploratory study, rats were exposed for 2 h to 100 mg WTC dust/m3 (while under isoflurane [ISO] anesthesia) or an air/ISO mixture; this dose conservatively modeled likely exposures by mouth-breathing FR facing ≈750–1000 mg WTC dust/m3. Lungs were harvested 2 h post-exposure and total RNA extracted for subsequent global gene expression analysis. Among the > 1000 genes affected by WTC dust (under ISO) or ISO alone, 166 were unique to the dust exposure. In many instances, genes maximally-induced by the WTC dust exposure (relative to in naïve rats) were unchanged/inhibited by ISO only; similarly, several genes maximally inhibited in WTC dust rats were largely induced/unchanged in rats that received ISO only. These outcomes reflect likely contrasting effects of ISO and the WTC dust on lung gene expression. Overall, the data show that lungs of rats exposed to WTC dust (under ISO) – after accounting for any impact from ISO alone – displayed increased expression of genes related to lung inflammation, oxidative stress, and cell cycle control, while several involved in anti-oxidant function were inhibited. These changes suggested acute inflammogenic effects and oxidative stress in the lungs of WTC dust-exposed rats. This study, thus, concludes that a single very high exposure to WTC dusts could

Acute high-level exposure to WTC particles alters expression of genes associated with oxidative stress and immune function in the lung.

PubMed

Cohen, Mitchell D; Vaughan, Joshua M; Garrett, Brittany; Prophete, Colette; Horton, Lori; Sisco, Maureen; Kodavanti, Urmila P; Ward, William O; Peltier, Richard E; Zelikoff, Judith; Chen, Lung-chi

2015-01-01

First responders (FR) present at Ground Zero in the first 72 h after the World Trade Center (WTC) collapsed have progressively exhibited significant respiratory injuries. The few toxicology studies performed to date evaluated effects from just fine (< 2.5 µm) WTC dusts; none examined health effects/toxicities from atmospheres bearing larger particle sizes, despite the fact the majority (> 96%) of dusts were > 10 µm and most FR likely entrained dusts by mouth breathing. Using a system that generated/delivered supercoarse (10-53 µm) WTC dusts to F344 rats (in a manner that mimicked FR exposures), this study sought to examine potential toxicities in the lungs. In this exploratory study, rats were exposed for 2 h to 100 mg WTC dust/m(3) (while under isoflurane [ISO] anesthesia) or an air/ISO mixture; this dose conservatively modeled likely exposures by mouth-breathing FR facing ≈750-1000 mg WTC dust/m(3). Lungs were harvested 2 h post-exposure and total RNA extracted for subsequent global gene expression analysis. Among the >  1000 genes affected by WTC dust (under ISO) or ISO alone, 166 were unique to the dust exposure. In many instances, genes maximally-induced by the WTC dust exposure (relative to in naïve rats) were unchanged/inhibited by ISO only; similarly, several genes maximally inhibited in WTC dust rats were largely induced/unchanged in rats that received ISO only. These outcomes reflect likely contrasting effects of ISO and the WTC dust on lung gene expression. Overall, the data show that lungs of rats exposed to WTC dust (under ISO) - after accounting for any impact from ISO alone - displayed increased expression of genes related to lung inflammation, oxidative stress, and cell cycle control, while several involved in anti-oxidant function were inhibited. These changes suggested acute inflammogenic effects and oxidative stress in the lungs of WTC dust-exposed rats. This study, thus, concludes that a single very high exposure

Hypothalamic-Pituitary-Adrenal Reactivity to Acute Stress: an Investigation into the Roles of Perceived Stress and Family Resources.

PubMed

Obasi, Ezemenari M; Shirtcliff, Elizabeth A; Cavanagh, Lucia; Ratliff, Kristen L; Pittman, Delishia M; Brooks, Jessica J

2017-11-01

Rurally situated African Americans suffer from chronic exposure to stress that may have a deleterious effect on health outcomes. Unfortunately, research on potential mechanisms that underlie health disparities affecting the African American community has received limited focus in the scientific literature. This study investigated the relationship between perceived stress, family resources, and cortisol reactivity to acute stress. A rural sample of African American emerging adults (N = 60) completed a battery of assessments, the Trier Social Stress Test (TSST), and provided four samples of salivary cortisol: prior to receiving TSST instructions, prior to conducting the speech task, immediately following the TSST, and 15-20 min following the TSST. As predicted, cortisol levels increased in response to a controlled laboratory inducement of acute stress. Moreover, diminished levels of family resources were associated with blunted cortisol reactivity to acute stress. Of note, higher levels of perceived stress over the past month and being male were independently associated with lower levels of cortisol at baseline. Lack of family resources had a blunting relationship on the hypothalamic-pituitary-adrenal axis reactivity. These findings provide biomarker support for the relationship between family resources-an indicator associated with social determinants of health-and stress physiology within a controlled laboratory experiment. Identifying mechanisms that work toward explanation of within-group differences in African American health disparities is both needed and informative for culturally informed prevention and intervention efforts.

Reversible inactivation of rostral nucleus raphe pallidus attenuates acute autonomic responses but not their habituation to repeated audiogenic stress in rats.

PubMed

Nyhuis, Tara J; Masini, Cher V; Taufer, Kirsten L; Day, Heidi E W; Campeau, Serge

2016-01-01

The medullary nucleus raphe pallidus (RPa) mediates several autonomic responses evoked by acute stress exposure, including tachycardia and hyperthermia. The present study assessed whether the RPa contributes to the decline/habituation of these responses observed during repeated audiogenic stress. Adult male rats were implanted with cannulae aimed at the RPa, and abdominal E-mitters that wirelessly acquire heart rate and core body temperature. After surgical recovery, animals were injected with muscimol or vehicle (aCSF) in the RPa region, followed by 30 min of 95-dBA loud noise or no noise control exposures on 3 consecutive days at 24-h intervals. Forty-eight hours after the third exposure, animals were exposed to an additional, but injection-free, loud noise or no noise test to assess habituation of hyperthermia and tachycardia. Three days later, rats were restrained for 30-min to evaluate their ability to display normal acute autonomic responses following the repeated muscimol injection regimen. The results indicated that the inhibition of cellular activity induced by the GABAA-receptor agonist muscimol centered in the RPa region reliably attenuated acute audiogenic stress-evoked tachycardia and hyperthermia, compared with vehicle-injected rats. Animals in the stress groups exhibited similar attenuated tachycardia and hyperthermia during the injection-free fourth audiogenic stress exposure, and displayed similar and robust increases in these responses to the subsequent restraint test. These results suggest that cellular activity in neurons of the RPa region is necessary for the expression of acute audiogenic stress-induced tachycardia and hyperthermia, but may not be necessary for the acquisition of habituated tachycardic responses to repeated stress.

Reversible inactivation of rostral nucleus raphe pallidus attenuates acute autonomic responses but not their habituation to repeated audiogenic stress in rats

PubMed Central

Nyhuis, Tara J.; Masini, Cher V.; Taufer, Kirsten L.; Day, Heidi E.W.; Campeau, Serge

2016-01-01

The medullary nucleus raphe pallidus (RPa) mediates several autonomic responses evoked by acute stress exposure, including tachycardia and hyperthermia. The present study assessed whether the RPa contributes to the decline/habituation of these responses observed during repeated audiogenic stress. Adult male rats were implanted with cannulae aimed at the RPa, and abdominal E-mitters that wirelessly acquire heart rate and core body temperature. After surgical recovery, animals were injected with muscimol or vehicle (aCSF) in the RPa region, followed by 30 minutes of 95-dBA loud noise or no noise control exposures on 3 consecutive days at 24-hr intervals. Forty-eight hours after the third exposure, animals were exposed to an additional, but injection-free, loud noise or no noise test to assess habituation of hyperthermia and tachycardia. Three days later, rats were restrained for 30-minutes to evaluate their ability to display normal acute autonomic responses following the repeated muscimol injection regimen. The results indicated that the inhibition of cellular activity induced by the GABAA-receptor agonist muscimol centered in the RPa region reliably attenuated acute audiogenic stress-evoked tachycardia and hyperthermia, compared with vehicle-injected rats. Animals in the stress groups exhibited similarly attenuated tachycardia and hyperthermia during the injection-free fourth audiogenic stress exposure, and displayed similar and robust increases in these responses to the subsequent restraint test. These results suggest that cellular activity in neurons of the RPa region is necessary for the expression of acute audiogenic stress-induced tachycardia and hyperthermia, but may not be necessary for the acquisition of habituated tachycardic responses to repeated stress. PMID:26998558

Triathletes Lose Their Advantageous Pain Modulation under Acute Psychosocial Stress.

PubMed

Geva, Nirit; Pruessner, Jens; Defrin, Ruth

2017-02-01

Triathletes, who constantly engage in intensely stressful sport, were recently found to exhibit greater pain tolerance and more efficient pain inhibition capabilities than nonathletes. However, pain inhibition correlated negatively with retrospective reports of mental stress during training and competition. The aim of the current study was to test pain inhibition capabilities of triathletes under acute, controlled psychological stress manipulation. Participants were 25 triathletes and ironman triathletes who underwent the measurement of pain threshold, pain intolerance, tonic suprathreshold pain, and conditioned pain modulation before and during exposure to the Montreal Imaging Stress Task (MIST). Perceived ratings of stress and anxiety, autonomic variables, and salivary cortisol levels were obtained as indices of stress. The MIST induced a significant stress reaction manifested in the subjective and objective indices. Overall, a significant reduction in pain threshold and in conditioned pain modulation efficacy was observed after the MIST, which reached the baseline levels observed previously in nonathletes. Paradoxically, the magnitude of this stress-induced hyperalgesia (SIH) correlated negatively with the magnitude of the stress response; low-stress responders exhibited greater SIH than high-stress responders. The results suggest that under acute psychological stress, triathletes not only react with SIH and a reduction in pain modulation but also lose their advantageous pain modulation over nonathletes. The stronger the stress response recorded, the weaker the SIH. It appears that triathletes are not resilient to stress, responding with an increase in the sensitivity to pain as well as a decrease in pain inhibition. The possible effects of athletes' baseline pain profile and stress reactivity on SIH are discussed.

Acute stress induces hyperacusis in women with high levels of emotional exhaustion.

PubMed

Hasson, Dan; Theorell, Töres; Bergquist, Jonas; Canlon, Barbara

2013-01-01

Hearing problems is one of the top ten public health disorders in the general population and there is a well-established relationship between stress and hearing problems. The aim of the present study was to explore if an acute stress will increase auditory sensitivity (hyperacusis) in individuals with high levels of emotional exhaustion (EE). Hyperacusis was assessed using uncomfortable loudness levels (ULL) in 348 individuals (140 men; 208 women; age 23-71 years). Multivariate analyses (ordered logistic regression), were used to calculate odds ratios, including interacting or confounding effects of age, gender, ear wax and hearing loss (PTA). Two-way ANCOVAs were used to assess possible differences in mean ULLs between EE groups pre- and post-acute stress task (a combination of cold pressor, emotional Stroop and Social stress/video recording). There were no baseline differences in mean ULLs between the three EE groups (one-way ANOVA). However, after the acute stress exposure there were significant differences in ULL means between the EE-groups in women. Post-hoc analyses showed that the differences in mean ULLs were between those with high vs. low EE (range 5.5-6.5 dB). Similar results were found for frequencies 0.5 and 1 kHz. The results demonstrate that women with high EE-levels display hyperacusis after an acute stress task. The odds of having hyperacusis were 2.5 (2 kHz, right ear; left ns) and 2.2 (4 kHz, right ear; left ns) times higher among those with high EE compared to those with low levels. All these results are adjusted for age, hearing loss and ear wax. Women with high levels of emotional exhaustion become more sensitive to sound after an acute stress task. This novel finding highlights the importance of including emotional exhaustion in the diagnosis and treatment of hearing problems.

Effects of voluntary wheel running on heart rate, body temperature, and locomotor activity in response to acute and repeated stressor exposures in rats.

PubMed

Masini, Cher V; Nyhuis, Tara J; Sasse, Sarah K; Day, Heidi E W; Campeau, Serge

2011-05-01

Stress often negatively impacts physical and mental health but it has been suggested that voluntary physical activity may benefit health by reducing some of the effects of stress. The present experiments tested whether voluntary exercise can reduce heart rate, core body temperature and locomotor activity responses to acute (novelty or loud noise) or repeated stress (loud noise). After 6 weeks of running-wheel access, rats exposed to a novel environment had reduced heart rate, core body temperature, and locomotor activity responses compared to rats housed under sedentary conditions. In contrast, none of these measures were different between exercised and sedentary rats following acute 30-min noise exposures, at either 85 or 98 dB. Following 10 weeks of running-wheel access, both groups displayed significant habituation of all these responses to 10 consecutive daily 30-min presentations of 98 dB noise stress. However, the extent of habituation of all three responses was significantly enhanced in exercised compared to sedentary animals on the last exposure to noise. These results suggest that in physically active animals, under some conditions, acute responses to stress exposure may be reduced, and response habituation to repeated stress may be enhanced, which ultimately may reduce the negative and cumulative impact of stress.

Effects of voluntary wheel running on heart rate, body temperature, and locomotor activity in response to acute and repeated stressor exposures in rats

PubMed Central

MASINI, CHER V.; NYHUIS, TARA J.; SASSE, SARAH K.; DAY, HEIDI E. W.; CAMPEAU, SERGE

2015-01-01

Stress often negatively impacts physical and mental health but it has been suggested that voluntary physical activity may benefit health by reducing some of the effects of stress. The present experiments tested whether voluntary exercise can reduce heart rate, core body temperature and locomotor activity responses to acute (novelty or loud noise) or repeated stress (loud noise). After 6 weeks of running-wheel access, rats exposed to a novel environment had reduced heart rate, core body temperature, and locomotor activity responses compared to rats housed under sedentary conditions. In contrast, none of these measures were different between exercised and sedentary rats following acute 30-min noise exposures, at either 85 or 98 dB. Following 10 weeks of running-wheel access, both groups displayed significant habituation of all these responses to 10 consecutive daily 30-min presentations of 98 dB noise stress. However, the extent of habituation of all three responses was significantly enhanced in exercised compared to sedentary animals on the last exposure to noise. These results suggest that in physically active animals, under some conditions, acute responses to stress exposure may be reduced, and response habituation to repeated stress may be enhanced, which ultimately may reduce the negative and cumulative impact of stress. PMID:21438772

Development of acute exposure guideline levels for airborne exposures to hazardous substances.

PubMed

Krewski, Daniel; Bakshi, Kulbir; Garrett, Roger; Falke, Ernest; Rusch, George; Gaylor, David

2004-04-01

Hazardous substances can be released into the atmosphere due to industrial and transportation accidents, fires, tornadoes, earthquakes, and terrorists, thereby exposing workers and the nearby public to potential adverse health effects. Various enforceable guidelines have been set by regulatory agencies for worker and ambient air quality. However, these exposure levels generally are not applicable to rare lifetime acute exposures, which possibly could occur at high concentrations. Acute exposure guideline levels (AEGLs) provide estimates of concentrations for airborne exposures for an array of short durations that possibly could cause mild (AEGL-1), severe, irreversible, potentially disabling adverse health effects (AEGL-2), or life threatening effects (AEGL-3). These levels can be useful for emergency responders and planners in reducing or eliminating potential risks to the public. Procedures and methodologies for deriving AEGLs are reviewed in this paper that have been developed in the United States, with direct input from international representatives of OECD member-countries, by the National Advisory Committee for Acute Exposure Guidelines for Hazardous Substances and reviewed by the National Research Council. Techniques are discussed for the extrapolation of effects across different exposure durations. AEGLs provide a viable approach for assisting in the prevention, planning, and response to acute airborne exposures to toxic agents.

Corrigendum to "Acute and repeated exposure to social stress reduces gut microbiota diversity in Syrian hamsters" [Behav. Brain Res. 345 (2018) 39-48].

PubMed

Partrick, Katherine A; Chassaing, Benoit; Beach, Linda Q; McCann, Katharine E; Gewirtz, Andrew T; Huhman, Kim L

2018-08-01

Social stress can promote a variety of neuropsychiatric illnesses, many of which have a high co-morbidity with gastrointestinal disorders. Recent data indicate that gastrointestinal microbiota can affect their host's brain and behavior. Syrian hamsters are ideal subjects for social stress research because they are territorial, aggressive, and rapidly form dominant/subordinate relationships. The purpose of this study was to determine if exposure to social stress in hamsters alters gut microbiota in dominants and subordinates after an agonistic encounter and if pre-stress gut microbiota composition is correlated with the outcome of such a conflict. Microbiota composition was assessed via 16S mRNA Illumina sequencing on fecal samples. One agonistic encounter caused a decrease in alpha diversity in both dominant and subordinate animals with a more pronounced decrease after repeated encounters. PERMANOVA analysis of the unweighted unifrac distance revealed a distinct change in beta diversity after one and nine encounters in both dominants and subordinates. Linear discriminant analysis (LEfSE) showed bacteria from the order Lactobacillales were significantly reduced following social stress in both dominants and subordinates, and both groups exhibited increases in phyla Bacteroidetes and decreases in phyla Firmicutes following repeated encounters. LEfSE analysis on samples collected prior to social interaction revealed that some microbial taxa were correlated with a hamster achieving dominant or subordinate status. These data suggest that even an acute exposure to social stress can impact gastrointestinal microbiota and that the state of the microbial community before social stress may predict dominant/subordinate status following a subsequent agonistic encounter. Copyright © 2018.

Acute stress disorder in older, middle-aged and younger adults in reaction to the second Lebanon war.

PubMed

Cohen, Miri

2008-01-01

To compare rate of acute stress disorder (ASD) and intensity of acute stress symptoms (ASS) in younger, middle-aged and older Israeli citizens exposed to missile attacks during the second Lebanon war. A telephone survey of a random sample of residents in the northern area of Israel was conducted in July 2006, during the third week of Lebanon war. Respondents were divided into groups aged 18-40, 41-69 and 70+. ASD and ASS were measured by the Acute Stress Interview questionnaire and by war-related exposure variables and demographic data. Exposure variables were similar in the three age groups. Older respondents reported lower intensity of ASS and obtained lower means for each of the symptoms criteria than the young adults, while the middle-aged adults were in between the younger and the older group. ASD criteria were met by 13.2% of the younger, 4.7% of middle-aged and 4.3% of older respondents (p > 0.05), and subsyndromal ASD was found in 20.5%, 14.1% and 4.4% (p < 0.05) respectively. Twenty-two percent of ASS variance was explained by younger age, female gender and higher perceived proximity to missile falling. Older adults reacted to the war situation with lower level of acute stress symptoms. Long-term effects of war on different age groups should be further studied.

Chronic and acute effects of stress on energy balance: are there appropriate animal models?

PubMed

Harris, Ruth B S

2015-02-15

Stress activates multiple neural and endocrine systems to allow an animal to respond to and survive in a threatening environment. The corticotropin-releasing factor system is a primary initiator of this integrated response, which includes activation of the sympathetic nervous system and the hypothalamic-pituitary-adrenal (HPA) axis. The energetic response to acute stress is determined by the nature and severity of the stressor, but a typical response to an acute stressor is inhibition of food intake, increased heat production, and increased activity with sustained changes in body weight, behavior, and HPA reactivity. The effect of chronic psychological stress is more variable. In humans, chronic stress may cause weight gain in restrained eaters who show increased HPA reactivity to acute stress. This phenotype is difficult to replicate in rodent models where chronic psychological stress is more likely to cause weight loss than weight gain. An exception may be hamsters subjected to repeated bouts of social defeat or foot shock, but the data are limited. Recent reports on the food intake and body composition of subordinate members of group-housed female monkeys indicate that these animals have a similar phenotype to human stress-induced eaters, but there are a limited number of investigators with access to the model. Few stress experiments focus on energy balance, but more information on the phenotype of both humans and animal models during and after exposure to acute or chronic stress may provide novel insight into mechanisms that normally control body weight. Copyright © 2015 the American Physiological Society.

Chronic and acute effects of stress on energy balance: are there appropriate animal models?

PubMed Central

2014-01-01

Stress activates multiple neural and endocrine systems to allow an animal to respond to and survive in a threatening environment. The corticotropin-releasing factor system is a primary initiator of this integrated response, which includes activation of the sympathetic nervous system and the hypothalamic-pituitary-adrenal (HPA) axis. The energetic response to acute stress is determined by the nature and severity of the stressor, but a typical response to an acute stressor is inhibition of food intake, increased heat production, and increased activity with sustained changes in body weight, behavior, and HPA reactivity. The effect of chronic psychological stress is more variable. In humans, chronic stress may cause weight gain in restrained eaters who show increased HPA reactivity to acute stress. This phenotype is difficult to replicate in rodent models where chronic psychological stress is more likely to cause weight loss than weight gain. An exception may be hamsters subjected to repeated bouts of social defeat or foot shock, but the data are limited. Recent reports on the food intake and body composition of subordinate members of group-housed female monkeys indicate that these animals have a similar phenotype to human stress-induced eaters, but there are a limited number of investigators with access to the model. Few stress experiments focus on energy balance, but more information on the phenotype of both humans and animal models during and after exposure to acute or chronic stress may provide novel insight into mechanisms that normally control body weight. PMID:25519732

Acute psychophysiological stress impairs human associative learning.

PubMed

Ehlers, M R; Todd, R M

2017-11-01

Addiction is increasingly discussed asa disorder of associative learning processes, with both operant and classical conditioning contributing to the development of maladaptive habits. Stress has long been known to promote drug taking and relapse and has further been shown to shift behavior from goal-directed actions towards more habitual ones. However, it remains to be investigated how acute stress may influence simple associative learning processes that occur before a habit can be established. In the present study, healthy young adults were exposed to either acute stress or a control condition half an hour before performing simple classical and operant conditioning tasks. Psychophysiological measures confirmed successful stress induction. Results of the operant conditioning task revealed reduced instrumental responding under delayed acute stress that resembled behavioral responses to lower levels of reward. The classical conditioning experiment revealed successful conditioning in both experimental groups; however, explicit knowledge of conditioning as indicated by stimulus ratings differentiated the stress and control groups. These findings suggest that operant and classical conditioning are differentially influenced by the delayed effects of acute stress with important implications for the understanding of how new habitual behaviors are initially established. Copyright © 2017 Elsevier Inc. All rights reserved.

Chronic stress decreases availability of heat shock proteins to glucocorticoid receptor in response to novel acute stress in Wistar rat hypothalamus.

PubMed

Simic, Iva; Mitic, Milos; Djordjevic, Jelena; Radojcic, Marija; Adzic, Miroslav

2012-05-01

Chronic psychosocial isolation (CPSI) is known to cause several maladaptive changes in the limbic brain structures, which regulate the hypothalamic-pituitary-adrenal (HPA) axis activity. In this study, we focused our investigation on CPSI effects in the hypothalamus (HT) since it is a major driver of HPA axis activity. We also investigated whether the exposure to CPSI could alter the response to subsequent acute stress (30-min immobilization). In the HT, we followed cytosolic and nuclear levels of the glucocorticoid receptor (GR), as a mediator of HPA axis feedback inhibition, and its chaperones, the heat shock proteins (HSPs), hsp70 and hsp90. The CPSI did not cause any changes in either GR or HSPs levels. However, we observed increase of the GR and hsp70 in both HT cellular compartments as a response of naïve rats to acute stress, whereas the response of CPSI rats to acute stress was associated with elevation of the GR in the cytosol and decrease of HSPs in the nucleus. Thus, our data indicated reduced availability of HSPs to GR in both cytosol and nucleus of the HT under acute stress of CPSI animals, and therefore, pointed out to potentially negative effects of CPSI on GR function in the HT.

Acute changes in community violence and increases in hospital visits and deaths from stress-responsive diseases.

PubMed

Ahern, Jennifer; Matthay, Ellicott C; Goin, Dana E; Farkas, Kriszta; Rudolph, Kara E

2018-06-06

Community violence may affect a broad range of health outcomes through physiologic stress responses and changes in health behaviors among residents. However, existing research on the health impacts of community violence suffers from problems with bias. We examined the relations of acute changes in community violence with hospital visits and deaths due to stress-responsive diseases (mental, respiratory, and cardiac conditions) in statewide data from California 2005-2013. The community violence exposure was measured as both binary spikes and continuous acute changes. We applied a combined fixed-effects and time-series design that separates the effects of violence from those of community- and individual-level confounders more effectively than past research. Temporal patterning was removed from community violence rates and disease rates in each place using a Kalman smoother, resulting in residual rates. We used linear regression with place fixed-effects to examine within-place associations of acute changes in community violence with residual rates of each outcome, controlling for local time-varying covariates. We found acute increases in hospital visits and deaths due to anxiety disorders (0.31 per 100,000; 95% Confidence Interval (CI) 0.02,0.59), substance use (0.47 per 100,000; 95%CI 0.14,0.80), asthma (0.56 per 100,000; 95%CI 0.16,0.95), and fatal acute myocardial infarction (0.09 per 100,000; 95%CI 0.00,0.18) co-occurring with violence spikes. The pattern of findings was similar for the exposure of continuous acute violence changes. Although the associations were small, the identified increases in stress-responsive conditions suggest the possibility of health impacts of acute changes in community violence.

Having your cake and eating it too: A habit of comfort food may link chronic social stress exposure and acute stress-induced cortisol hyporesponsiveness.

USDA-ARS?s Scientific Manuscript database

Stress has been tied to changes in eating behavior and food choice. Previous studies in rodents have shown that chronic stress increases palatable food intake which, in turn, increases mesenteric fat and inhibits acute stress-induced hypothalamic-pituitary-adrenal (HPA) axis activity. The effect of...

Influence of Regularity of Exposure to Chronic Stress on the Pattern of Habituation of Pituitary-Adrenal Hormones, Prolactin and Glucose.

PubMed

Martí; Armario

1997-05-01

The effect of regularity of exposure to two different chronic stressors (noise or immobilization (IMO)) on the pattern of habituation of pituitary-adrenal (PA) hormones, prolactin and glucose was evaluated in adult male rats. Animals were chronically subjected to either regular or irregular time schedule of noise (30 min/day) or IMO (2 h/day) for two weeks. The day after the last stress session the rats were killed without stress or after having been subjected to 30 min of the homotypic stressor. Whereas regular noise did not affect food intake, body weight gain or adrenal weight, irregular noise decreased body weight gain and induced a moderate adrenal hypertrophy. In addition, previous daily exposure to regular but not to irregular noise reduced both prolactin and corticosterone responses to acute noise. In contrast, glucose response to acute noise was reduced after both regular and irregular exposure to chronic noise. Either regular or irregular exposure to chronic IMO decreased food intake and body weight and increased adrenal weight to the same extent. Likewise, no influence of regularity of exposure to chronic IMO on corticosterone and prolactin responses to acute IMO was observed. However, habituation of the ACTH response to acute IMO was observed in rats subjected to chronic regular IMO, but not in rats subjected to chronic irregular IMO. Finally, acute IMO-induced hyperglycemia diminished to the same extent after regular and irregular IMO. From these results we can conclude that: first, the process of habituation of the PA axis to chronic stress is greatly dependent upon factors such as regularity of exposure to the stressor and stressor intensity, and second, the influence of regularity on the pattern of habituation to a repeated stressor is dependent on the physiological variable we are dealing with.

Development and psychometric evaluation of child acute stress measures in Spanish and English.

PubMed

Kassam-Adams, Nancy; Gold, Jeffrey I; Montaño, Zorash; Kohser, Kristen L; Cuadra, Anai; Muñoz, Cynthia; Armstrong, F Daniel

2013-02-01

Clinicians and researchers need tools for accurate early assessment of children's acute stress reactions and acute stress disorder (ASD). There is a particular need for independently validated Spanish-language measures. The current study reports on 2 measures of child acute stress (a self-report checklist and a semistructured interview), describing the development of the Spanish version of each measure and psychometric evaluation of both the Spanish and English versions. Children between the ages of 8 to 17 years who had experienced a recent traumatic event completed study measures in Spanish (n = 225) or in English (n = 254). Results provide support for reliability (internal consistency of the measures in both languages ranged from .83 to .89; cross-language reliability of the checklist was .93) and for convergent validity (with later PTSD symptoms, and with concurrent anxiety symptoms). Comparing checklist and interview results revealed a strong association between severity scores within the Spanish and English samples. Differences between the checklist and interview in evaluating the presence of ASD appear to be linked to different content coverage for dissociation symptoms. Future studies should further assess the impact of differing assessment modes, content coverage, and the use of these measures in children with diverse types of acute trauma exposure in English- and Spanish-speaking children. Copyright © 2013 International Society for Traumatic Stress Studies.

Acute Stress Induces Hyperacusis in Women with High Levels of Emotional Exhaustion

PubMed Central

Hasson, Dan; Theorell, Töres; Bergquist, Jonas; Canlon, Barbara

2013-01-01

Background Hearing problems is one of the top ten public health disorders in the general population and there is a well-established relationship between stress and hearing problems. The aim of the present study was to explore if an acute stress will increase auditory sensitivity (hyperacusis) in individuals with high levels of emotional exhaustion (EE). Methods Hyperacusis was assessed using uncomfortable loudness levels (ULL) in 348 individuals (140 men; 208 women; age 23–71 years). Multivariate analyses (ordered logistic regression), were used to calculate odds ratios, including interacting or confounding effects of age, gender, ear wax and hearing loss (PTA). Two-way ANCOVAs were used to assess possible differences in mean ULLs between EE groups pre- and post-acute stress task (a combination of cold pressor, emotional Stroop and Social stress/video recording). Results There were no baseline differences in mean ULLs between the three EE groups (one-way ANOVA). However, after the acute stress exposure there were significant differences in ULL means between the EE-groups in women. Post-hoc analyses showed that the differences in mean ULLs were between those with high vs. low EE (range 5.5–6.5 dB). Similar results were found for frequencies 0.5 and 1 kHz. The results demonstrate that women with high EE-levels display hyperacusis after an acute stress task. The odds of having hyperacusis were 2.5 (2 kHz, right ear; left ns) and 2.2 (4 kHz, right ear; left ns) times higher among those with high EE compared to those with low levels. All these results are adjusted for age, hearing loss and ear wax. Conclusion Women with high levels of emotional exhaustion become more sensitive to sound after an acute stress task. This novel finding highlights the importance of including emotional exhaustion in the diagnosis and treatment of hearing problems. PMID:23301005

Acute Heat Stress Changes Protein Expression in the Testes of a Broiler-Type Strain of Taiwan Country Chickens.

PubMed

Wang, Shih-Han; Cheng, Chuen-Yu; Chen, Chao-Jung; Chan, Hong-Lin; Chen, Hsin-Hsin; Tang, Pin-Chi; Chen, Chih-Feng; Lee, Yen-Pai; Huang, San-Yuan

2018-03-19

Heat stress leads to decreased fertility in roosters. This study investigated the global protein expression in response to acute heat stress in the testes of a broiler-type strain of Taiwan country chickens (TCCs). Twelve 45-week-old roosters were randomly allocated to the control group maintained at 25°C, and three groups subjected to acute heat stress at 38°C for 4 h, with 0, 2, and 6 h of recovery, respectively. Testis samples were collected for hematoxylin and eosin staining, apoptosis assay, and protein analysis. The results revealed 101 protein spots that differed significantly from the control following exposure to acute heat stress. The proteins that were differentially expressed participated mainly in protein metabolism and other metabolic processes, responses to stimuli, apoptosis, cellular organization, and spermatogenesis. Proteins that negatively regulate apoptosis were downregulated and proteins involved in autophagy and major heat shock proteins (HSP90α, HSPA5, and HSPA8) were upregulated in the testes of heat-stressed chickens. In conclusion, acute heat stress causes a change in protein expression in the testes of broiler-type B strain TCCs and may thus impair cell morphology, spermatogenesis, and apoptosis. The expression of heat shock proteins increased to attenuate the testicular injury induced by acute heat stress.

Response inhibition and cognitive appraisal in clients with acute stress disorder and posttraumatic stress disorder.

PubMed

Abolghasemi, Abass; Bakhshian, Fereshteh; Narimani, Mohammad

2013-08-01

The purpose of the present study was to compare response inhibition and cognitive appraisal in clients with acute stress disorder, clients with posttraumatic stress disorder, and normal individuals. This was a comparative study. The sample consisted of 40 clients with acute stress disorder, 40 patients with posttraumatic stress disorder, and 40 normal individuals from Mazandaran province selected through convenience sampling method. Data were collected using Composite International Diagnostic Interview, Stroop Color-Word Test, Posttraumatic Cognitions Inventory, and the Impact of Event Scale. Results showed that individuals with acute stress disorder are less able to inhibit inappropriate responses and have more impaired cognitive appraisals compared to those with posttraumatic stress disorder. Moreover, results showed that response inhibition and cognitive appraisal explain 75% of the variance in posttraumatic stress disorder symptoms and 38% of the variance in posttraumatic stress disorder symptoms. The findings suggest that response inhibition and cognitive appraisal are two variables that influence the severity of posttraumatic stress disorder and acute stress disorder symptoms. Also, these results have important implications for pathology, prevention, and treatment of posttraumatic stress disorder and acute stress disorder.

Chronic Psychosocial Factors and Acute Physiological Responses to Laboratory-Induced Stress in Healthy Populations: A Quantitative Review of 30 Years of Investigations

ERIC Educational Resources Information Center

Chida, Yoichi; Hamer, Mark

2008-01-01

This meta-analysis included 729 studies from 161 articles investigating how acute stress responsivity (including stress reactivity and recovery of hypothalamic-pituitary-adrenal [HPA] axis, autonomic, and cardiovascular systems) changes with various chronic psychosocial exposures (job stress; general life stress; depression or hopelessness;…

Active war in Sri Lanka: Children's war exposure, coping, and posttraumatic stress disorder symptom severity.

PubMed

Soysa, Champika K; Azar, Sandra T

2016-01-01

Posttraumatic stress disorder (PTSD) in response to active war is understudied among Sinhalese children in Sri Lanka. We investigated PTSD symptom severity in children using child (n = 60) and mother (n = 60) reports; child-reported war exposure and coping; as well as self-reported maternal PTSD symptom severity. The study addressed active war in 2 rural locations (acute and chronic community war exposure). Child-reports were significantly greater than mother-reports of child PTSD symptom severity. Furthermore, children's war exposure, child-reported and mother-reported child PTSD symptom severity, and maternal PTSD symptom severity were significantly greater in the acute versus chronic community war exposure location, but children's approach and avoidance coping did not significantly differ, indicating a potential ceiling effect. Children's war exposure significantly, positively predicted child-reported child PTSD symptom severity, controlling for age, gender, and maternal PTSD symptom severity, but only maternal PTSD symptom severity significantly, positively predicted mother-reported child PTSD symptom severity. Avoidance coping (in both acute and chronic war) significantly positively mediated the children's war exposure-child-reported child PTSD symptom severity relation, but not mother-reports of the same. Approach coping (in chronic but not acute war) significantly, positively mediated the children's war exposure-child-reported and mother-reported child PTSD symptom severity relations. We advanced the literature on long-term active war by confirming the value of children's self-reports, establishing that both approach and avoidance coping positively mediated the war-exposure-PTSD symptom severity relation, and that the mediation effect of approach coping was situationally moderated by acute verses chronic community war exposure among Sri Lankan children. (PsycINFO Database Record (c) 2016 APA, all rights reserved).

Symptoms of acute stress in Jewish and Arab Israeli citizens during the Second Lebanon War.

PubMed

Yahav, Rivka; Cohen, Miri

2007-10-01

The "Second Lebanon War" exposed northern Israel to massive missile attacks, aimed at civilian centers, Jewish and Arab, for a period of several weeks. To assess prevalence of acute stress disorder (ASD) and acute stress symptoms (ASS) in Jewish and Arab samples, and their correlates with demographic and exposure variables. Telephone survey conducted in the third week of the second Lebanon war with a random sample of 133 Jewish and 66 Arab adult residents of northern Israel. ASD, ASS and symptoms-related impairment were measured by the Acute Stress Disorder Interview (ASDI) questionnaire, in addition to war-related exposure and demographic data. The majority of respondents experienced at least one of four symptom groups of ASD, 5.5% of the Jewish respondents and 20.3% of the Arabs met the criteria of ASD. Higher rates of Arab respondents reported symptoms of dissociation, reexperiencing and arousal, but a similar rate of avoidance was reported by the two samples. Higher mean scores of ASS and of symptoms-related impairment were reported by the Arab respondents. According to multiple regression analyses, younger age, female gender, Arab ethnicity and experiencing the war more intensely as a stressor significantly explained ASS variance, while Arab ethnicity and proximity to missiles exploding significantly explained the variance of symptoms-related impairment. A substantial rate of participants experienced symptoms of acute stress, while for only small proportion were the symptoms consistent with ASD. Higher ASD and ASS were reported by the Arab sample, calling attention to the need to build interventions to reduce the present symptoms and to help prepare for possible similar situations in the future.

Development and Psychometric Evaluation of Child Acute Stress Measures in Spanish and English

PubMed Central

Kassam-Adams, Nancy; Gold, Jeffrey I.; Montaño, Zorash; Kohser, Kristen L.; Cuadra, Anai; Muñoz, Cynthia; Armstrong, F. Daniel

2015-01-01

Clinicians and researchers need tools for accurate early assessment of children’s acute stress reactions and acute stress disorder (ASD). There is a particular need for independently validated Spanish-language measures. The current study reports on 2 measures of child acute stress (a self-report checklist and a semi-structured interview), describing the development of the Spanish version of each measure and psychometric evaluation of both the Spanish and English versions. Children between the ages of 8 to 17 years who had experienced a recent traumatic event completed study measures in Spanish (n = 225) or in English (n = 254). Results provide support for reliability (internal consistency of the measures in both languages ranges from .83 to .89; cross-language reliability of the checklist is .93) and for convergent validity (with later PTSD symptoms, and with concurrent anxiety symptoms). Comparing checklist and interview results revealed a strong association between severity scores within the Spanish and English samples. Checklist-interview differences in evaluating the presence of ASD appear to be linked to different content coverage for dissociation symptoms. Future studies should further assess the impact of differing assessment modes, content coverage, and the use of these measures in children with diverse types of acute trauma exposure in English- and Spanish-speaking children. PMID:23371337

Oxidative stress adaptation with acute, chronic, and repeated stress.

PubMed

Pickering, Andrew M; Vojtovich, Lesya; Tower, John; A Davies, Kelvin J

2013-02-01

Oxidative stress adaptation, or hormesis, is an important mechanism by which cells and organisms respond to, and cope with, environmental and physiological shifts in the level of oxidative stress. Most studies of oxidative stress adaption have been limited to adaptation induced by acute stress. In contrast, many if not most environmental and physiological stresses are either repeated or chronic. In this study we find that both cultured mammalian cells and the fruit fly Drosophila melanogaster are capable of adapting to chronic or repeated stress by upregulating protective systems, such as their proteasomal proteolytic capacity to remove oxidized proteins. Repeated stress adaptation resulted in significant extension of adaptive responses. Repeated stresses must occur at sufficiently long intervals, however (12-h or more for MEF cells and 7 days or more for flies), for adaptation to be successful, and the levels of both repeated and chronic stress must be lower than is optimal for adaptation to acute stress. Regrettably, regimens of adaptation to both repeated and chronic stress that were successful for short-term survival in Drosophila nevertheless also caused significant reductions in life span for the flies. Thus, although both repeated and chronic stress can be tolerated, they may result in a shorter life. Copyright © 2012 Elsevier Inc. All rights reserved.

Prior exposure to a single stress session facilitates subsequent contextual fear conditioning in rats. Evidence for a role of corticosterone.

PubMed

Cordero, M Isabel; Venero, Cesar; Kruyt, Nyika D; Sandi, Carmen

2003-11-01

Previous studies showed that exposure of rats to chronic restraint stress for 21 days enhances subsequent contextual fear conditioning. Since recent evidence suggest that this effect is not dependent on stress-induced neurodegenerative processes, but to elevated training-elicited glucocorticoid release in chronically stressed animals, we aimed to explore here whether a single exposure to restraint stress, which is not expected to induce neuronal damage, would also affect contextual fear conditioning. We also questioned whether post-training corticosterone levels might be associated with any potential effect of stress on fear conditioning. Adult male Wistar rats were exposed to acute restraint stress for 2 h and, two days later, trained in the contextual fear conditioning task, under training conditions involving either moderate (0.4 mA shock) or high (1 mA shock) stress levels. The results showed that acute stress enhanced conditioned freezing at both training conditions, although data from the 1 mA shock intensity experiment only approached significance. Stressed animals were shown to display higher post-training corticosterone levels. Furthermore, the facilitating effect of prior stress was not evident when animals were trained in the hippocampal-independent auditory-cued conditioning task. Therefore, these findings support the idea that stress experiences preceding exposure to new types of stressors facilitate the development of contextual fear conditioning. They also indicate that not only repeated, but also a single exposure to aversive stimulation is sufficient to facilitate context-dependent fear conditioning, and suggest that increased glucocorticoid release at training might be implicated in the mechanisms mediating the memory facilitating effects induced by prior stress experiences.

Human physiological responses to cold exposure: Acute responses and acclimatization to prolonged exposure.

PubMed

Castellani, John W; Young, Andrew J

2016-04-01

Cold exposure in humans causes specific acute and chronic physiological responses. This paper will review both the acute and long-term physiological responses and external factors that impact these physiological responses. Acute physiological responses to cold exposure include cutaneous vasoconstriction and shivering thermogenesis which, respectively, decrease heat loss and increase metabolic heat production. Vasoconstriction is elicited through reflex and local cooling. In combination, vasoconstriction and shivering operate to maintain thermal balance when the body is losing heat. Factors (anthropometry, sex, race, fitness, thermoregulatory fatigue) that influence the acute physiological responses to cold exposure are also reviewed. The physiological responses to chronic cold exposure, also known as cold acclimation/acclimatization, are also presented. Three primary patterns of cold acclimatization have been observed, a) habituation, b) metabolic adjustment, and c) insulative adjustment. Habituation is characterized by physiological adjustments in which the response is attenuated compared to an unacclimatized state. Metabolic acclimatization is characterized by an increased thermogenesis, whereas insulative acclimatization is characterized by enhancing the mechanisms that conserve body heat. The pattern of acclimatization is dependent on changes in skin and core temperature and the exposure duration. Published by Elsevier B.V.

The additive benefit of hypnosis and cognitive-behavioral therapy in treating acute stress disorder.

PubMed

Bryant, Richard A; Moulds, Michelle L; Guthrie, Rachel M; Nixon, Reginald D V

2005-04-01

This research represents the first controlled treatment study of hypnosis and cognitive- behavioral therapy (CBT) of acute stress disorder (ASD). Civilian trauma survivors (N=87) who met criteria for ASD were randomly allocated to 6 sessions of CBT, CBT combined with hypnosis (CBT-hypnosis), or supportive counseling (SC). CBT comprised exposure, cognitive restructuring, and anxiety management. CBT-hypnosis comprised the CBT components with each imaginal exposure preceded by a hypnotic induction and suggestions to engage fully in the exposure. In terms of treatment completers (n=69), fewer participants in the CBT and CBT-hypnosis groups met criteria for posttraumatic stress disorder at posttreatment and 6-month follow-up than those in the SC group. CBT-hypnosis resulted in greater reduction in reexperiencing symptoms at posttreatment than CBT. These findings suggest that hypnosis may have use in facilitating the treatment effects of CBT for posttraumatic stress. Copyright (c) 2005 APA, all rights reserved

The Additive Benefit of Hypnosis and Cognitive-Behavioral Therapy in Treating Acute Stress Disorder

ERIC Educational Resources Information Center

Bryant, Richard A.; Moulds, Michelle L.; Guthrie, Rachel M.; Nixon, Reginald D. V.

2005-01-01

This research represents the first controlled treatment study of hypnosis and cognitive- behavioral therapy (CBT) of acute stress disorder (ASD). Civilian trauma survivors (N = 87) who met criteria for ASD were randomly allocated to 6 sessions of CBT, CBT combined with hypnosis (CBT-hypnosis), or supportive counseling (SC). CBT comprised exposure,…

Protective effect of exercise and sildenafil on acute stress and cognitive function.

PubMed

Ozbeyli, Dilek; Gokalp, Ayse Gizem; Koral, Tolga; Ocal, Onur Yuksel; Dogan, Berkay; Akakin, Dilek; Yuksel, Meral; Kasimay, Ozgur

2015-11-01

There are contradictory results about the effects of exercise and sildenafil on cognitive functions. To investigate the effects of sildenafil pretreatment and chronic exercise on anxiety and cognitive functions. Wistar rats (n=42) were divided as sedentary and exercise groups. A moderate-intensity swimming exercise was performed for 6 weeks, 5 days/week, 1h/day. Some of the rats were administered orogastrically with sildenafil (25mg/kg/day) either acutely or chronically. Exposure to cat odor was used for induction of stress. The level of anxiety was evaluated by elevated plus maze test, while object recognition test was used to determine cognitive functions. Brain tissues were removed for the measurement of myeloperoxidase (MPO), malondialdehyde (MDA), nitric oxide levels, lucigenin-enhanced chemiluminescence, and for histological analysis. Increased MPO and MDA levels in sedentary-stressed rats were decreased with sildenafil applications. Chronic exercise inhibited the increase in MPO levels. Increased nitric oxide and lucigenin chemiluminescence levels in sedentary-stressed rats, were diminished with chronic sildenafil pretreatment. The time spent in the open arms of the plus maze was declined in sedentary-stressed rats, while chronic sildenafil pretreatment increased the time back to that in non-stressed rats. Acute sildenafil application to exercised rats prolonged the time spent in open arms as compared to non-treated exercise group. The time spent with the novel object, which was decreased in sedentary-stressed rats, was increased with sildenafil pretreatment. Our results suggest that sildenafil pretreatment or exercise exerts a protective effect against acute stress and improves cognitive functions by decreasing oxidative damage. Copyright © 2015 Elsevier Inc. All rights reserved.

The acute autonomic stress response and amniotic fluid glucocorticoids in second-trimester pregnant women.

PubMed

La Marca-Ghaemmaghami, Pearl; Dainese, Sara M; La Marca, Roberto; Zimmermann, Roland; Ehlert, Ulrike

2015-01-01

The maternal autonomic nervous system (ANS) has received little attention in the investigation of biological mechanisms linking prenatal stress to fetal cortisol (F) excess. In vitro, norepinephrine and epinephrine inhibit placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which protects the fetus from F overexposure by inactivating it to cortisone (E). Here, we investigated the acute ANS stress response to an amniocentesis and its association with amniotic fluid F, E, and E/(E + F) as a marker of fetoplacental 11β-HSD2 activity. An aliquot of amniotic fluid was obtained from 34 healthy, second-trimester pregnant women undergoing amniocentesis. Repeated assessment of mood states served to examine the psychological stress response to amniocentesis. Saliva samples were collected to measure stress-induced changes in salivary α-amylase concentrations in response to amniocentesis. Cardiac parameters were measured continuously. Undergoing amniocentesis induced significant psychological and autonomic alterations. Low-frequency (LF)/high-frequency (HF) baseline, suggested to reflect sympathovagal balance, was negatively correlated with amniotic E/(E + F) (r=-0.53, p = .002) and positively with F (r = 0.62, p < .001). In contrast, a stronger acute LF/HF response was positively associated with E/(E + F) (r = 0.44, p = .012) and negatively with F (r=-0.40, p = .025). These findings suggest that the maternal ANS is involved in the regulation of the fetoplacental barrier to stress. Allostatic processes may have been initiated to counterbalance acute stress effects. In contrast, higher LF/HF baseline values, possibly indicative of chronic stress exposure, may have inhibited 11β-HSD2 activity in the fetoplacental unit. These results parallel animal findings of up-regulated placental 11β-HSD2 in response to acute stress but impairment under chronic stress.

Risky choice and brain CRF after adolescent ethanol vapor exposure and social stress in adulthood.

PubMed

Boutros, Nathalie; Der-Avakian, Andre; Semenova, Svetlana; Lee, Soon; Markou, Athina

2016-09-15

Adolescent ethanol exposure increases risky choice and alters corticotropin releasing factor (CRF) systems in adulthood. The impact of stress on risky choice after adolescent intermittent ethanol (AIE) exposure is not known. We investigated time-specific effects of AIE vapor exposure during early adolescence on risky choice after stress or no stress in adulthood. Male Wistar rats were exposed to air or AIE vapor on postnatal days 28-42 (adolescence) and were exposed to 10days of social defeat or no stress on postnatal days 172-181 (adulthood). Risky choice was assessed in the probability discounting task under baseline conditions and after days 1 and 10 of social defeat. CRF and CRF receptor 1 (CRFR1) mRNA levels were assessed in the prefrontal cortex (PFC) and the central nucleus of the amygdala (CeA) 24h post-stress to evaluate persistent effects of stress on the brain. AIE exposure had no effect on risky choice either at baseline or after social defeat. Additionally, neither acute nor chronic social defeat affected risky choice in air-exposed rats. In the PFC, chronic social defeat selectively decreased CRF mRNA levels in air-exposed rats and increased CRFR1 mRNA levels in all rats. AIE exposure increased CRF mRNA levels in the CeA with no effect of social stress. Our results indicate no effect of ethanol exposure via vapor during early adolescence on risky choice, while our previous findings indicated that AIE exposure via gavage affected risky choice. Both AIE exposure and social defeat altered CRF and CRFR1 mRNA levels in the brain. Copyright © 2016 Elsevier B.V. All rights reserved.

Chronic Desipramine Prevents Acute Stress-Induced Reorganization of Medial Prefrontal Cortex Architecture by Blocking Glutamate Vesicle Accumulation and Excitatory Synapse Increase

PubMed Central

Treccani, Giulia; Liebenberg, Nico; Chen, Fenghua; Popoli, Maurizio; Wegener, Gregers; Nyengaard, Jens Randel

2015-01-01

Background: Although a clear negative influence of chronic exposure to stressful experiences has been repeatedly demonstrated, the outcome of acute stress on key brain regions has only just started to be elucidated. Although it has been proposed that acute stress may produce enhancement of brain plasticity and that antidepressants may prevent such changes, we still lack ultrastructural evidence that acute stress-induced changes in neurotransmitter physiology are coupled with structural synaptic modifications. Methods: Rats were pretreated chronically (14 days) with desipramine (10mg/kg) and then subjected to acute foot-shock stress. By means of serial section electron microscopy, the structural remodeling of medial prefrontal cortex glutamate synapses was assessed soon after acute stressor cessation and stress hormone levels were measured. Results: Foot-shock stress induced a remarkable increase in the number of docked vesicles and small excitatory synapses, partially and strongly prevented by desipramine pretreatment, respectively. Acute stress-induced corticosterone elevation was not affected by drug treatment. Conclusions: Since desipramine pretreatment prevented the stress-induced structural plasticity but not the hormone level increase, we hypothesize that the preventing action of desipramine is located on pathways downstream of this process and/or other pathways. Moreover, because enhancement of glutamate system remodeling may contribute to overexcitation dysfunctions, this aspect could represent a crucial component in the pathophysiology of stress-related disorders. PMID:25522419

Brain aromatase and circulating corticosterone are rapidly regulated by combined acute stress and sexual interaction in a sex specific manner

PubMed Central

Dickens, M.J.; Balthazart, J.; Cornil, C. A.

2012-01-01

Neural production of 17β-oestradiol via aromatisation of testosterone may play a critical role in rapid, non-genomic regulation of physiological and behavioural processes. In brain nuclei implicated in the control of sexual behaviour, sexual or stressfull stimuli induce respectively a rapid inhibition or increase in preoptic aromatase activity (AA). Here, we tested quail that were either non-stressed or acutely stressed (15 min restraint) immediately prior to sexual interaction (5 min) with stressed or non-stressed partners. We measured nuclei-specific AA changes, corresponding behavioural output, fertilisation rates and corticosterone (CORT) concentrations. In males, sexual interaction rapidly reversed stress-induced increases of AA in the medial preoptic nucleus (POM). This time scale (<5min) highlights the dynamic potential of the aromatase system to integrate input from stimuli that drive AA in opposing directions. Moreover, acute stress had minimal effects on male behaviour suggesting that the input from the sexual stimuli on POM AA may actively preserve sexual behaviour despite stress exposure. We also found distinct sex differences in contextual physiological responses: while males did not show any effect of partner status, females responded to both their stress exposure and the male partner’s stress exposure at the level of circulating CORT and AA. In addition, fertilisation rates and female CORT correlated with the male partner’s exhibition of sexually aggressive behaviour suggesting that female perception of the male can affect their physiology as much as direct stress. Overall, male reproduction appears relatively simple – sexual stimuli, irrespective of stress, drives major neural changes including rapid reversal of stress-induced changes of AA. In contrast, female reproduction appears more nuanced and context specific, with subjects responding physiologically and behaviourally to stress, the male partner’s stress exposure, and female

Acute and past subjective stress influence working memory and related neural substrates.

PubMed

Luettgau, Lennart; Schlagenhauf, Florian; Sjoerds, Zsuzsika

2018-05-28

Stress has been proposed to affect cognitive control capacities, including working memory (WM) maintenance. This effect may depend on variability in stress reactivity and past subjective stress. However, as most studies employed between-subjects designs, evidence for within-subject stress effects remains scarce. To understand the role of intra-individual stress effects on WM, we adopted a within-subject design to study how acute stress, variability in stress reactivity, and past subjective stress influence behavioral and neural WM mechanisms. Thirty-four healthy males performed a WM task during functional magnetic resonance imaging (fMRI) in a control versus acute stress condition following the Trier Social Stress Test, a validated psychosocial stressor method. We tested for stress effects on WM performance and related neural activation by associating them with individual acute stress responsivity and past subjective stress experience using retrospective self-report questionnaires. We found no evidence of an effect of acute stress or related stress-reactivity on intra-individual WM performance. However, past subjective stress negatively influenced acute stress-induced changes to WM. On the neural level, acute stress reduced WM-related activation in the dorsolateral prefrontal cortex (dlPFC). The observed negative influence of inter-individual variability in past subjective stress experience on changes in WM performance, suggests that past subjective stress might induce vulnerability for impairing effects of acute stress on cognitive functioning. Because acute stress reduced WM-related dlPFC activation while WM performance remained unaffected, acute stress might boost neural processing efficiency in this group of high performing healthy individuals. Our study suggests that measures of past subjective stress should be considered when studying and interpreting the effects of acute stress on cognition. Copyright © 2018. Published by Elsevier Ltd.

Exploring DSM-5 criterion A in Acute Stress Disorder symptoms following natural disaster.

PubMed

Lavenda, Osnat; Grossman, Ephraim S; Ben-Ezra, Menachem; Hoffman, Yaakov

2017-10-01

The present study examines the DSM-5 Acute Stress Disorder (ASD) diagnostic criteria of exposure, in the context of a natural disaster. The study is based on the reports of 1001 Filipinos following the aftermath of super typhoon Haiyan in 2013. Participants reported exposure to injury, psychological distress and ASD symptoms. Findings indicated the association of criterion A with the prevalence of meeting all other ASD diagnostic criteria and high psychological distress. The diagnostic properties of Criterion A are discussed. Copyright © 2017 Elsevier B.V. All rights reserved.

Acute Stress Decreases but Chronic Stress Increases Myocardial Sensitivity to Ischemic Injury in Rodents

PubMed Central

Eisenmann, Eric D.; Rorabaugh, Boyd R.; Zoladz, Phillip R.

2016-01-01

Cardiovascular disease (CVD) is the largest cause of mortality worldwide, and stress is a significant contributor to the development of CVD. The relationship between acute and chronic stress and CVD is well evidenced. Acute stress can lead to arrhythmias and ischemic injury. However, recent evidence in rodent models suggests that acute stress can decrease sensitivity to myocardial ischemia–reperfusion injury (IRI). Conversely, chronic stress is arrhythmogenic and increases sensitivity to myocardial IRI. Few studies have examined the impact of validated animal models of stress-related psychological disorders on the ischemic heart. This review examines the work that has been completed using rat models to study the effects of stress on myocardial sensitivity to ischemic injury. Utilization of animal models of stress-related psychological disorders is critical in the prevention and treatment of cardiovascular disorders in patients experiencing stress-related psychiatric conditions. PMID:27199778

Acute Stress Decreases but Chronic Stress Increases Myocardial Sensitivity to Ischemic Injury in Rodents.

PubMed

Eisenmann, Eric D; Rorabaugh, Boyd R; Zoladz, Phillip R

2016-01-01

Cardiovascular disease (CVD) is the largest cause of mortality worldwide, and stress is a significant contributor to the development of CVD. The relationship between acute and chronic stress and CVD is well evidenced. Acute stress can lead to arrhythmias and ischemic injury. However, recent evidence in rodent models suggests that acute stress can decrease sensitivity to myocardial ischemia-reperfusion injury (IRI). Conversely, chronic stress is arrhythmogenic and increases sensitivity to myocardial IRI. Few studies have examined the impact of validated animal models of stress-related psychological disorders on the ischemic heart. This review examines the work that has been completed using rat models to study the effects of stress on myocardial sensitivity to ischemic injury. Utilization of animal models of stress-related psychological disorders is critical in the prevention and treatment of cardiovascular disorders in patients experiencing stress-related psychiatric conditions.

Brain aromatase and circulating corticosterone are rapidly regulated by combined acute stress and sexual interaction in a sex-specific manner.

PubMed

Dickens, M J; Balthazart, J; Cornil, C A

2012-10-01

Neural production of 17β-oestradiol via aromatisation of testosterone may play a critical role in rapid, nongenomic regulation of physiological and behavioural processes. In brain nuclei implicated in the control of sexual behaviour, sexual or stressfull stimuli induce, respectively, a rapid inhibition or increase in preoptic aromatase activity (AA). In the present study, we tested quail that were either nonstressed or acutely stressed (15 min of restraint) immediately before sexual interaction (5 min) with stressed or nonstressed partners. We measured nuclei-specific AA changes, corresponding behavioural output, fertilisation rates and corticosterone (CORT) concentrations. In males, sexual interaction rapidly reversed stress-induced increases of AA in the medial preoptic nucleus (POM). This time scale (< 5 min) highlights the dynamic potential of the aromatase system to integrate input from stimuli that drive AA in opposing directions. Moreover, acute stress had minimal effects on male behaviour, suggesting that the input from the sexual stimuli on POM AA may actively preserve sexual behaviour despite stress exposure. We also found distinct sex differences in contextual physiological responses: males did not show any effect of partner status, whereas females responded to both their stress exposure and the male partner's stress exposure at the level of circulating CORT and AA. In addition, fertilisation rates and female CORT correlated with the male partner's exhibition of sexually aggressive behaviour, suggesting that female perception of the male can affect their physiology as much as direct stress. Overall, male reproduction appears relatively simple: sexual stimuli, irrespective of stress, drives major neural changes including rapid reversal of stress-induced changes of AA. By contrast, female reproduction appears more nuanced and context specific, with subjects responding physiologically and behaviourally to stress, the male partner's stress exposure, and

Mood and cortisol responses following tryptophan-rich hydrolyzed protein and acute stress in healthy subjects with high and low cognitive reactivity to depression.

PubMed

Firk, Christine; Markus, C Rob

2009-06-01

It is suggested that stress particularly in subjects with high cognitive reactivity (CR), a psychological vulnerability marker of depression, may increase or even induce serotonergic vulnerability, which in turn may lead to reduced serotonin (5-HT) function, decreased stress coping and an increased risk to develop depressive symptoms. The aim of the present study was to investigate the beneficial effects of 5-HT augmentation through a tryptophan-rich hydrolyzed protein (HP) on mood and stress coping in subjects with high and low CR. We hypothesized that subjects with high CR are more responsive to the beneficial effects of HP than subjects with low CR particularly after acute stress exposure. In a double-blind, crossover study, participants' mood and cortisol was assessed before and after acute stress exposure either following intake of HP or a standard casein protein (CP) as control condition. HP significantly increased positive mood in all subjects and dampened the cortisol response to acute stress. No differences were found between high and low CR subjects. To conclude, because dietary treatment with HP has beneficial effects on mood and physiological stress coping in both high and low CR subjects, HP may be a good dietary method for augmenting brain TRP and 5-HT and thus 5-HT linked stress resilience.

Peritraumatic dissociation, acute stress, and early posttraumatic stress disorder in victims of general crime.

PubMed

Birmes, P; Carreras, D; Ducassé, J L; Charlet, J P; Warner, B A; Lauque, D; Schmitt, L

2001-09-01

To compare the relation between peritraumatic dissociation and acute stress and the early development of posttraumatic stress disorder (PTSD) in victims of general crime. A total of 48 subjects were assessed within 24 hours of the trauma, using the Peritraumatic Dissociative Experiences Questionnaire Self-Report Version (PDEQ-SRV). They were followed longitudinally to assess acute stress (2 weeks after the assault,) using the Standford Acute Stress Reaction Questionnaire (SASRQ), and posttraumatic stress (at 5 weeks), using the Clinician-Administered PTSD Scale (CAPS) and the Impact of Event Scale (IES). Among PTSD subjects mean PDEQ scores were significantly higher (mean 3, SD 0.9) than in those without PTSD (mean 2.3, SD 0.7) (t = 2.78, df 46, P = 0.007). Among PTSD subjects, mean SASRQ scores were significantly higher (mean 97.9, SD 29.2) than in those without PTSD (mean 54.8, SD 28.2) (t = 4.9, df 46, P = 0.00007). High levels of peritraumatic dissociation and acute stress following violent assault are risk factors for early PTSD. Identifying acute reexperiencing can help the clinician identify subjects at highest risk.

Acute Stress Symptoms in Seriously Injured Patients: Precipitating Versus Cumulative Trauma and the Contribution of Peritraumatic Distress.

PubMed

Briere, John; Dias, Colin P; Semple, Randye J; Scott, Catherine; Bigras, Noémie; Godbout, Natacha

2017-08-01

The relationship between type of trauma exposure, cumulative trauma, peritraumatic distress, and subsequent acute stress disorder (ASD) symptoms was examined prospectively in 96 individuals presenting with acute medical injuries to a Level 1 emergency/trauma department. Common precipitating traumas included motor vehicle-related events, stabbings, shootings, and physical assaults. At 2 to 3 weeks follow-up, 22.9% of participants had developed ASD. Univariate analysis revealed no relationship between type of precipitating trauma and ASD symptoms, whereas robust path analysis indicated direct effects of gender, lifetime cumulative trauma exposure, and peritraumatic distress. Peritraumatic distress did not mediate the association between cumulative trauma and symptoms, but did mediate the association between gender and symptomatology. These results, which account for 23.1% of the variance in ASD symptoms, suggest that ASD may be more due to cumulative trauma exposure than the nature of the precipitating trauma, but that cumulative trauma does not exert its primary effect by increasing peritraumatic distress to the most recent trauma. Copyright © 2017 International Society for Traumatic Stress Studies.

Acute and subchronic toxicity of inhaled toluene in male Long Evans rats: oxidative stress markers in brain

EPA Pesticide Factsheets

Research interested in oxidative stress markers following exposure to VOCsThis dataset is associated with the following publication:Kodavanti , P., J. Royland , D.A. Moore-Smith, J. Beas, J. Richards , T. Beasley , P. Evansky , and P.J. Bushnell. Acute and Subchronic Toxicity of Inhaled Toluene in Male Long-Evans Rats: Oxidative Stress Markers in Brain. NEUROTOXICOLOGY. Elsevier B.V., Amsterdam, NETHERLANDS, 51: 10-19, (2015).

Exposure to traffic pollution, acute inflammation and autonomic response in a panel of car commuters.

PubMed

Sarnat, Jeremy A; Golan, Rachel; Greenwald, Roby; Raysoni, Amit U; Kewada, Priya; Winquist, Andrea; Sarnat, Stefanie E; Dana Flanders, W; Mirabelli, Maria C; Zora, Jennifer E; Bergin, Michael H; Yip, Fuyuen

2014-08-01

Exposure to traffic pollution has been linked to numerous adverse health endpoints. Despite this, limited data examining traffic exposures during realistic commutes and acute response exists. We conducted the Atlanta Commuters Exposures (ACE-1) Study, an extensive panel-based exposure and health study, to measure chemically-resolved in-vehicle exposures and corresponding changes in acute oxidative stress, lipid peroxidation, pulmonary and systemic inflammation and autonomic response. We recruited 42 adults (21 with and 21 without asthma) to conduct two 2-h scripted highway commutes during morning rush hour in the metropolitan Atlanta area. A suite of in-vehicle particulate components were measured in the subjects' private vehicles. Biomarker measurements were conducted before, during, and immediately after the commutes and in 3 hourly intervals after commutes. At measurement time points within 3h after the commute, we observed mild to pronounced elevations relative to baseline in exhaled nitric oxide, C-reactive-protein, and exhaled malondialdehyde, indicative of pulmonary and systemic inflammation and oxidative stress initiation, as well as decreases relative to baseline levels in the time-domain heart-rate variability parameters, SDNN and rMSSD, indicative of autonomic dysfunction. We did not observe any detectable changes in lung function measurements (FEV1, FVC), the frequency-domain heart-rate variability parameter or other systemic biomarkers of vascular injury. Water soluble organic carbon was associated with changes in eNO at all post-commute time-points (p<0.0001). Our results point to measureable changes in pulmonary and autonomic biomarkers following a scripted 2-h highway commute. Copyright © 2014 Elsevier Inc. All rights reserved.

Exposure to traffic pollution, acute inflammation and autonomic response in a panel of car commuters

PubMed Central

Sarnat, Jeremy A.; Golan, Rachel; Greenwald, Roby; Raysoni, Amit U.; Kewada, Priya; Winquist, Andrea; Sarnat, Stefanie E.; Flanders, W. Dana; Mirabelli, Maria C.; Zora, Jennifer E.; Bergin, Michael H.; Yip, Fuyuen

2015-01-01

Background Exposure to traffic pollution has been linked to numerous adverse health endpoints. Despite this, limited data examining traffic exposures during realistic commutes and acute response exists. Objectives: We conducted the Atlanta Commuters Exposures (ACE-1) Study, an extensive panel-based exposure and health study, to measure chemically-resolved in-vehicle exposures and corresponding changes in acute oxidative stress, lipid peroxidation, pulmonary and systemic inflammation and autonomic response. Methods We recruited 42 adults (21 with and 21 without asthma) to conduct two 2-h scripted highway commutes during morning rush hour in the metropolitan Atlanta area. A suite of in-vehicle particulate components were measured in the subjects’ private vehicles. Biomarker measurements were conducted before, during, and immediately after the commutes and in 3 hourly intervals after commutes. Results At measurement time points within 3 h after the commute, we observed mild to pronounced elevations relative to baseline in exhaled nitric oxide, C-reactive-protein, and exhaled malondialdehyde, indicative of pulmonary and systemic inflammation and oxidative stress initiation, as well as decreases relative to baseline levels in the time-domain heart-rate variability parameters, SDNN and rMSSD, indicative of autonomic dysfunction. We did not observe any detectable changes in lung function measurements (FEV1, FVC), the frequency-domain heart-rate variability parameter or other systemic biomarkers of vascular injury. Water soluble organic carbon was associated with changes in eNO at all post-commute time-points (p < 0.0001). Conclusions Our results point to measureable changes in pulmonary and autonomic biomarkers following a scripted 2-h highway commute. PMID:24906070

The stressed female brain: neuronal activity in the prelimbic but not infralimbic region of the medial prefrontal cortex suppresses learning after acute stress.

PubMed

Maeng, Lisa Y; Shors, Tracey J

2013-01-01

Women are nearly twice as likely as men to suffer from anxiety and post-traumatic stress disorder (PTSD), indicating that many females are especially vulnerable to stressful life experience. A profound sex difference in the response to stress is also observed in laboratory animals. Acute exposure to an uncontrollable stressful event disrupts associative learning during classical eyeblink conditioning in female rats but enhances this same type of learning process in males. These sex differences in response to stress are dependent on neuronal activity in similar but also different brain regions. Neuronal activity in the basolateral nucleus of the amygdala (BLA) is necessary in both males and females. However, neuronal activity in the medial prefrontal cortex (mPFC) during the stressor is necessary to modify learning in females but not in males. The mPFC is often divided into its prelimbic (PL) and infralimbic (IL) subregions, which differ both in structure and function. Through its connections to the BLA, we hypothesized that neuronal activity within the PL, but not IL, during the stressor is necessary to suppress learning in females. To test this hypothesis, either the PL or IL of adult female rats was bilaterally inactivated with GABAA agonist muscimol during acute inescapable swim stress. About 24 h later, all subjects were trained with classical eyeblink conditioning. Though stressed, females without neuronal activity in the PL learned well. In contrast, females with IL inactivation during the stressor did not learn well, behaving similarly to stressed vehicle-treated females. These data suggest that exposure to a stressful event critically engages the PL, but not IL, to disrupt associative learning in females. Together with previous studies, these data indicate that the PL communicates with the BLA to suppress learning after a stressful experience in females. This circuit may be similarly engaged in women who become cognitively impaired after stressful life

Chronic Pain Under Missile Attacks: Role of Pain Catastrophizing, Media, and Stress-Related Exposure.

PubMed

Noyman-Veksler, Gal; Shalev, Hadar; Brill, Silviu; Rudich, Zvia; Shahar, Golan

2017-10-09

We examined the effects of exposure to missile attacks on patients' pain and depressive symptoms, moderated by pain-related catastrophizing. One-hundred Israeli chronic pain patients were assessed both prior and subsequent to military operation "Protective Edge," during which thousands of missiles landed on populated areas across the country. Baseline assessment included pain, depression, and catastrophizing, and postwar assessment tapped exposure to missiles, pain, and depression. Media exposure predicted an increase in sensory pain under high levels of catastrophizing (1 SD above the mean; unstandardized simple slope = 0.57, p = .01), and depression in the entire sample (b = 0.61, p = .01). Perceived stress related to the missiles exhibited an expected effect, predicting an increase in depressive symptoms (b = 1.45, p = .03). Unexpectedly, perceived stress predicted a decrease in sensory pain under high levels of catastrophizing (unstandardized simple slope = -0.49, p = .02). Media exposure to acute stress may render chronic pain patients more vulnerable to experiencing pain and depressive symptoms, depending on their use of pain-based catastrophizing. High catastrophizers may attend more to outside threats, amplifying the sensory and affective aspects of pain they experience. Perceived stress also plays a significant role in eliciting depressive symptoms in this population. (PsycINFO Database Record (c) 2017 APA, all rights reserved).

Repeated handling, restraint, or chronic crowding impair the hypothalamic-pituitary-adrenocortical response to acute restraint stress.

PubMed

Gadek-Michalska, A; Bugajski, J

2003-09-01

The purpose of the present study was to assess whether, and to what extent prior handling, restraint or social crowding stress during 3-10 days affects the hypothalamic-pituitary-adrenocortical (HPA) response to an acute short-lasting restraint stress. Also the effect of a feedback inhibitory mechanism of corticosterone in the impairment of HPA axis by these stressors was investigated. Male Wistar rats were pretreated with handling 1 min/day for 3-10 days, restraint 2 times daily for 3-7 days and crowding stress for 7 days before exposure to acute restraint stress in metal tubes for 10 min. Some group of rats received exogenous s.c. corticosterone either once 25 mg/kg or 2 times daily 10 mg/kg for 3-10 days before restraint stress. After the last restraint the rats were decapitated and their trunk blood was collected for the measurement of plasma ACTH and serum corticosterone levels. Handling for 3-7 days, restraint for 3-7 days, and crowding for 7 days and a single pretreatment with corticosterone--all significantly and to a similar extent inhibited the restraint stress-induced increase in ACTH and corticosterone secretion. Chronic pretreatment with corticosterone blunted the restraint stress-induced increase in HPA axis activity. These results indicate that repeated short-lasting stress induced by handling, restraint, or crowding potently attenuates the acute restraint stress-induced stimulatory action of the HPA axis. They also indicate adaptive action of moderate stress on the HPA axis response to acute stress. The results also suggest that a short-lasting hypersecretion of corticosterone during psychological stress may induce a prolonged feedback inhibition of the HPA axis activity. The attenuation of HPA axis response by prior handling has also obvious methodological implications.

Impairments of spatial working memory and attention following acute psychosocial stress.

PubMed

Olver, James S; Pinney, Myra; Maruff, Paul; Norman, Trevor R

2015-04-01

Few studies have investigated the effect of an acute psychosocial stress paradigm on impaired attention and working memory in humans. Further, the duration of any stress-related cognitive impairment remains unclear. The aim of this study was to examine the effect of an acute psychosocial stress paradigm, the Trier Social Stress, on cognitive function in healthy volunteers. Twenty-three healthy male and female subjects were exposed to an acute psychosocial stress task. Physiological measures (salivary cortisol, heart rate and blood pressure) and subjective stress ratings were measured at baseline, in anticipation of stress, immediately post-stress and after a period of rest. A neuropsychological test battery including spatial working memory and verbal memory was administered at each time point. Acute psychosocial stress produced significant increases in cardiovascular and subjective measures in the anticipatory and post-stress period, which recovered to baseline after rest. Salivary cortisol steadily declined over the testing period. Acute psychosocial stress impaired delayed verbal recall, attention and spatial working memory. Attention remained impaired, and delayed verbal recall continued to decline after rest. Acute psychosocial stress is associated with an impairment of a broad range of cognitive functions in humans and with prolonged abnormalities in attention and memory. Copyright © 2014 John Wiley & Sons, Ltd.

Acute stress in adulthood impoverishes social choices and triggers aggressiveness in preclinical models.

PubMed

Nosjean, Anne; Cressant, Arnaud; de Chaumont, Fabrice; Olivo-Marin, Jean-Christophe; Chauveau, Frédéric; Granon, Sylvie

2014-01-01

Adult C57BL/6J mice are known to exhibit high level of social flexibility while mice lacking the β2 subunit of nicotinic receptors (β2(-/-) mice) present social rigidity. We asked ourselves what would be the consequences of a restraint acute stress (45 min) on social interactions in adult mice of both genotypes, hence the contribution of neuronal nicotinic receptors in this process. We therefore dissected social interaction complexity of stressed and not stressed dyads of mice in a social interaction task. We also measured plasma corticosterone levels in our experimental conditions. We showed that a single stress exposure occurring in adulthood reduced and disorganized social interaction complexity in both C57BL/6J and β2(-/-) mice. These stress-induced maladaptive social interactions involved alteration of distinct social categories and strategies in both genotypes, suggesting a dissociable impact of stress depending on the functioning of the cholinergic nicotinic system. In both genotypes, social behaviors under stress were coupled to aggressive reactions with no plasma corticosterone changes. Thus, aggressiveness appeared a general response independent of nicotinic function. We demonstrate here that a single stress exposure occurring in adulthood is sufficient to impoverish social interactions: stress impaired social flexibility in C57BL/6J mice whereas it reinforced β2(-/-) mice behavioral rigidity.

Acute stress in adulthood impoverishes social choices and triggers aggressiveness in preclinical models

PubMed Central

Nosjean, Anne; Cressant, Arnaud; de Chaumont, Fabrice; Olivo-Marin, Jean-Christophe; Chauveau, Frédéric; Granon, Sylvie

2015-01-01

Adult C57BL/6J mice are known to exhibit high level of social flexibility while mice lacking the β2 subunit of nicotinic receptors (β2−/− mice) present social rigidity. We asked ourselves what would be the consequences of a restraint acute stress (45 min) on social interactions in adult mice of both genotypes, hence the contribution of neuronal nicotinic receptors in this process. We therefore dissected social interaction complexity of stressed and not stressed dyads of mice in a social interaction task. We also measured plasma corticosterone levels in our experimental conditions. We showed that a single stress exposure occurring in adulthood reduced and disorganized social interaction complexity in both C57BL/6J and β2−/− mice. These stress-induced maladaptive social interactions involved alteration of distinct social categories and strategies in both genotypes, suggesting a dissociable impact of stress depending on the functioning of the cholinergic nicotinic system. In both genotypes, social behaviors under stress were coupled to aggressive reactions with no plasma corticosterone changes. Thus, aggressiveness appeared a general response independent of nicotinic function. We demonstrate here that a single stress exposure occurring in adulthood is sufficient to impoverish social interactions: stress impaired social flexibility in C57BL/6J mice whereas it reinforced β2−/− mice behavioral rigidity. PMID:25610381

Effects of acute and chronic stress on telencephalic neurochemistry and gene expression in rainbow trout (Oncorhynchus mykiss).

PubMed

Moltesen, Maria; Laursen, Danielle Caroline; Thörnqvist, Per-Ove; Andersson, Madelene Åberg; Winberg, Svante; Höglund, Erik

2016-12-15

By filtering relevant sensory inputs and initiating stress responses, the brain is an essential organ in stress coping and adaptation. However, exposure to chronic or repeated stress can lead to allostatic overload, where neuroendocrinal and behavioral reactions to stress become maladaptive. This work examines forebrain mechanisms involved in allostatic processes in teleost fishes. Plasma cortisol, forebrain serotonergic (5-HTergic) neurochemistry, and mRNA levels of corticotropin-releasing factor (CRF), CRF-binding protein (CRF-BP), CRF receptors (CRFR1 and CRFR2), mineralocorticoid receptor (MR), glucocorticoid receptors (GR1 and GR2) and serotonin type 1A (5-HT 1A ) receptors (5-HT 1Aα and 5-HT 1Aβ ) were investigated at 1 h before and 0, 1 and 4 h after acute stress, in two groups of rainbow trout held in densities of 25 and 140 kg m -3 for 28 days. Generally, being held at 140 kg m -3 resulted in a less pronounced cortisol response. This effect was also reflected in lower forebrain 5-HTergic turnover, but not in mRNA levels in any of the investigated genes. This lends further support to reports that allostatic load causes fish to be incapable of mounting a proper cortisol response to an acute stressor, and suggests that changes in forebrain 5-HT metabolism are involved in allostatic processes in fish. Independent of rearing densities, mRNA levels of 5-HT 1Aα and MR were downregulated 4 h post-stress compared with values 1 h post-stress, suggesting that these receptors are under feedback control and take part in the downregulation of the hypothalamic-pituitary-interrenal (HPI) axis after exposure to an acute stressor. © 2016. Published by The Company of Biologists Ltd.

Acute stress affects free recall and recognition of pictures differently depending on age and sex.

PubMed

Hidalgo, Vanesa; Pulopulos, Matias M; Puig-Perez, Sara; Espin, Laura; Gomez-Amor, Jesus; Salvador, Alicia

2015-10-01

Little is known about age differences in the effects of stress on memory retrieval. Our aim was to perform an in-depth examination of acute psychosocial stress effects on memory retrieval, depending on age and sex. For this purpose, data from 52 older subjects (27 men and 25 women) were reanalyzed along with data from a novel group of 50 young subjects (26 men and 24 women). Participants were exposed to an acute psychosocial stress task (Trier Social Stress Test) or a control task. After the experimental manipulation, the retrieval of positive, negative and neutral pictures learned the previous day was tested. As expected, there was a significant response to the exposure to the stress task, but the older participants had a lower cortisol response to TSST than the younger ones. Stress impaired free recall of emotional (positive and negative) and neutral pictures only in the group of young men. Also in this group, correlation analyses showed a marginally significant association between cortisol and free recall. However, exploratory analyses revealed only a negative relationship between the stress-induced cortisol response and free recall of negative pictures. Moreover, stress impaired recognition memory of positive pictures in all participants, although this effect was not related to the cortisol or alpha-amylase response. These results indicate that both age and sex are critical factors in acute stress effects on specific aspects of long-term memory retrieval of emotional and neutral material. They also point out that more research is needed to better understand their specific role. Copyright © 2015 Elsevier B.V. All rights reserved.

Chironomus riparius exposure to fullerene-contaminated sediment results in oxidative stress and may impact life cycle parameters

PubMed Central

Waissi, G.C; Bold, S; Pakarinen, K; Akkanen, J; Leppänen, M.T; Petersen, E.J; Kukkonen, J.V.K

2016-01-01

A key component of understanding the potential environmental risks of fullerenes (C60) is their potential effects on benthic invertebrates. Using the sediment dwelling invertebrate Chironomus riparius we explored the effects of acute (12 h and 24 h) and chronic (10 d, 15 d, and 28 d) exposures of sediment associated fullerenes. The aims of this study were to assess the impact of exposure to C60 in the sediment top layer ((0.025, 0.18 and 0.48) C60 mg/cm2) on larval growth, oxidative stress and emergence rates and to quantify larval body burdens in similarly exposed organisms. Oxidative stress localization was observed in the tissues next to the microvilli and exoskeleton through a method for identifying oxidative stress reactions generated by reactive oxygen species. Rapid intake of fullerenes was shown in acute experiments, whereas body residues decreased after chronic exposure. Transmission electron microscopy analysis revealed oxidative damage and structural changes in cells located between the lipid droplets and next to the microvilli layer in fullerene exposed samples. Fullerene associated sediments also caused changes in the emergence rate of males and females, suggesting that the cellular interactions described above or other effects from the fullerenes may influence reproduction rates. PMID:27178647

Acute exposure to offshore produced water has an effect on stress- and secondary stress responses in three-spined stickleback Gasterosteus aculeatus.

PubMed

Knag, Anne Christine; Taugbøl, Annette

2013-09-01

Pollution is one of today's greatest problems, and the release of contaminants into the environment can cause adverse changes in vitally important biological pathways. In this study, we exposed three-spined stickleback Gasterosteus aculeatus to produced water (PW), i.e. wastewater from offshore petroleum production. PW contains substances such as alkylphenols (APs) and aromatic hydrocarbons (PAHs) known to induce toxicant stress and endocrine disruption in a variety of organisms. Following exposure to PW, a standardized confinement treatment was applied as a second stressor (PW-stress), testing how fish already under stress from the pollutant would respond to an additional stressor. The endpoint for analysis was a combination of blood levels of cortisol and glucose, in addition to transcribed levels of a set of genes related to toxicant stress, endocrine disruption and general stress. The findings of this study indicate that low doses of PW do not induce vitellogenin in immature female stickleback, but do cause an upregulation of cytochrome (CYP1A) and UDP-glucuronsyltransferase (UDP-GT), two biomarkers related to toxicant stress. However, when the second stressor was applied, both genes were downregulated, indicating that the confinement exposure had a suppressive effect on the expression of toxicant biomarkers (CYP1A and UDP-GT). Further, two of the stress related genes, heat shock protein 90 (HSP90) and stress-induced phosphoprotein (STIP), were upregulated in both PW- and PW-stress-treatment, but not in the water control confinement treatment, indicating that PW posed as a larger stress-factor than confinement for these genes. The confinement stressor caused an increased level of glucose in both control and PW-treated fish, indicating hyperglycemia, a commonly reported stress response in fish. © 2013.

Obesity-Induced Endoplasmic Reticulum Stress Causes Lung Endothelial Dysfunction and Promotes Acute Lung Injury.

PubMed

Shah, Dilip; Romero, Freddy; Guo, Zhi; Sun, Jianxin; Li, Jonathan; Kallen, Caleb B; Naik, Ulhas P; Summer, Ross

2017-08-01

Obesity is a significant risk factor for acute respiratory distress syndrome. The mechanisms underlying this association are unknown. We recently showed that diet-induced obese mice exhibit pulmonary vascular endothelial dysfunction, which is associated with enhanced susceptibility to LPS-induced acute lung injury. Here, we demonstrate that lung endothelial dysfunction in diet-induced obese mice coincides with increased endoplasmic reticulum (ER) stress. Specifically, we observed enhanced expression of the major sensors of misfolded proteins, including protein kinase R-like ER kinase, inositol-requiring enzyme α, and activating transcription factor 6, in whole lung and in primary lung endothelial cells isolated from diet-induced obese mice. Furthermore, we found that primary lung endothelial cells exposed to serum from obese mice, or to saturated fatty acids that mimic obese serum, resulted in enhanced expression of markers of ER stress and the induction of other biological responses that typify the lung endothelium of diet-induced obese mice, including an increase in expression of endothelial adhesion molecules and a decrease in expression of endothelial cell-cell junctional proteins. Similar changes were observed in lung endothelial cells and in whole-lung tissue after exposure to tunicamycin, a compound that causes ER stress by blocking N-linked glycosylation, indicating that ER stress causes endothelial dysfunction in the lung. Treatment with 4-phenylbutyric acid, a chemical protein chaperone that reduces ER stress, restored vascular endothelial cell expression of adhesion molecules and protected against LPS-induced acute lung injury in diet-induced obese mice. Our work indicates that fatty acids in obese serum induce ER stress in the pulmonary endothelium, leading to pulmonary endothelial cell dysfunction. Our work suggests that reducing protein load in the ER of pulmonary endothelial cells might protect against acute respiratory distress syndrome in obese

Sleep and stress in man: an approach through exercise and exposure to extreme environments.

PubMed

Buguet, A; Cespuglio, R; Radomski, M W

1998-05-01

In this paper, the effects of exercise on human sleep (in temperate, cold, and hot climates) are compared with those of exposure to extreme environments (tropical, polar climates). Exercise has two effect: (i) when the exercise load is too heavy or if the subject is not trained to the exercise conditions, the hypothalamo-pituitary-adrenocortical axis (HPA) is strongly activated (somatic stress reaction), and a diachronic (delayed) decrease in total sleep time and slow-wave sleep (SWS) occurs with a synchronic (concomitant) sleep disruption (such as a decrease in REM sleep); (ii) a diachronic enhancement of SWS and (or) REM sleep occurs during moderate training and in athletes, with a moderate HPA activation (neurogenic stress reaction). Heat acclimatization (neurogenic stress response) results in a diachronic increase in SWS, contrary to acute heat exposure (somatic stress) which leads to a diachronic decrease in SWS. Nocturnal cold exposure (somatic and (or) neurogenic stress) provokes a synchronic decrease in REM sleep with an activation of stress hormones, which are reduced by previous acclimation (neurogenic pathway); SWS remains undisturbed in the cold, as it occurs at the beginning of the night before body cooling. In conclusion, when the brain can deal with the stressor (neurogenic stress), diachronic increases in SWS and (or) REM sleep occur. When these "central" mechanisms are overloaded, the classical "somatic" stress reaction occurs with diachronic and synchronic disruptions of the sleep structure.

Alpha adrenergic regulation of celiac blood flow and plasma catecholamine response during acute heat stress in fed cockerels.

PubMed

Bottje, W G; Harrison, P C

1986-08-01

Hubbard cockerels with chronically implanted electromagnetic blood flow probes on the celiac artery were used to establish a relationship between changes in postprandial celiac mean blood flow (MBF) and plasma catecholamines during a acute heat exposure. Five min after the elevation of ambient temperature from 25 to 37 C, there were concomitant reductions (P less than .05) in celiac MBF, norepinephrine (NE), and heart rate (HR). After 50 min of heat stress, rectal temperature (Tr), respiratory rate (RR), plasma epinephrine (E), and celiac vascular resistance (CVR) were significantly greater (P less than .05) than preheat stress thermoneutral control values. During the thermoneutral recovery period, all parameters returned to values comparable to preheat exposure control with the exception of NE, which tended (P less than .1) to remain lower. To determine the role of the sympathetic nervous system in regulating postprandial celiac MBF during acute heat exposure, chronically instrumented cockerels were infused with phenoxybenzamine, an alpha-adrenergic receptor-blocking agent. Alpha-receptor blockade attenuated both postprandial intestinal hyperemia under thermoneutral conditions as well as the heat-induced reduction of postprandial celiac MBF. The results of these studies implicate the sympathetic nervous system in the regulation of postprandial celiac MBF in heat-stressed cockerels and indicate a possible alpha-adrenergic-mediated mechanism involved in postprandial intestinal hyperemia.

The role of maladaptive appraisals in child acute stress reactions.

PubMed

Salmon, Karen; Sinclair, Emma; Bryant, Richard A

2007-06-01

To test the prediction of cognitive models of trauma that negative, catastrophic appraisals central to the development of psychopathological stress reactions. A cross-sectional, concurrent design was used. Sixty-six children (aged 7-13 years), who were hospitalized after traumatic injury were assessed within 4 weeks of their trauma for acute stress disorder, depression, and administered the Child Post-traumatic Cognitions Inventory (cPTCI). Parental acute stress was also assessed. Children's negative appraisals of their ongoing vulnerability accounted for 44% of the variance of acute stress reactions in children. Injury severity, depression, age, and parental acute stress levels did not account for significant additional variance. The findings provide support for cognitive models of trauma adaptation and highlight the importance of assessing children's appraisals of their traumatic experience in order to develop effective interventions.

Acute Stress Symptoms in Young Children with Burns

ERIC Educational Resources Information Center

Stoddard, Frederick J.; Saxe, Glenn; Ronfeldt, Heidi; Drake, Jennifer E.; Burns, Jennifer; Edgren, Christy; Sheridan, Robert

2006-01-01

Objective: Posttraumatic stress disorder symptoms are a focus of much research with older children, but little research has been conducted with young children, who account for about 50% of all pediatric burn injuries. This is a 3-year study of 12- to 48-month-old acutely burned children to assess acute traumatic stress outcomes. The aims were to…

Chronic repeated exposure to weather-related stimuli elicits few symptoms of chronic stress in captive molting and non-molting European starlings (Sturnus vulgaris).

PubMed

de Bruijn, Robert; Reed, J Michael; Romero, L Michael

2017-10-01

Repeated exposure to acute stressors causes dramatic changes in an animal's stress physiology and the cumulative effects are often called chronic stress. Recently we showed that short-term exposure to weather-related stimuli, such as temperature change, artificial precipitation, and food restriction, cause acute responses in captive European starlings (Sturnus vulgaris). Here, we examined the effect of repeated exposure to weather-related stressors on heart rate and corticosterone (CORT) of captive non-molting and molting European starlings. Four times every day for 3 weeks, birds were exposed to either 30 min of a subtle (3°C) decrease in temperature, a short bout of simulated rain, or 2 hr of food removal. The order and time of presentation were randomly assigned on each day. We found no differences in heart rate or heart rate variability. Furthermore, there were no changes in baseline CORT levels, CORT negative feedback efficacy, or maximal adrenal capacity. Mass increased across the experimental period only in molting birds. CORT responses to restraint were decreased in both groups following treatment, suggesting the birds had downregulated their responses to acute stress. Molting birds showed evidence of suppression of the HPA axis compared with non-molting birds, which is consistent with previous research. Overall, our data show that repeated exposure to weather-related stressors does not elicit most of the symptoms normally associated with chronic stress. © 2018 Wiley Periodicals, Inc.

The Adverse Effects of Environmental Noise Exposure on Oxidative Stress and Cardiovascular Risk

PubMed Central

Sørensen, Mette; Schmidt, Frank; Schmidt, Erwin; Steven, Sebastian; Kröller-Schön, Swenja; Daiber, Andreas

2018-01-01

Abstract Epidemiological studies have provided evidence that traffic noise exposure is linked to cardiovascular diseases such as arterial hypertension, myocardial infarction, and stroke. Noise is a nonspecific stressor that activates the autonomous nervous system and endocrine signaling. According to the noise reaction model introduced by Babisch and colleagues, chronic low levels of noise can cause so-called nonauditory effects, such as disturbances of activity, sleep, and communication, which can trigger a number of emotional responses, including annoyance and subsequent stress. Chronic stress in turn is associated with cardiovascular risk factors, comprising increased blood pressure and dyslipidemia, increased blood viscosity and blood glucose, and activation of blood clotting factors, in animal models and humans. Persistent chronic noise exposure increases the risk of cardiometabolic diseases, including arterial hypertension, coronary artery disease, diabetes mellitus type 2, and stroke. Recently, we demonstrated that aircraft noise exposure during nighttime can induce endothelial dysfunction in healthy subjects and is even more pronounced in coronary artery disease patients. Importantly, impaired endothelial function was ameliorated by acute oral treatment with the antioxidant vitamin C, suggesting that excessive production of reactive oxygen species contributes to this phenomenon. More recently, we introduced a novel animal model of aircraft noise exposure characterizing the underlying molecular mechanisms leading to noise-dependent adverse oxidative stress-related effects on the vasculature. With the present review, we want to provide an overview of epidemiological, translational clinical, and preclinical noise research addressing the nonauditory, adverse effects of noise exposure with focus on oxidative stress. Antioxid. Redox Signal. 28, 873–908. PMID:29350061

Responses of the soft coral Xenia elongata following acute exposure to a chemical dispersant.

PubMed

Studivan, Michael S; Hatch, Walter I; Mitchelmore, Carys L

2015-01-01

Limited toxicology data are available regarding oil dispersant exposure to coral species. Corexit® EC9500A (Corexit) is a commonly applied dispersant most well known for its use after the Deepwater Horizon spill in April, 2010. There is limited evidence that Corexit can cause a bleaching response in corals. The aims of the study were: (1) to determine the extent of bleaching after acute 24 h and 72 h exposures of sublethal concentrations (0-50 ppm) of Corexit to the pulsing soft coral Xenia elongata and (2) to investigate a percent symbiont loss calculation using zooxanthellae density. The percent symbiont loss calculation was compared to a traditional metric of normalizing zooxanthellae density to soluble protein content. Percent symbiont loss was an effective measure of coral stress in acute Corexit exposures, while protein normalized zooxanthellae density was more variable. The bleaching data suggest a positive relationship between dispersant concentration and percent symbiont loss, culminating in excessive tissue necrosis and coral mortality within 72 h in high concentration exposures (p < 0.001). Percent beaching ranged from 25% in 5 ppm exposures to 100% in 50 ppm exposures. Corexit also caused a significant decrease in pulse activity (p < 0.0001) and relative oxygen saturation (p < 0.001), possibly indicating a reduction in photosynthetic efficiency. This study and other similar research indicate that dispersant exposure is highly damaging to marine organisms, including ecologically important coral species.

Acute stress responses: A review and synthesis of ASD, ASR, and CSR.

PubMed

Isserlin, Leanna; Zerach, Gadi; Solomon, Zahava

2008-10-01

Toward the development of a unifying diagnosis for acute stress responses this article attempts to find a place for combat stress reaction (CSR) within the spectrum of other defined acute stress responses. This article critically compares the diagnostic criteria of acute stress disorder (ASD), acute stress reaction (ASR), and CSR. Prospective studies concerning the predictive value of ASD, ASR, and CSR are reviewed. Questions, recommendations, and implications for clinical practice are raised concerning the completeness of the current acute stress response diagnoses, the heterogeneity of different stressors, the scope of expected outcomes, and the importance of decline in function as an indicator of future psychological, psychiatric, and somatic distress. PsycINFO Database Record 2009 APA.

Ozone-induced foliar damage and release of stress volatiles is highly dependent on stomatal openness and priming by low-level ozone exposure in Phaseolus vulgaris

PubMed Central

Li, Shuai; Harley, Peter C.; Niinemets, Ülo

2018-01-01

Acute ozone exposure triggers major emissions of volatile organic compounds (VOC), but quantitatively, it is unclear how different ozone doses alter the start and the total amount of these emissions, and the induction rate of different stress volatiles. It is also unclear whether priming (i.e., pre-exposure to lower O3 concentrations) can modify the magnitude and kinetics of volatile emissions. We investigated photosynthetic characteristics and VOC emissions in Phaseolus vulgaris following acute ozone exposure (600 nmol mol-1 for 30 min) under illumination and in darkness and after priming with 200 nmol mol-1 O3 for 30 min. Methanol and lipoxygenase (LOX) pathway product emissions were induced rapidly, followed by moderate emissions of methyl salicylate (MeSA). Stomatal conductance prior to acute exposure was lower in darkness and after low O3 priming than in light and without priming. After low O3 priming, no MeSA and lower LOX emissions were detected under acute exposure. Overall, maximum emission rates and the total amount of emitted LOX products and methanol were quantitatively correlated with total stomatal ozone uptake. These results indicate that different stress volatiles scale differently with ozone dose and highlight the key role of stomatal conductance in controlling ozone uptake, leaf injury and volatile release. PMID:28623868

Effects of acute and chronic psychological stress on isolated islets' insulin release

PubMed Central

Zardooz, Homeira; Zahediasl, Saleh; Rostamkhani, Fatemeh; Farrokhi, Babak; Nasiraei, Shiva; Kazeminezhad, Behrang; Gholampour, Roohollah

2012-01-01

This study investigated the effects of acute and chronic psychological stress on glucose-stimulated insulin secretion from isolated pancreatic islets. Male Wistar rats were divided into two control and stressed groups; each further was allocated into fed and fasted groups. Stress was induced by communication box for one (acute), fifteen and thirty (chronic) days. After islet isolation, their number, size and insulin output were assessed. Plasma corticosterone level was determined. In fasted animals, acute stress increased basal and post stress plasma corticosterone level, while 30 days stress decreased it compared to day 1. In fed rats, acute stress increased only post stress plasma corticosterone concentration, however, after 15 days stress, it was decreased compared to day 1. Acute stress did not change insulin output; however, the insulin output was higher in the fed acutely stressed rats at 8.3 and 16.7 mM glucose than fasted ones. Chronic stress increased insulin output on day 15 in the fasted animals but decreased it on day 30 in the fed animals at 8.3 and 16.7 mM glucose. In the fasted control rats insulin output was lower than fed ones. In the chronic stressed rats insulin output at 8.3 and 16.7 mM glucose was higher in the fasted than fed rats. The number of islets increased in the fasted rats following 15 days stress. This study indicated that the response of the isolated islets from acute and chronically stressed rats are different and depends on the feeding status. PMID:27385956

Acute stress affects risk taking but not ambiguity aversion.

PubMed

Buckert, Magdalena; Schwieren, Christiane; Kudielka, Brigitte M; Fiebach, Christian J

2014-01-01

Economic decisions are often made in stressful situations (e.g., at the trading floor), but the effects of stress on economic decision making have not been systematically investigated so far. The present study examines how acute stress influences economic decision making under uncertainty (risk and ambiguity) using financially incentivized lotteries. We varied the domain of decision making as well as the expected value of the risky prospect. Importantly, no feedback was provided to investigate risk taking and ambiguity aversion independent from learning processes. In a sample of 75 healthy young participants, 55 of whom underwent a stress induction protocol (Trier Social Stress Test for Groups), we observed more risk seeking for gains. This effect was restricted to a subgroup of participants that showed a robust cortisol response to acute stress (n = 26). Gambling under ambiguity, in contrast to gambling under risk, was not influenced by the cortisol response to stress. These results show that acute psychosocial stress affects economic decision making under risk, independent of learning processes. Our results further point to the importance of cortisol as a mediator of this effect.

Endoplasmic Reticulum Stress in Ischemic and Nephrotoxic Acute Kidney Injury.

PubMed

Yan, Mingjuan; Shu, Shaoqun; Guo, Chunyuan; Tang, Chengyuan; Dong, Zheng

2018-06-12

Acute kidney injury is a medical condition characterized by kidney damage with a rapid decline of renal function, which is associated with high mortality and morbidity. Recent research has further established an intimate relationship between acute kidney injury and chronic kidney disease. Perturbations of kidney cells in acute kidney injury result in the accumulation of unfolded and misfolded proteins in the endoplasmic reticulum, leading to unfolded protein response or endoplasmic reticulum stress. In this review, we analyze the role and regulation of endoplasmic reticulum stress in acute kidney injury triggered by renal ischemia-reperfusion and cisplatin nephrotoxicity. The balance between the two major components of unfolded protein response, the adaptive pathway and the apoptotic pathway, plays a critical role in determining the cell fate in endoplasmic reticulum stress. The adaptive pathway is evoked to attenuate translation, induce chaperones, maintain protein homeostasis, and promote cell survival. Prolonged endoplasmic reticulum stress activates the apoptotic pathway, resulting in the elimination of dysfunctional cells. Therefore, regulating ER stress in kidney cells may provide a therapeutic target in acute kidney injury.

Acute stress affects prospective memory functions via associative memory processes.

PubMed

Szőllősi, Ágnes; Pajkossy, Péter; Demeter, Gyula; Kéri, Szabolcs; Racsmány, Mihály

2018-01-01

Recent findings suggest that acute stress can improve the execution of delayed intentions (prospective memory, PM). However, it is unclear whether this improvement can be explained by altered executive control processes or by altered associative memory functioning. To investigate this issue, we used physical-psychosocial stressors to induce acute stress in laboratory settings. Then participants completed event- and time-based PM tasks requiring the different contribution of control processes and a control task (letter fluency) frequently used to measure executive functions. According to our results, acute stress had no impact on ongoing task performance, time-based PM, and verbal fluency, whereas it enhanced event-based PM as measured by response speed for the prospective cues. Our findings indicate that, here, acute stress did not affect executive control processes. We suggest that stress affected event-based PM via associative memory processes. Copyright © 2017 Elsevier B.V. All rights reserved.

Laying hen responses to acute heat stress and carbon dioxide supplementation: I. Blood gas changes and plasma lactate accumulation.

PubMed

Koelkebeck, K W; Odom, T W

1994-04-01

Exposure to heat stress lowered partial pressure of arterial blood carbon dioxide (paCO2), arterial blood bicarbonate ion (HCO3-), but increased arterial blood pH (pHa) and plasma lactate (LA). Increasing ambient carbon dioxide (CO2) to 1.5% increased paCO2 from hypocapnic levels to normocapnic levels, raised HCO3-, lowered pHa and plasma LA to pre-heat stress levels. Following CO2 treatment, respiratory alkalosis conditions returned. It was evident in this study that increasing ambient chamber CO2 to 1.5% was effective in ameliorating acid-base disturbances and reducing elevated levels of plasma LA which normally develops when laying hens are subjected to an acute heat stress exposure.

Acute stress worsens the deficits in appetitive behaviors for social and sexual stimuli displayed by rats after long-term withdrawal from morphine.

PubMed

Bai, Yunjing; Belin, David; Zheng, Xigeng; Liu, Zhengkui; Zhang, Yue

2017-06-01

Negative affective states, e.g., anhedonia, are suggested to be involved in the long-lasting motivational processes associated with relapse. Here, we investigated whether anhedonic behaviors could be elicited by an acute stress after protracted abstinence from morphine. The behavioral responses to natural stimuli following exposure to an acute stress were examined after 14 days of withdrawal from morphine. Male rats were pretreated with either a binge-like morphine regimen or daily saline injections for 5 days. The motivation for two natural stimuli, i.e., a social stimulus (male rat) and a sexual stimulus (estrous female rat), was measured, following exposure to an acute stress (intermittent foot shock, 0.5 mA * 0.5 s * 10 min; mean inter-shock interval 40 s), under three conditions: free approach and effort- and conflict-based approaches. Foot-shock-induced stress did not influence free-approach behavior (sniffing time) towards the social or sexual stimulus. However, in the effort-based approach task, the stressed morphine-withdrawn rats demonstrated an attenuated motivation to climb over a partition to approach the social stimulus while the stressed saline-pretreated rats showed an increased motivation to approach the social stimulus. When an aversive stimulus (pins) was introduced in order to induce an approach-avoidance conflict, both drug-withdrawn and drug-naïve groups exhibited a bimodal distribution of approach behavior towards the sexual stimulus after the stress was introduced, i.e., the majority of rats had low risky appetitive behaviors but a minority of them showed rather highly "risky" approach behavior. The acute stress induces differential motivational deficits for social and sexual rewards in protracted drug-abstinent rats.

Intrauterine and lactation exposure to fluoxetine blunted in the offspring the aortic adaptive response induced by acute restraint stress.

PubMed

Marques, Bruno V D; Higashi, Carolina M; da S Novi, Daniella R B; Zanluqui, Nagela G; Gregório, Thais F; Pinge-Filho, Phileno; Gerardin, Daniela C C; Pelosi, Gislaine G; Moreira, Estefânia G; Ceravolo, Graziela S

2017-10-15

Selective serotonin reuptake inhibitors are the most widely prescribed antidepressants to women during pregnancy. Maternal treatment with fluoxetine can expose fetuses and neonates to higher levels of serotonin that plays a role in stress response. Thus, the aim of the study was to evaluate whether maternal treatment with fluoxetine interferes with aorta reactivity of adult male offspring after acute restraint stress. Wistar rats were gavaged with fluoxetine (5mg/kg/day) or water (control) during pregnancy and lactation. The experiments were performed in adult male offspring, treated or not with reserpine (4mg/Kg, ip, 28h before the experimental protocol). Fluoxetine and control rats were submitted to a single restraint stress session (ST) for 1h. Curves to phenylephrine were performed in thoracic aorta with endothelium. Aortic nitric oxide (NOx) were evaluated by the Griess method. The aortic contraction induced by phenylephrine was similar between control and fluoxetine rats. The acute stress reduced contraction in aorta of control ST compared to control, and L-NAME equaled this response. In fluoxetine rats, ST did not change the aortic constriction. Reserpine treatment restored the vasoconstriction in control ST, but did not interfere with aortic contraction in control, fluoxetine or fluoxetine ST. The NOx concentration was higher in aortas from control ST than control rats, and reserpine reduced NOx levels of control ST. The NOx concentration was similar between fluoxetine and fluoxetine ST rats, treated or not with reserpine. In conclusion, maternal treatment with fluoxetine blunted acute restraint stress-induced NO system activation and aortic adaptation in adult offspring. Copyright © 2017 Elsevier B.V. All rights reserved.

Acute stress symptoms, dissociation, and depression among rescue personnel 24 hours after the Bet-Yehoshua train crash in Israel:the effect of gender.

PubMed

Palgi, Yuval; Ben-Ezra, Menachem; Essar, Nir; Sofer, Hilik; Haber, Yeela

2009-01-01

The effect of immediate exposure to traumatic events and gender differences is under-studied in the literature. Most studies focus on acute stress disorder (ASD) and post-traumatic stress disorder (PTSD) phases in order to measure gender differences, and tend to neglect the immediate exposure to the disaster. The main hypothesis was that female rescue personnel would exhibit higher levels of acute stress symptoms, dissociation, and depressive symptoms in the 24 hours following a traumatic event. Twenty-three rescue personnel participated in a search and rescue operation at the Bet-Yehoshua train crash in Israel. The rescue personnel group was divided based on gender. Each participant completed a demographic questionnaire including questions that assessed psychological symptoms and issues such as perceived threat to life, the Impact of Event Scale Revised (IES-R), the Dissociative Experience Scale (DES), and the Center of Epidemiologic Studies Depression questionnaire (CES-D). Statistical inferences were calculated using t-tests and chi-square tests, along with testing of covariance (MANCOVA) in order to indentify which factors are related to psychiatric symptomatology following the immediate exposure to disaster. The results suggest that among rescue personnel, women did not differ in their levels of acute stress, dissociation, and depressive symptoms from men. These results suggest the possibility that the gender differences in reactions to traumatic events do not emerge in the acute stress reactions (ASR) phase (up to 24 hours after the event), but later on when people have time to process the trauma. Another possibility that may explain the discrepancy between this study and the common knowledge in the literature is that women rescue personnel are considered a highly selected group, which does not reflect on the general population of women. More studies are needed in order to substantiate these results.

Relationship of Stress, Leukocyte Functions and Acute Ulcerative Gingivitis.

DTIC Science & Technology

1982-10-22

IONAL 1jjl (I Y AN[)AAU> I,)(, 4 •. . . . .i -AD (Report Number 3 , Lf) RELATIONSHIP OF STRESS, LEUKOCYTE FUNCTION AND ACUTE ULCERATIVE GINGIVITIS...AIk £It. KEY WORDS (C~mntm. a reers old. A *1acoa and Identit by block number) Acute Necrotic Ulcerative Gingivitis (ANUG)), Stress 4 Leukocyte

Acute stress affects risk taking but not ambiguity aversion

PubMed Central

Buckert, Magdalena; Schwieren, Christiane; Kudielka, Brigitte M.; Fiebach, Christian J.

2014-01-01

Economic decisions are often made in stressful situations (e.g., at the trading floor), but the effects of stress on economic decision making have not been systematically investigated so far. The present study examines how acute stress influences economic decision making under uncertainty (risk and ambiguity) using financially incentivized lotteries. We varied the domain of decision making as well as the expected value of the risky prospect. Importantly, no feedback was provided to investigate risk taking and ambiguity aversion independent from learning processes. In a sample of 75 healthy young participants, 55 of whom underwent a stress induction protocol (Trier Social Stress Test for Groups), we observed more risk seeking for gains. This effect was restricted to a subgroup of participants that showed a robust cortisol response to acute stress (n = 26). Gambling under ambiguity, in contrast to gambling under risk, was not influenced by the cortisol response to stress. These results show that acute psychosocial stress affects economic decision making under risk, independent of learning processes. Our results further point to the importance of cortisol as a mediator of this effect. PMID:24834024

Prenatal exposure to escitalopram and/or stress in rats: a prenatal stress model of maternal depression and its treatment

PubMed Central

Bourke, Chase H.; Capello, Catherine F.; Rogers, Swati M.; Yu, Megan L.; Boss-Williams, Katherine A.; Weiss, Jay M.; Stowe, Zachary N.; Owens, Michael J.

2014-01-01

Rationale A rigorously investigated model of stress and antidepressant administration during pregnancy is needed to evaluate possible effects on the mother. Objective The objective of this study was to develop a model of clinically relevant prenatal exposure to an antidepressant and stress during pregnancy to evaluate the effects on maternal care behavior. Results Female rats implanted with 28 day osmotic minipumps delivering the SSRI escitalopram throughout pregnancy had serum escitalopram concentrations in a clinically observed range (17-65 ng/mL). A separate cohort of pregnant females exposed to a chronic unpredictable mild stress paradigm on gestational days 10-20 showed elevated baseline (305 ng/mL), and acute stress-induced (463 ng/mL), plasma corticosterone concentrations compared to unstressed controls (109 ng/mL). A final cohort of pregnant dams were exposed to saline (control), escitalopram, stress, or stress and escitalopram to determine the effects on maternal care. Maternal behavior was continuously monitored over the first 10 days post parturition. A reduction of 35% in maternal contact and 11% in nursing behavior was observed due to stress during the light cycle. Licking and grooming behavior was unaffected by stress or drug exposure in either the light or dark cycle. Conclusions These data indicate that: 1) clinically relevant antidepressant treatment during human pregnancy can be modeled in rats using escitalopram; 2) chronic mild stress can be delivered in a manner that does not compromise fetal viability; and 3) neither of these prenatal treatments substantially altered maternal care post parturition. PMID:23436130

The expression of plasticity-related genes in an acute model of stress is modulated by chronic desipramine in a time-dependent manner within medial prefrontal cortex.

PubMed

Nava, Nicoletta; Treccani, Giulia; Müller, Heidi Kaastrup; Popoli, Maurizio; Wegener, Gregers; Elfving, Betina

2017-01-01

It is well established that stress plays a major role in the pathogenesis of neuropsychiatric diseases. Stress-induced alteration of synaptic plasticity has been hypothesized to underlie the morphological changes observed by neuroimaging in psychiatric patients in key regions such as hippocampus and prefrontal cortex (PFC). We have recently shown that a single acute stress exposure produces significant short-term alterations of structural plasticity within medial PFC. These alterations were partially prevented by previous treatment with chronic desipramine (DMI). In the present study we evaluated the effects of acute Foot-shock (FS)-stress and pre-treatment with the traditional antidepressant DMI on the gene expression of key regulators of synaptic plasticity and structure. Expression of Homer, Shank, Spinophilin, Densin-180, and the small RhoGTPase related gene Rac1 and downstream target genes, Limk1, Cofilin1 and Rock1 were investigated 1 day (1d), 7 d and 14d after FS-stress exposure. We found that DMI specifically increases the short-term expression of Spinophilin, as well as Homer and Shank family genes, and that both acute stress and DMI exert significant long-term effects on mRNA levels of genes involved in spine plasticity. These findings support the knowledge that acute FS stress and antidepressant treatment induce both rapid and sustained time-dependent alterations in structural components of synaptic plasticity in rodent medial PFC. Copyright © 2016 Elsevier B.V. and ECNP. All rights reserved.

Assessing Lifetime Stress Exposure Using the Stress and Adversity Inventory for Adults (Adult STRAIN): An Overview and Initial Validation.

PubMed

Slavich, George M; Shields, Grant S

2018-01-01

Numerous theories have proposed that acute and chronic stressors may exert a cumulative effect on life-span health by causing biological "wear and tear," or allostatic load, which in turn promotes disease. Very few studies have directly tested such models, though, partly because of the challenges associated with efficiently assessing stress exposure over the entire life course. To address this issue, we developed the first online system for systematically assessing lifetime stress exposure, called the Stress and Adversity Inventory (STRAIN), and describe its initial validation here. Adults recruited from the community (n = 205) were administered the STRAIN, Childhood Trauma Questionnaire-Short Form, and Perceived Stress Scale, as well as measures of socioeconomic status, personality, social desirability, negative affect, mental and physical health complaints, sleep quality, computer-assessed executive function, and doctor-diagnosed general health problems and autoimmune disorders. The STRAIN achieved high acceptability and was completed relatively quickly (mean = 18 minutes 39 seconds; interquartile range = 12-23 minutes). The structure of the lifetime stress data best fit two latent classes overall and five distinct trajectories over time. Concurrent associations with the Childhood Trauma Questionnaire-Short Form and Perceived Stress Scale were good (r values = .147-.552). Moreover, the STRAIN was not significantly related to personality traits or social desirability characteristics and, in adjusted analyses, emerged as the measure most strongly associated with all six of the health and cognitive outcomes assessed except current mental health complaints (β values = .16-.41; risk ratios = 1.02-1.04). Finally, test-retest reliability for the main stress exposure indices over 2-4 weeks was excellent (r values = .904-.919). The STRAIN demonstrated good usability and acceptability; very good concurrent, discriminant, and predictive validity; and excellent test

Assessing Lifetime Stress Exposure Using the Stress and Adversity Inventory for Adults (Adult STRAIN): An Overview and Initial Validation

PubMed Central

Slavich, George M.; Shields, Grant S.

2018-01-01

ABSTRACT Objective Numerous theories have proposed that acute and chronic stressors may exert a cumulative effect on life-span health by causing biological “wear and tear,” or allostatic load, which in turn promotes disease. Very few studies have directly tested such models, though, partly because of the challenges associated with efficiently assessing stress exposure over the entire life course. To address this issue, we developed the first online system for systematically assessing lifetime stress exposure, called the Stress and Adversity Inventory (STRAIN), and describe its initial validation here. Methods Adults recruited from the community (n = 205) were administered the STRAIN, Childhood Trauma Questionnaire—Short Form, and Perceived Stress Scale, as well as measures of socioeconomic status, personality, social desirability, negative affect, mental and physical health complaints, sleep quality, computer-assessed executive function, and doctor-diagnosed general health problems and autoimmune disorders. Results The STRAIN achieved high acceptability and was completed relatively quickly (mean = 18 minutes 39 seconds; interquartile range = 12–23 minutes). The structure of the lifetime stress data best fit two latent classes overall and five distinct trajectories over time. Concurrent associations with the Childhood Trauma Questionnaire—Short Form and Perceived Stress Scale were good (r values = .147–.552). Moreover, the STRAIN was not significantly related to personality traits or social desirability characteristics and, in adjusted analyses, emerged as the measure most strongly associated with all six of the health and cognitive outcomes assessed except current mental health complaints (β values = .16–.41; risk ratios = 1.02–1.04). Finally, test-retest reliability for the main stress exposure indices over 2–4 weeks was excellent (r values = .904–.919). Conclusions The STRAIN demonstrated good usability and acceptability; very good concurrent

Comparison of three acute stress models for simulating the pathophysiology of stress-related mucosal disease.

PubMed

Saxena, Bhagawati; Singh, Sanjay

2017-05-30

Stress-related mucosal disease (SRMD) is highly prevalent in intensive care patients leading to increasing treatment cost and mortality. SRMD is a disease elusive of ideal treatment. Evaluation of drugs is very pertinent for the efficient and safe treatment of SRMD. It relies mainly on in vivo screening models. There are various stress models, and till date, none of them is validated for simulating the SRMD pathophysiology. The present study aims to choose the best model, which reproduce pathophysiology of SRMD, among previously established stress models. This study evaluates ulcer index, hexosamine content, microvascular permeability, and gastric content in three acute stress models (cold-restraint, restraint, and water immersion restraint). Macroscopic pictures of the ulcerogenic stomach explain that in contrast to other models, cold-restraint stress (CRS) exposure produced marked ulcers on the fundic area of the stomach. Results of the present study depicted that each stress model significantly increased ulcer index, microvascular permeability and decreased hexosamine level, however, the maximum in the case of CRS-exposed rats. Total acidity and pH of the gastric content remains unchanged in all the stress models. On the contrary, the gastric volume significantly decreased only in case of CRS, while unchanged in other stress models. The overall results revealed that the CRS resembles the pathophysiology of SRMD closely. It is the best and feasible model among all the models to evaluate drugs for the treatment of SRMD.

Differential modulatory effects of morphine on acute and chronic stress induced neurobehavioral and cellular markers in rats.

PubMed

Joshi, Jagdish C; Ray, Arunabha; Gulati, Kavita

2014-04-15

The present study evaluated the effects of morphine treatments on elevated plus maze test parameters, oxidative stress markers and Hsp70 expression in normal and stressed rats. Acute and chronic stress caused neurobehavioral suppression, altered prooxidant-antioxidant balance and increased Hsp70 expression in brain homogenates in a differential manner. Morphine (1 and 5mg/kg) attenuated RS induced anxiogenesis, changes in MDA and GSH but further enhanced Hsp70 expression. Similar anxiolytic and Hsp70 enhancing effects were seen after morphine in normal rats (no RS). Exposure to chronic RS did not elicit any appreciable neurobehavioral response in EPM but enhanced MDA, lowered GSH and exaggerated the Hsp70 expression. Pretreatment with morphine did not affect the neurobehavioral response to chronic RS, but reverted the GSH and Hsp70 expression. The results suggest that morphine differentially influences acute and chronic stress induced changes in anxiety behavior and complex interactions between oxidative stress markers and Hsp70 expression which may contribute to these effects. Copyright © 2014 Elsevier B.V. All rights reserved.

Exposure to Stress: Occupational Hazards in Hospitals

MedlinePlus

EXPOSURE TO STRESS Occupational Hazards in Hospitals DEPARTMENT OF HEALTH AND HUMAN SERVICES Centers for Disease Control and Prevention National Institute for Occupational Safety and Health Exposure to Stress Occupational Hazards in Hospitals DEPARTMENT OF HEALTH AND ...

Ozone-induced foliar damage and release of stress volatiles is highly dependent on stomatal openness and priming by low-level ozone exposure in Phaseolus vulgaris.

PubMed

Li, Shuai; Harley, Peter C; Niinemets, Ülo

2017-09-01

Acute ozone exposure triggers major emissions of volatile organic compounds (VOCs), but quantitatively, it is unclear how different ozone doses alter the start and the total amount of these emissions, and the induction rate of different stress volatiles. It is also unclear whether priming (i.e. pre-exposure to lower O 3 concentrations) can modify the magnitude and kinetics of volatile emissions. We investigated photosynthetic characteristics and VOC emissions in Phaseolus vulgaris following acute ozone exposure (600 nmol mol -1 for 30 min) under illumination and in darkness and after priming with 200 nmol mol -1 O 3 for 30 min. Methanol and lipoxygenase (LOX) pathway product emissions were induced rapidly, followed by moderate emissions of methyl salicylate (MeSA). Stomatal conductance prior to acute exposure was lower in darkness and after low O 3 priming than in light and without priming. After low O 3 priming, no MeSA and lower LOX emissions were detected under acute exposure. Overall, maximum emission rates and the total amount of emitted LOX products and methanol were quantitatively correlated with total stomatal ozone uptake. These results indicate that different stress volatiles scale differently with ozone dose and highlight the key role of stomatal conductance in controlling ozone uptake, leaf injury and volatile release. © 2017 John Wiley & Sons Ltd.

Acute Alcohol Modulates Cardiac Function as PI3K/Akt Regulates Oxidative Stress

PubMed Central

Umoh, Nsini A.; Walker, Robin K.; Al-Rubaiee, Mustafa; Jeffress, Miara A.; Haddad, Georges E.

2015-01-01

Background Clinical manifestations of alcohol abuse on the cardiac muscle include defective contractility with the development of heart failure. Interestingly, low alcohol consumption has been associated with reduced risk of cardiovascular disease. Although several hypotheses have been postulated for alcoholic cardiomyopathy and for the low-dose beneficial cardiovascular effects, the precise mechanisms and mediators remain largely undefined. We hypothesize that modulation of oxidative stress by PI3K/Akt plays a key role in the cardiac functional outcome to acute alcohol exposure. Methods Thus, acutely exposed rat cardiac tissue and cardiocytes to low (LA: 5 mM), moderate (MA: 25 mM), and high (HA: 100 mM) alcohol were assessed for markers of oxidative stress in the presence and absence of PI3K/Akt activators (IGF-1 0.1 μM or constitutively active PI3K: Ad.BD110 transfection) or inhibitor (LY294002 1 μMor Akt-negative construct Ad.Akt(K179M) transfection). Results Acute LA reduced Akt, superoxide dismutase (SOD-3) and NFκB, ERK1, and p38 MAPK gene expression. Acute HA only increased that of SOD-3 and NFκB. These effects were generally inhibited by Ad.Akt(K179M) and enhanced with Ad.BD110 transfection. In parallel, LA reduced but HA enhanced Akt activity, which was reversed by IGF-1 and inhibited by Ad.Akt(K179M), respectively. Also, LA reduced caspase 3/7 activity and oxidative stress, while HA increased both. The former was blocked, while the latter effect was enhanced by Ad.Akt(K179M). The reverse was true with PI3K/Akt activation. This translated into reduced viability with HA, with no effect with LA. On the functional level, acute LA improved cardiac output and ejection fraction, mainly through increased stroke volume. This was accompanied with enhanced end-systolic pressure–volume relationship and preload recruitable stroke work. Opposite effect was recorded for HA. LA and HA in vivo functional effects were alleviated by LY and enhanced by IGF-1 treatment

Relationship between exposure to pesticides and occurrence of acute leukemia in Iran.

PubMed

Maryam, Zakerinia; Sajad, Amirghofran; Maral, Namdari; Zahra, Lesan; Sima, Pooralimohamad; Zeinab, Attabac; Zahra, Mehravar; Fariba, Ebrahimi; Sezaneh, Haghpanah; Davood, Mehrabani

2015-01-01

One of the causes of acute leukemia can be exposure to certain chemicals such as pesticides. This study determined the relationship between exposure to pesticides and the occurrence of acute leukemia in Fars province, south of Iran. Between April 2011 and April 2013 in a case-control study conducted in Nemazee Hospital in Shiraz, Southern Iran; 314 subjects diagnosed with acute leukemia (94 pediatric cases and 220 adults) were enrolled to determine any correlation between exposure to pesticides and the occurrence. Controls (n=314) were matched by sex and age. There was a history of exposure to pesticides among 85% of pediatric cases and 69% of their controls and 83% of adult cases and 75% of their controls while 87.5% of pediatric cases and 90% of adult cases reported exposure to intermediate and high doses of pesticides and among the controls, the exposure to low doses of pesticides was 70.5% and 65%, respectively. Exposure to indoor pesticides was seen among most of cases and controls. Being a farmer was at a significantly more increased risk of developing acute leukemia in comparison to other jobs, especially for their children. Exposure to pesticides was shown to be one of the most important causes of acute leukemia. It seems that there is a need to educate the people on public health importance of exposure to pesticides especially during school time to reduce the risk of malignancies during childhood.

Seawater inhalation induces acute lung injury via ROS generation and the endoplasmic reticulum stress pathway

PubMed Central

Li, Cong-Cong; Lu, Xi; Qian, Wei-Sheng; Li, Yu-Juan; Jin, Fa-Guang; Mu, De-Guang

2018-01-01

Seawater (SW) inhalation can induce acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). In the present study, SW induced apoptosis of rat alveolar epithelial cells and histopathological alterations to lung tissue. Furthermore, SW administration increased generation of reactive oxygen species (ROS), whereas pretreatment with the ROS scavenger, N-acetyl-L-cysteine (NAC), significantly decreased ROS generation, apoptosis and histopathological alterations. In addition, SW exposure upregulated the expression levels of glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP), which are critical proteins in the endoplasmic reticulum (ER) stress response, thus indicating that SW may activate ER stress. Conversely, blocking ER stress with 4-phenylbutyric acid (4-PBA) significantly improved SW-induced apoptosis and histopathological alterations, whereas an ER stress inducer, thapsigargin, had the opposite effect. Furthermore, blocking ROS with NAC inhibited SW-induced ER stress, as evidenced by the downregulation of GRP78, phosphorylated (p)-protein kinase R-like ER kinase (PERK), p-inositol-requiring kinase 1α (IRE1α), p-50 activating transcription factor 6α and CHOP. In addition, blocking ER stress with 4-PBA decreased ROS generation. In conclusion, the present study indicated that ROS and ER stress pathways, which are involved in alveolar epithelial cell apoptosis, are important in the pathogenesis of SW-induced ALI. PMID:29436612

Oxidative stress induced necroptosis activation is involved in the pathogenesis of hyperoxic acute lung injury.

PubMed

Han, C H; Guan, Z B; Zhang, P X; Fang, H L; Li, L; Zhang, H M; Zhou, F J; Mao, Y F; Liu, W W

2018-01-15

Necroptosis has been found to be involved in the pathogenesis of some lung diseases, but its role in hyperoxic acute lung injury (HALI) is still unclear. This study aimed to investigate contribution of necroptosis to the pathogenesis of HALI induced by hyperbaric hyperoxia exposure in a rat model. Rats were divided into control group, HALI group, Nec-1 (necroptosis inhibitor) group and edaravone group. Rats were exposed to pure oxygen at 250 kPa for 6 h to induce HALI. At 30 min before hyperoxia exposure, rats were intraperitoneally injected with Nec-1 or edaravone, and sacrificed at 24 h after hyperoxia exposure. Lung injury was evaluated by histology, lung water to dry ratio (W/D) and bronchoalveolar lavage fluid (BALF) biochemistry; the serum and plasma oxidative stress, expression of RIP1, RIP3 and MLKL, and interaction between RIP1 and RIP3 were determined. Results showed hyperoxia exposure significantly caused damage to lung and increased necroptotic cells and the expression of RIP1, RIP3 and MLKL. Edaravone pre-treatment not only inhibited the oxidative stress in HALI, but also reduced necroptotic cells, decreased the expression of RIP1, RIP3 and MLKL and improved lung pathology. Nec-1 pretreatment inhibited necroptosis and improved lung pathology, but had little influence on oxidative stress. This study suggests hyperoxia exposure induces oxidative stress may activate necroptosis, involving in the pathology of HALI, and strategies targeting necroptosis may become promising treatments for HALI. Copyright © 2017. Published by Elsevier Inc.

Malondialdehyde-Derived Epitopes In Human Skin Result From Acute Exposure To Solar UV And Occur In Nonmelanoma Skin Cancer Tissue

PubMed Central

Williams, Joshua D.; Bermudez, Yira; Park, Sophia L.; Stratton, Steven P.; Uchida, Koji; Hurst, Craig A.; Wondrak, Georg T.

2014-01-01

Cutaneous exposure to solar ultraviolet radiation (UVR) is a causative factor in photoaging and photocarcinogenesis. In human skin, oxidative stress is widely considered a key mechanism underlying the detrimental effects of acute and chronic UVR exposure. The lipid peroxidation product malondialdehyde (MDA) accumulates in tissue under conditions of increased oxidative stress, and the occurrence of MDA-derived protein epitopes, including dihydropyridine-lysine (DHP), has recently been substantiated in human skin. Here we demonstrate for the first time that acute exposure to sub-apoptogenic doses of solar simulated UV light (SSL) causes the formation of free MDA and protein-bound MDA-derived epitopes in cultured human HaCaT keratinocytes and healthy human skin. Immunohistochemical staining revealed that acute exposure to SSL is sufficient to cause an almost twenty-fold increase in general MDA- and specific DHP-epitope content in human skin. When compared to dose-matched solar simulated UVA, complete SSL was more efficient generating both free MDA and MDA-derived epitopes. Subsequent tissue microarray (TMA) analysis revealed the prevalence of MDA- and DHP-epitopes in nonmelanoma skin cancer (NMSC). In squamous cell carcinoma tissue, both MDA- and DHP-epitopes were increased more than three-fold as compared to adjacent normal tissue. Taken together, these date demonstrate the occurrence of MDA-derived epitopes in both solar UVR-exposed healthy human skin and NMSC TMA tissue; however, the potential utility of these epitopes as novel biomarkers of cutaneous photodamage and a functional role in the process of skin photocarcinogenesis remain to be explored. PMID:24584085

Malondialdehyde-derived epitopes in human skin result from acute exposure to solar UV and occur in nonmelanoma skin cancer tissue.

PubMed

Williams, Joshua D; Bermudez, Yira; Park, Sophia L; Stratton, Steven P; Uchida, Koji; Hurst, Craig A; Wondrak, Georg T

2014-03-05

Cutaneous exposure to solar ultraviolet radiation (UVR) is a causative factor in photoaging and photocarcinogenesis. In human skin, oxidative stress is widely considered a key mechanism underlying the detrimental effects of acute and chronic UVR exposure. The lipid peroxidation product malondialdehyde (MDA) accumulates in tissue under conditions of increased oxidative stress, and the occurrence of MDA-derived protein epitopes, including dihydropyridine-lysine (DHP), has recently been substantiated in human skin. Here we demonstrate for the first time that acute exposure to sub-apoptogenic doses of solar simulated UV light (SSL) causes the formation of free MDA and protein-bound MDA-derived epitopes in cultured human HaCaT keratinocytes and healthy human skin. Immunohistochemical staining revealed that acute exposure to SSL is sufficient to cause an almost twenty-fold increase in general MDA- and specific DHP-epitope content in human skin. When compared to dose-matched solar simulated UVA, complete SSL was more efficient generating both free MDA and MDA-derived epitopes. Subsequent tissue microarray (TMA) analysis revealed the prevalence of MDA- and DHP-epitopes in nonmelanoma skin cancer (NMSC). In squamous cell carcinoma tissue, both MDA- and DHP-epitopes were increased more than threefold as compared to adjacent normal tissue. Taken together, these date demonstrate the occurrence of MDA-derived epitopes in both solar UVR-exposed healthy human skin and NMSC TMA tissue; however, the potential utility of these epitopes as novel biomarkers of cutaneous photodamage and a functional role in the process of skin photocarcinogenesis remain to be explored. Copyright © 2014 Elsevier B.V. All rights reserved.

Trait Hostility and Acute Inflammatory Responses to Stress in the Laboratory

PubMed Central

Girard, Dominique; Tardif, Jean-Claude; Boisclair Demarble, Julie; D’Antono, Bianca

2016-01-01

Hostility has been associated with higher basal levels of inflammation. The present study evaluated the association of hostility with acute stress-induced changes in inflammatory activity. One hundred and ninety-nine healthy men and women, aged 19–64 years, were exposed to a stress protocol involving four interpersonal stressors. Participants completed the Cook-Medley Hostility questionnaire and provided two blood samples for the measurement of inflammatory biomarkers (CRP, Il-6, MPO, TNF-α, MCP-1, Il-8, Il-10, and Il-18), prior to and following exposure to a standardized stress protocol. In univariate analyses, hostility was associated with significantly higher TNF-α, but lower Il-8 and Il-18 values post-stress, though only Il-8 remained significant after controlling for baseline differences. In multivariate analyses, a significant Age by Hostility interaction emerged for Il-6, while sex moderated the relation between hostility and Il-10 reactivity. Following stress, hostility was associated with greater pro-inflammatory Il-6 activity among younger individuals and to decreased anti-inflammatory Il-10 activity in women. Future research is needed to replicate these findings and to evaluate their implication for disease. PMID:27270459

Prior exposure to capture heightens the corticosterone and behavioural responses of little penguins (Eudyptula minor) to acute stress

PubMed Central

Carroll, Gemma; Turner, Emma; Dann, Peter; Harcourt, Rob

2016-01-01

Studies of physiology can provide important insight into how animals are coping with challenges in their environment and can signal the potential effects of exposure to human activity in both the short and long term. In this study, we measured the physiological and behavioural response of little penguins (Eudyptula minor) that were naïve to human activity over 30 min of capture and handling. We assessed relationships between corticosterone secretion, behaviour, sex and time of day in order to characterize the determinants of the natural stress response. We then compared the response of these naïve penguins with the responses of female little penguins that had been exposed to research activity (bimonthly nest check and weighing) and to both research activity (monthly nest check and weighing) and evening viewing by tourists. We found that corticosterone concentrations increased significantly over 30 min of capture, with naïve penguins demonstrating a more acute stress response during the day than at night. Penguins that had previously been exposed to handling at the research and research/visitor sites showed elevated corticosterone concentrations and consistently more aggressive behaviour after 30 min compared with naïve birds, although there were no significant differences in baseline corticosterone concentrations. Our findings demonstrate that these little penguins have not habituated to routine capture, but rather mount a heightened physiological and behavioural response to handling by humans. Less invasive research monitoring techniques, such as individual identification with PIT tags and automatic recording and weighing, and a reduction in handling during the day should be considered to mitigate some of the potentially negative effects of disturbance. Given the paucity of data on the long-term consequences of heightened stress on animal physiology, our study highlights the need for further investigation of the relationship between the corticosterone

Prior exposure to capture heightens the corticosterone and behavioural responses of little penguins (Eudyptula minor) to acute stress.

PubMed

Carroll, Gemma; Turner, Emma; Dann, Peter; Harcourt, Rob

2016-01-01

Studies of physiology can provide important insight into how animals are coping with challenges in their environment and can signal the potential effects of exposure to human activity in both the short and long term. In this study, we measured the physiological and behavioural response of little penguins (Eudyptula minor) that were naïve to human activity over 30 min of capture and handling. We assessed relationships between corticosterone secretion, behaviour, sex and time of day in order to characterize the determinants of the natural stress response. We then compared the response of these naïve penguins with the responses of female little penguins that had been exposed to research activity (bimonthly nest check and weighing) and to both research activity (monthly nest check and weighing) and evening viewing by tourists. We found that corticosterone concentrations increased significantly over 30 min of capture, with naïve penguins demonstrating a more acute stress response during the day than at night. Penguins that had previously been exposed to handling at the research and research/visitor sites showed elevated corticosterone concentrations and consistently more aggressive behaviour after 30 min compared with naïve birds, although there were no significant differences in baseline corticosterone concentrations. Our findings demonstrate that these little penguins have not habituated to routine capture, but rather mount a heightened physiological and behavioural response to handling by humans. Less invasive research monitoring techniques, such as individual identification with PIT tags and automatic recording and weighing, and a reduction in handling during the day should be considered to mitigate some of the potentially negative effects of disturbance. Given the paucity of data on the long-term consequences of heightened stress on animal physiology, our study highlights the need for further investigation of the relationship between the corticosterone

Does Acute Stress Disorder Predict Posttraumatic Stress Disorder Following Bank Robbery?

ERIC Educational Resources Information Center

Hansen, Maj; Elklit, Ask

2013-01-01

Unfortunately, the number of bank robberies is increasing and little is known about the subsequent risk of posttraumatic stress disorder (PTSD). Several studies have investigated the prediction of PTSD through the presence of acute stress disorder (ASD). However, there have only been a few studies following nonsexual assault. The present study…

Prefrontal Cortex Corticotropin-Releasing Factor Receptor 1 Conveys Acute Stress-Induced Executive Dysfunction.

PubMed

Uribe-Mariño, Andrés; Gassen, Nils C; Wiesbeck, Maximilian F; Balsevich, Georgia; Santarelli, Sara; Solfrank, Beate; Dournes, Carine; Fries, Gabriel R; Masana, Merce; Labermeier, Christiana; Wang, Xiao-Dong; Hafner, Kathrin; Schmid, Bianca; Rein, Theo; Chen, Alon; Deussing, Jan M; Schmidt, Mathias V

2016-11-15

The medial prefrontal cortex (mPFC) subserves complex cognition and is impaired by stress. Corticotropin-releasing factor (CRF), through CRF receptor 1 (CRFR1), constitutes a key element of the stress response. However, its contribution to the effects of stress in the mPFC remains unclear. Mice were exposed to acute social defeat stress and subsequently to either the temporal order memory (n = 11-12) or reversal learning (n = 9-11) behavioral test. Changes in mPFC Crhr1 messenger RNA levels were measured in acutely stressed mice (n = 12). Crhr1 loxP/loxP mice received either intra-mPFC adeno-associated virus-Cre or empty microinjections (n = 17-20) and then were submitted to acute stress and later to the behavioral tests. Co-immunoprecipitation was used to detect activation of the protein kinase A (PKA) signaling pathway in the mPFC of acutely stressed mice (n = 8) or intra-mPFC CRF injected mice (n = 7). Finally, mice received intra-mPFC CRF (n = 11) and/or Rp-isomer cyclic adenosine 3',5' monophosphorothioate (Rp-cAMPS) (n = 12) microinjections and underwent behavioral testing. We report acute stress-induced effects on mPFC-mediated cognition, identify CRF-CRFR1-containing microcircuits within the mPFC, and demonstrate stress-induced changes in Crhr1 messenger RNA expression. Importantly, intra-mPFC CRFR1 deletion abolishes acute stress-induced executive dysfunction, whereas intra-mPFC CRF mimics acute stress-induced mPFC dysfunction. Acute stress and intra-mPFC CRF activate the PKA signaling pathway in the mPFC, leading to cyclic AMP response element binding protein phosphorylation in intra-mPFC CRFR1-expressing neurons. Finally, PKA blockade reverses the intra-mPFC CRF-induced executive dysfunction. Taken together, these results unravel a molecular mechanism linking acute stress to executive dysfunction via CRFR1. This will aid in the development of novel therapeutic targets for stress-induced cognitive dysfunction. Copyright © 2016 Society of Biological

Effects of acute ethanol exposure on cytokine production by primary airway smooth muscle cells

DOE Office of Scientific and Technical Information (OSTI.GOV)

Kaphalia, Lata; Kalita, Mridul; Kaphalia, Bhupendra S.

Both chronic and binge alcohol abuse can be significant risk factors for inflammatory lung diseases such as acute respiratory distress syndrome and chronic obstructive pulmonary disease. However, metabolic basis of alcohol-related lung disease is not well defined, and may include key metabolites of ethanol [EtOH] in addition to EtOH itself. Therefore, we investigated the effects of EtOH, acetaldehyde [ACE], and fatty acid ethyl esters [FAEEs] on oxidative stress, endoplasmic reticulum (ER) stress, AMP-activated protein kinase (AMPK) signaling and nuclear translocation of phosphorylated (p)-NF-κB p65 in primary human airway smooth muscle (HASM) cells stimulated to produce cytokines using LPS exposure. Bothmore » FAEEs and ACE induced evidence of cellular oxidative stress and ER stress, and increased p-NF-κB in nuclear extracts. EtOH and its metabolites decreased p-AMPKα activation, and induced expression of fatty acid synthase, and decreased expression of sirtuin 1. In general, EtOH decreased secretion of IP-10, IL-6, eotaxin, GCSF, and MCP-1. However, FAEEs and ACE increased these cytokines, suggesting that both FAEEs and ACE as compared to EtOH itself are proinflammatory. A direct effect of EtOH could be consistent with blunted immune response. Collectively, these two features of EtOH exposure, coupled with the known inhibition of innate immune response in our model might explain some clinical manifestations of EtOH exposure in the lung. - Highlights: • Metabolic basis for EtOH toxicity was studied in human airway smooth muscle (HASM) cells. • In HASM cells, EtOH metabolites were found to be relatively more toxic than EtOH itself. • EtOH metabolites mediate deactivation of AMPK via oxidative stress and ER stress. • EtOH metabolites were found to be more proinflammatory than EtOH itself in HASM cells.« less

Increases in anxiety-like behavior induced by acute stress are reversed by ethanol in adolescent but not adult rats.

PubMed

Varlinskaya, Elena I; Spear, Linda P

2012-01-01

Repeated exposure to stressors has been found to increase anxiety-like behavior in laboratory rodents, with the social anxiety induced by repeated restraint being extremely sensitive to anxiolytic effects of ethanol in both adolescent and adult rats. No studies, however, have compared social anxiogenic effects of acute stress or the capacity of ethanol to reverse this anxiety in adolescent and adult animals. Therefore, the present study was designed to investigate whether adolescent [postnatal day (P35)] Sprague-Dawley rats differ from their adult counterparts (P70) in the impact of acute restraint stress on social anxiety and in their sensitivity to the social anxiolytic effects of ethanol. Animals were restrained for 90 min, followed by examination of stress- and ethanol-induced (0, 0.25, 0.5, 0.75, and 1 g/kg) alterations in social behavior using a modified social interaction test in a familiar environment. Acute restraint stress increased anxiety, as indexed by reduced levels of social investigation at both ages, and decreased social preference among adolescents. These increases in anxiety were dramatically reversed among adolescents by acute ethanol. No anxiolytic-like effects of ethanol emerged following restraint stress in adults. The social suppression seen in response to higher doses of ethanol was reversed by restraint stress in animals of both ages. To the extent that these data are applicable to humans, the results of the present study provide some experimental evidence that stressful life events may increase the attractiveness of alcohol as an anxiolytic agent for adolescents. Copyright © 2011 Elsevier Inc. All rights reserved.

Serotonin regulates brain-derived neurotrophic factor expression in select brain regions during acute psychological stress

PubMed Central

Jiang, De-guo; Jin, Shi-li; Li, Gong-ying; Li, Qing-qing; Li, Zhi-ruo; Ma, Hong-xia; Zhuo, Chuan-jun; Jiang, Rong-huan; Ye, Min-jie

2016-01-01

Previous studies suggest that serotonin (5-HT) might interact with brain-derived neurotrophic factor (BDNF) during the stress response. However, the relationship between 5-HT and BDNF expression under purely psychological stress is unclear. In this study, one hour before psychological stress exposure, the 5-HT1A receptor agonist 8-OH-DPAT or antagonist MDL73005, or the 5-HT2A receptor agonist DOI or antagonist ketanserin were administered to rats exposed to psychological stress. Immunohistochemistry and in situ hybridization revealed that after psychological stress, with the exception of the ventral tegmental area, BDNF protein and mRNA expression levels were higher in the 5-HT1A and the 5-HT2A receptor agonist groups compared with the solvent control no-stress or psychological stress group in the CA1 and CA3 of the hippocampus, prefrontal cortex, central amygdaloid nucleus, dorsomedial hypothalamic nucleus, dentate gyrus, shell of the nucleus accumbens and the midbrain periaqueductal gray. There was no significant difference between the two agonist groups. In contrast, after stress exposure, BDNF protein and mRNA expression levels were lower in the 5-HT1A and 5-HT2A receptor antagonist groups than in the solvent control non-stress group, with the exception of the ventral tegmental area. Our findings suggest that 5-HT regulates BDNF expression in a rat model of acute psychological stress. PMID:27857753

Social media as a shield: Facebook buffers acute stress.

PubMed

Rus, Holly M; Tiemensma, Jitske

2018-03-01

Facebook remains the most widely used social media platform. Research suggests that Facebook may both enhance and undermine psychosocial constructs related to well-being, and that it may impair physiological stress recovery. However, little is known about its influence on stress reactivity. Using novel experimental methods, this study examined how Facebook influences reactivity to an acute social stressor. Facebook users (n=104, 53 males, mean age 19.50, SD=1.73) were randomly assigned to use their own Facebook account or sit quietly with the option of reading electronic magazines before experiencing an acute social stressor. All participants showed significant changes in subjective and physiological stress markers in response to the stressor. However, participants who used Facebook experienced lower levels of psychosocial stress, physiological stress, and rated the stressor as less threatening (p's<0.05) when controlling for gender and emotional investment in the website compared to controls. Results suggest that Facebook use may buffer stress-in particular psychosocial stress-if used before experiencing an acute social stressor. This study is among the first to incorporate both objective and subjective measures in investigating the complex relationship between Facebook use and well-being. Copyright © 2017 Elsevier Inc. All rights reserved.

Seasonal variations in the physiological stress response to discrete bouts of aerial exposure in the little skate, Leucoraja erinacea.

PubMed

Cicia, Angela M; Schlenker, Lela S; Sulikowski, James A; Mandelman, John W

2012-06-01

Aerial exposure and acute thermal stress have been shown to elicit profound physiological disruptions in obligate water-breathing teleosts. However, no study has investigated these responses in an elasmobranch. To address this, venous blood samples were collected and evaluated from little skates (Leucoraja erinacea) subjected to discrete aerial exposure durations (0, 15, and 50 min) coupled with differing abrupt thermal changes (gradient between seawater and air; winter: ΔT=-3 °C; summer: ΔT=+9 °C) in two distinct laboratory studies. In general, blood acid-base properties (e.g. decline in pH; elevation in PCO(2)) and select metabolites (elevated whole-blood lactate) and electrolytes (elevated plasma K(+)) were significantly disrupted by aerial exposure, and were most disturbed after skates were exposed to air for 50 min. However, the magnitude of the blood acid-base perturbations, metabolic contribution to the resulting blood acidosis, elevations to ionic and metabolic parameters, and delayed mortality were more extreme during the summer study, suggesting that acute thermal stress exacerbates the physiological impairments associated with aerial exposure in little skates. Conversely, a reduced thermal gradient (from seawater to air) may attenuate the magnitude of metabolic and ionic perturbations, resulting in a high physiological threshold for coping with extended aerial exposure. Copyright © 2011 Elsevier Inc. All rights reserved.

Microglial activation as a measure of stress in mouse brains exposed acutely (60 minutes) and long-term (2 years) to mobile telephone radiofrequency fields.

PubMed

Finnie, John W; Cai, Zhao; Manavis, Jim; Helps, Stephen; Blumbergs, Peter C

2010-02-01

To determine whether acute or long-term exposure of the brain to mobile telephone radiofrequency (RF) fields produces activation of microglia, which normally respond rapidly to any change in their microenvironment. Using a purpose designed exposure system at 900 MHz, mice were given a single, far-field whole body exposure at a specific absorption rate (SAR) of 4 W/kg for 60 min (acute) or on five successive days per week for 104 weeks (long-term). Control mice were sham-exposed or freely mobile in a cage to control for any stress caused by immobilisation in the exposure module. Positive control brains subjected to a stab wound were also included to confirm the ability of microglia to react to any neural stress. Brains were perfusion-fixed with 4% paraformaldehyde and representative regions of the cerebral cortex and hippocampus immunostained for ionised calcium binding adaptor molecule (Iba1), a specific microglial marker. There was no increase in microglial Iba1 expression in brains short or long-term exposed to mobile telephony microwaves compared to control (sham-exposed or freely moving caged mice) brains, while substantial microglial activation occurred in damaged positive control neural tissue. Acute (60 minutes) or longer duration (2 years) exposure of murine brains to mobile telephone RF fields did not produce any microglial activation detectable by Iba1 immunostaining.

Effects of acute ethanol administration and chronic stress exposure on social investigation and 50kHz ultrasonic vocalizations in adolescent and adult male Sprague-Dawley rats.

PubMed

Willey, Amanda R; Spear, Linda P

2013-04-01

Adolescents drink largely in social situations, likely in an attempt to facilitate social interactions. This study sought to examine alterations in the incentive salience of a social stimulus following repeated stress exposure and acute ethanol administration in adolescent and adult male Sprague-Dawley rats. Subjects were either exposed to 5days of restraint stress, chronic variable stress (CVS), which consisted of a different stressor every day, or non-stressed. On test day, the animals were injected with 0, 0.25, 0.5, or 0.75g/kg ethanol and placed in a social approach test in which they could see, hear, and smell a social conspecific, but could not physically interact with it. All the animals showed an interest in the social stimulus, with adolescents engaging in more social investigation than adults. Restraint stressed adults showed ethanol-induced increases in social investigation, while ethanol effects were not seen in any other group. An ethanol-associated increase in 50kHz ultrasonic vocalization (USV) production was only evident in restraint stressed adolescents following 0.75g/kg ethanol. 50kHz USVs were not correlated with time spent investigating the social stimulus in any test condition. These results show that age differences in the facilitatory effects of ethanol on incentive salience of social stimuli are moderated by stress, with the facilitation of social approach by ethanol only evident in restraint stressed adults. Copyright © 2013 Elsevier Inc. All rights reserved.

Loneliness and acute stress reactivity: A systematic review of psychophysiological studies.

PubMed

Brown, Eoin G; Gallagher, Stephen; Creaven, Ann-Marie

2018-05-01

Physiological reactivity to acute stress has been proposed as a potential biological mechanism by which loneliness may lead to negative health outcomes such as cardiovascular disease. This review was conducted to investigate the association between loneliness and physiological responses to acute stress. A series of electronic databases were systematically searched (PsycARTICLES, PsycINFO, Medline, CINAHL Plus, EBSCOhost, PubMed, SCOPUS, Web of Science, Science Direct) for relevant studies, published up to October 2016. Eleven studies were included in the review. Overall, the majority of studies reported positive associations between loneliness and acute stress responses, such that higher levels of loneliness were predictive of exaggerated physiological reactions. However, in a few studies, loneliness was also linked with decreased stress responses for particular physiological outcomes, indicating the possible existence of blunted relationships. There was no clear pattern suggesting any sex- or stressor-based differences in these associations. The available evidence supports a link between loneliness and atypical physiological reactivity to acute stress. A key finding of this review was that greater levels of loneliness are associated with exaggerated blood pressure and inflammatory reactivity to acute stress. However, there was some indication that loneliness may also be related to blunted cardiac, cortisol, and immune responses. Overall, this suggests that stress reactivity could be one of the biological mechanisms through which loneliness impacts upon health. © 2017 Society for Psychophysiological Research.

Parent-Child Agreement Regarding Children's Acute Stress: The Role of Parent Acute Stress Reactions

ERIC Educational Resources Information Center

Kassam-Adams, Nancy; Garcia-Espana, J. Felipe; Miller, Victoria A.; Winston, Flaura

2006-01-01

Objective: We examined parent--child agreement regarding child acute stress disorder (ASD) and the relationship between parent ASD symptoms and parent ratings of child ASD. Method: Parent-child dyads (N = 219; child age 8-17 years) were assessed within 1 month of child injury. Parent--child agreement was examined regarding child ASD presence,…

Manganese-enhanced magnetic resonance imaging (MEMRI) reveals brain circuitry involved in responding to an acute novel stress in rats with a history of repeated social stress.

PubMed

Bangasser, Debra A; Lee, Catherine S; Cook, Philip A; Gee, James C; Bhatnagar, Seema; Valentino, Rita J

2013-10-02

Responses to acute stressors are determined in part by stress history. For example, a history of chronic stress results in facilitated responses to a novel stressor and this facilitation is considered to be adaptive. We previously demonstrated that repeated exposure of rats to the resident-intruder model of social stress results in the emergence of two subpopulations that are characterized by different coping responses to stress. The submissive subpopulation failed to show facilitation to a novel stressor and developed a passive strategy in the Porsolt forced swim test. Because a passive stress coping response has been implicated in the propensity to develop certain psychiatric disorders, understanding the unique circuitry engaged by exposure to a novel stressor in these subpopulations would advance our understanding of the etiology of stress-related pathology. An ex vivo functional imaging technique, manganese-enhanced magnetic resonance imaging (MEMRI), was used to identify and distinguish brain regions that are differentially activated by an acute swim stress (15 min) in rats with a history of social stress compared to controls. Specifically, Mn(2+) was administered intracerebroventricularly prior to swim stress and brains were later imaged ex vivo to reveal activated structures. When compared to controls, all rats with a history of social stress showed greater activation in specific striatal, hippocampal, hypothalamic, and midbrain regions. The submissive subpopulation of rats was further distinguished by significantly greater activation in amygdala, bed nucleus of the stria terminalis, and septum, suggesting that these regions may form a circuit mediating responses to novel stress in individuals that adopt passive coping strategies. The finding that different circuits are engaged by a novel stressor in the two subpopulations of rats exposed to social stress implicates a role for these circuits in determining individual strategies for responding to stressors

Acute stress induces selective alterations in cost/benefit decision-making.

PubMed

Shafiei, Naghmeh; Gray, Megan; Viau, Victor; Floresco, Stan B

2012-09-01

Acute stress can exert beneficial or detrimental effects on different forms of cognition. In the present study, we assessed the effects of acute restraint stress on different forms of cost/benefit decision-making, and some of the hormonal and neurochemical mechanisms that may underlie these effects. Effort-based decision-making was assessed where rats chose between a low effort/reward (1 press=2 pellets) or high effort/reward option (4 pellets), with the effort requirement increasing over 4 blocks of trials (2, 5, 10, and 20 lever presses). Restraint stress for 1 h decreased preference for the more costly reward and induced longer choice latencies. Control experiments revealed that the effects on decision-making were not mediated by general reductions in motivation or preference for larger rewards. In contrast, acute stress did not affect delay-discounting, when rats chose between a small/immediate vs larger/delayed reward. The effects of stress on decision-making were not mimicked by treatment with physiological doses of corticosterone (1-3 mg/kg). Blockade of dopamine receptors with flupenthixol (0.25 mg/kg) before restraint did not attenuate stress-induced effects on effort-related choice, but abolished effects on choice latencies. These data suggest that acute stress interferes somewhat selectively with cost/benefit evaluations concerning effort costs. These effects do not appear to be mediated solely by enhanced glucocorticoid activity, whereas dopaminergic activation may contribute to increased deliberation times induced by stress. These findings may provide insight into impairments in decision-making and anergia associated with stress-related disorders, such as depression.

Acute Stress Induces Selective Alterations in Cost/Benefit Decision-Making

PubMed Central

Shafiei, Naghmeh; Gray, Megan; Viau, Victor; Floresco, Stan B

2012-01-01

Acute stress can exert beneficial or detrimental effects on different forms of cognition. In the present study, we assessed the effects of acute restraint stress on different forms of cost/benefit decision-making, and some of the hormonal and neurochemical mechanisms that may underlie these effects. Effort-based decision-making was assessed where rats chose between a low effort/reward (1 press=2 pellets) or high effort/reward option (4 pellets), with the effort requirement increasing over 4 blocks of trials (2, 5, 10, and 20 lever presses). Restraint stress for 1 h decreased preference for the more costly reward and induced longer choice latencies. Control experiments revealed that the effects on decision-making were not mediated by general reductions in motivation or preference for larger rewards. In contrast, acute stress did not affect delay-discounting, when rats chose between a small/immediate vs larger/delayed reward. The effects of stress on decision-making were not mimicked by treatment with physiological doses of corticosterone (1–3 mg/kg). Blockade of dopamine receptors with flupenthixol (0.25 mg/kg) before restraint did not attenuate stress-induced effects on effort-related choice, but abolished effects on choice latencies. These data suggest that acute stress interferes somewhat selectively with cost/benefit evaluations concerning effort costs. These effects do not appear to be mediated solely by enhanced glucocorticoid activity, whereas dopaminergic activation may contribute to increased deliberation times induced by stress. These findings may provide insight into impairments in decision-making and anergia associated with stress-related disorders, such as depression. PMID:22569506

Negative Energy Balance Blocks Neural and Behavioral Responses to Acute Stress by "Silencing" Central Glucagon-Like Peptide 1 Signaling in Rats.

PubMed

Maniscalco, James W; Zheng, Huiyuan; Gordon, Patrick J; Rinaman, Linda

2015-07-29

Previous reports indicate that caloric restriction attenuates anxiety and other behavioral responses to acute stress, and blunts the ability of stress to increase anterior pituitary release of adrenocorticotropic hormone. Since hindbrain glucagon-like peptide-1 (GLP-1) neurons and noradrenergic prolactin-releasing peptide (PrRP) neurons participate in behavioral and endocrine stress responses, and are sensitive to the metabolic state, we examined whether overnight food deprivation blunts stress-induced recruitment of these neurons and their downstream hypothalamic and limbic forebrain targets. A single overnight fast reduced anxiety-like behavior assessed in the elevated-plus maze and acoustic startle test, including marked attenuation of light-enhanced startle. Acute stress [i.e., 30 min restraint (RES) or 5 min elevated platform exposure] robustly activated c-Fos in GLP-1 and PrRP neurons in fed rats, but not in fasted rats. Fasting also significantly blunted the ability of acute stress to activate c-Fos expression within the anterior ventrolateral bed nucleus of the stria terminalis (vlBST). Acute RES stress suppressed dark-onset food intake in rats that were fed ad libitum, whereas central infusion of a GLP-1 receptor antagonist blocked RES-induced hypophagia, and reduced the ability of RES to activate PrRP and anterior vlBST neurons in ad libitum-fed rats. Thus, an overnight fast "silences" GLP-1 and PrRP neurons, and reduces both anxiety-like and hypophagic responses to acute stress. The partial mimicking of these fasting-induced effects in ad libitum-fed rats after GLP-1 receptor antagonism suggests a potential mechanism by which short-term negative energy balance attenuates neuroendocrine and behavioral responses to acute stress. The results from this study reveal a potential central mechanism for the "metabolic tuning" of stress responsiveness. A single overnight fast, which markedly reduces anxiety-like behavior in rats, reduces or blocks the ability of

Seawater inhalation induces acute lung injury via ROS generation and the endoplasmic reticulum stress pathway.

PubMed

Li, Peng-Cheng; Wang, Bo-Rong; Li, Cong-Cong; Lu, Xi; Qian, Wei-Sheng; Li, Yu-Juan; Jin, Fa-Guang; Mu, De-Guang

2018-05-01

Seawater (SW) inhalation can induce acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). In the present study, SW induced apoptosis of rat alveolar epithelial cells and histopathological alterations to lung tissue. Furthermore, SW administration increased generation of reactive oxygen species (ROS), whereas pretreatment with the ROS scavenger, N‑acetyl‑L‑cysteine (NAC), significantly decreased ROS generation, apoptosis and histopathological alterations. In addition, SW exposure upregulated the expression levels of glucose‑regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP), which are critical proteins in the endoplasmic reticulum (ER) stress response, thus indicating that SW may activate ER stress. Conversely, blocking ER stress with 4‑phenylbutyric acid (4‑PBA) significantly improved SW‑induced apoptosis and histopathological alterations, whereas an ER stress inducer, thapsigargin, had the opposite effect. Furthermore, blocking ROS with NAC inhibited SW‑induced ER stress, as evidenced by the downregulation of GRP78, phosphorylated (p)‑protein kinase R‑like ER kinase (PERK), p‑inositol‑requiring kinase 1α (IRE1α), p‑50 activating transcription factor 6α and CHOP. In addition, blocking ER stress with 4‑PBA decreased ROS generation. In conclusion, the present study indicated that ROS and ER stress pathways, which are involved in alveolar epithelial cell apoptosis, are important in the pathogenesis of SW‑induced ALI.

Psychopathy, traumatic exposure, and lifetime posttraumatic stress.

PubMed

Willemsen, Jochem; De Ganck, Julie; Verhaeghe, Paul

2012-06-01

This study examined two theoretical models on the interaction between psychopathy, traumatic exposure, and lifetime posttraumatic stress in a sample of 81 male detainees. In Model 1, the interpersonal and affective features of psychopathy were assumed to protect against posttraumatic stress. In Model 2, the lifestyle and antisocial traits of psychopathy were assumed to lead to a lifestyle that increases the risk of traumatic exposure and subsequent posttraumatic stress. The authors found significant negative bivariate associations between Psychopathy Checklist-Revised (PCL-R) total, Interpersonal and Affective facet scores, and posttraumatic stress. Model 1 was confirmed, as they found the interaction between the Affective facet and traumatic exposure had a significant negative effect on posttraumatic stress. Model 2 was rejected. The authors' findings confirm that the interpersonal and affective features of psychopathy are associated with an emotional deficit and that the affective features of psychopathy are crucial for understanding the relationship between psychopathy and anxiety.

Cold stress aggravates inflammatory responses in an LPS-induced mouse model of acute lung injury

NASA Astrophysics Data System (ADS)

Joo, Su-Yeon; Park, Mi-Ju; Kim, Kyun-Ha; Choi, Hee-Jung; Chung, Tae-Wook; Kim, Yong Jin; Kim, Joung Hee; Kim, Keuk-Jun; Joo, Myungsoo; Ha, Ki-Tae

2016-08-01

Although the relationship between environmental cold temperature and susceptibility to respiratory infection is generally accepted, the effect of ambient cold temperature on host reactivity in lung inflammation has not been fully studied. To examine the function of ambient cold temperature on lung inflammation, mice were exposed to 4 °C for 8 h each day for 14 days. In the lungs of mice exposed to cold stress, inflammatory cells in bronchoalveolar lavage (BAL) fluid and lung tissues were slightly increased by about twofold. However, the structures of pulmonary epithelial cells were kept within normal limits. Next, we examined the effect of cold stress on the inflammatory responses in a lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse model. The infiltration of neutrophils and inflammation of lung tissue determined by histology were significantly increased by exposure to ambient cold temperature. In addition, the production of pro-inflammatory cytokines including interleukin (IL)-12, IL-17, and monokine induced by gamma interferon (MIG) was elevated by exposure to cold stress. Therefore, we suggest that cold stress is a factor that exacerbates lung inflammation including ALI. To our knowledge, this is the first report on the relationship between cold stress and severity of lung inflammation.

Stress-dependent changes in neuroinflammatory markers observed after common laboratory stressors are not seen following acute social defeat of the Sprague Dawley rat.

PubMed

Hueston, Cara M; Barnum, Christopher J; Eberle, Jaime A; Ferraioli, Frank J; Buck, Hollin M; Deak, Terrence

2011-08-03

Exposure to acute stress has been shown to increase the expression of pro-inflammatory cytokines in brain, blood and peripheral organs. However, the nature of the inflammatory response evoked by acute stress varies depending on the stressor used and species examined. The goal of the following series of studies was to characterize the consequences of social defeat in the Sprague Dawley (SD) rat using three different social defeat paradigms. In Experiments 1 and 2, adult male SD rats were exposed to a typical acute resident-intruder paradigm of social defeat (60 min) by placement into the home cage of a larger, aggressive Long Evans rat and brain tissue was collected at multiple time points for analysis of IL-1β protein and gene expression changes in the PVN, BNST and adrenal glands. In subsequent experiments, rats were exposed to once daily social defeat for 7 or 21 days (Experiment 3) or housed continuously with an aggressive partner (separated by a partition) for 7 days (Experiment 4) to assess the impact of chronic social stress on inflammatory measures. Despite the fact that social defeat produced a comparable corticosterone response as other stressors (restraint, forced swim and footshock; Experiment 5), acute social defeat did not affect inflammatory measures. A small but reliable increase in IL-1 gene expression was observed immediately after the 7th exposure to social defeat, while other inflammatory measures were unaffected. In contrast, restraint, forced swim and footshock all significantly increased IL-1 gene expression in the PVN; other inflammatory factors (IL-6, cox-2) were unaffected in this structure. These findings provide a comprehensive evaluation of stress-dependent inflammatory changes in the SD rat, raising intriguing questions regarding the features of the stress challenge that may be predictive of stress-dependent neuroinflammation. Copyright © 2011 Elsevier Inc. All rights reserved.

Aging Exacerbates Neuroinflammatory Outcomes Induced by Acute Ozone Exposure.

PubMed

Tyler, Christina R; Noor, Shahani; Young, Tamara L; Rivero, Valeria; Sanchez, Bethany; Lucas, Selita; Caldwell, Kevin K; Milligan, Erin D; Campen, Matthew J

2018-05-01

The role of environmental stressors, particularly exposure to air pollution, in the development of neurodegenerative disease remains underappreciated. We examined the neurological effects of acute ozone (O3) exposure in aged mice, where increased blood-brain barrier (BBB) permeability may confer vulnerability to neuroinflammatory outcomes. C57BL/6 male mice, aged 8-10 weeks or 12-18 months were exposed to either filtered air or 1.0 ppm O3 for 4 h; animals received a single IP injection of sodium fluorescein (FSCN) 20 h postexposure. One-hour post-FSCN injection, animals were transcardially perfused for immunohistochemical analysis of BBB permeability. β-amyloid protein expression was assessed via ELISA. Flow cytometric characterization of infiltrating immune cells, including neutrophils, macrophages, and microglia populations was performed 20 h post-O3 exposure. Flow cytometry analysis of brains revealed increased microglia "activation" and presentation of CD11b, F4/80, and MHCII in aged animals relative to younger ones; these age-induced differences were potentiated by acute O3 exposure. Cortical and limbic regions in aged brains had increased reactive microgliosis and β-amyloid protein expression after O3 insult. The aged cerebellum was particularly vulnerable to acute O3 exposure with increased populations of infiltrating neutrophils, peripheral macrophages/monocytes, and Ly6C+ inflammatory monocytes after insult, which were not significantly increased in the young cerebellum. O3 exposure increased the penetration of FSCN beyond the BBB, the infiltration of peripheral immune cells, and reactive gliosis of microglia. Thus, the aged BBB is vulnerable to insult and becomes highly penetrable in response to O3 exposure, leading to greater neuroinflammatory outcomes.

Low lifetime stress exposure is associated with reduced stimulus–response memory

PubMed Central

Goldfarb, Elizabeth V.; Shields, Grant S.; Daw, Nathaniel D.; Slavich, George M.; Phelps, Elizabeth A.

2017-01-01

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. PMID:28298555

Aging Exacerbates Neuroinflammatory Outcomes Induced by Acute Ozone Exposure

DOE PAGES

Tyler, Christina R.; Noor, Shahani; Young, Tamara; ...

2018-01-27

The role of environmental stressors, particularly exposure to air pollution, in the development of neurodegenerative disease remains underappreciated. We examined the neurological effects of acute ozone (O 3) exposure in aged mice, where increased blood brain barrier (BBB) permeability may confer vulnerability to neuroinflammatory outcomes. C 57BL/6 male mice, aged 8-10 weeks or 12–18 months were exposed to either filtered air (FA) or 1.0 ppm O 3 for 4 hours; animals received a single IP injection of sodium fluorescein (FSCN) 20 hours post-exposure. One-hour post-FSCN injection, animals were transcardially perfused for immunohistochemical analysis of BBB permeability. β-amyloid protein expression wasmore » assessed via ELISA. Flow cytometric characterization of infiltrating immune cells, including neutrophils, macrophages, and microglia populations was performed 20 hours post-O 3 exposure. Flow cytometry analysis of brains revealed increased microglia “activation” and presentation of CD11b, F4/80 and MHCII in aged animals relative to younger ones; these age-induced differences were potentiated by acute O 3 exposure. Cortical and limbic regions in aged brains had increased reactive microgliosis and β-amyloid protein expression after O 3 insult. The aged cerebellum was particularly vulnerable to acute O 3 exposure with increased populations of infiltrating neutrophils, peripheral macrophages/monocytes, and Ly6C + inflammatory monocytes after insult, which were not significantly increased in the young cerebellum. O 3 exposure increased the penetration of FSCN beyond the BBB, the infiltration of peripheral immune cells, and reactive gliosis of microglia. Furthermore, the aged BBB is vulnerable to insult and becomes highly penetrable in response to O 3 exposure, leading to greater neuroinflammatory outcomes.« less

Aging Exacerbates Neuroinflammatory Outcomes Induced by Acute Ozone Exposure

DOE Office of Scientific and Technical Information (OSTI.GOV)

Tyler, Christina R.; Noor, Shahani; Young, Tamara

The role of environmental stressors, particularly exposure to air pollution, in the development of neurodegenerative disease remains underappreciated. We examined the neurological effects of acute ozone (O 3) exposure in aged mice, where increased blood brain barrier (BBB) permeability may confer vulnerability to neuroinflammatory outcomes. C 57BL/6 male mice, aged 8-10 weeks or 12–18 months were exposed to either filtered air (FA) or 1.0 ppm O 3 for 4 hours; animals received a single IP injection of sodium fluorescein (FSCN) 20 hours post-exposure. One-hour post-FSCN injection, animals were transcardially perfused for immunohistochemical analysis of BBB permeability. β-amyloid protein expression wasmore » assessed via ELISA. Flow cytometric characterization of infiltrating immune cells, including neutrophils, macrophages, and microglia populations was performed 20 hours post-O 3 exposure. Flow cytometry analysis of brains revealed increased microglia “activation” and presentation of CD11b, F4/80 and MHCII in aged animals relative to younger ones; these age-induced differences were potentiated by acute O 3 exposure. Cortical and limbic regions in aged brains had increased reactive microgliosis and β-amyloid protein expression after O 3 insult. The aged cerebellum was particularly vulnerable to acute O 3 exposure with increased populations of infiltrating neutrophils, peripheral macrophages/monocytes, and Ly6C + inflammatory monocytes after insult, which were not significantly increased in the young cerebellum. O 3 exposure increased the penetration of FSCN beyond the BBB, the infiltration of peripheral immune cells, and reactive gliosis of microglia. Furthermore, the aged BBB is vulnerable to insult and becomes highly penetrable in response to O 3 exposure, leading to greater neuroinflammatory outcomes.« less

Impact of Acute Metal Stress in Saccharomyces cerevisiae

PubMed Central

Lichtenberg-Fraté, Hella; Glaser, Walter; Schüller, Christoph; Klipp, Edda

2014-01-01

Although considered as essential cofactors for a variety of enzymatic reactions and for important structural and functional roles in cell metabolism, metals at high concentrations are potent toxic pollutants and pose complex biochemical problems for cells. We report results of single dose acute toxicity testing in the model organism S. cerevisiae. The effects of moderate toxic concentrations of 10 different human health relevant metals, Ag+, Al3+, As3+, Cd2+, Co2+, Hg2+, Mn2+, Ni2+, V3+, and Zn2+, following short-term exposure were analyzed by transcription profiling to provide the identification of early-on target genes or pathways. In contrast to common acute toxicity tests where defined endpoints are monitored we focused on the entire genomic response. We provide evidence that the induction of central elements of the oxidative stress response by the majority of investigated metals is the basic detoxification process against short-term metal exposure. General detoxification mechanisms also comprised the induction of genes coding for chaperones and those for chelation of metal ions via siderophores and amino acids. Hierarchical clustering, transcription factor analyses, and gene ontology data further revealed activation of genes involved in metal-specific protein catabolism along with repression of growth-related processes such as protein synthesis. Metal ion group specific differences in the expression responses with shared transcriptional regulators for both, up-regulation and repression were also observed. Additionally, some processes unique for individual metals were evident as well. In view of current concerns regarding environmental pollution our results may support ongoing attempts to develop methods to monitor potentially hazardous areas or liquids and to establish standardized tests using suitable eukaryotic a model organism. PMID:24416162

Impact of acute metal stress in Saccharomyces cerevisiae.

PubMed

Hosiner, Dagmar; Gerber, Susanne; Lichtenberg-Fraté, Hella; Glaser, Walter; Schüller, Christoph; Klipp, Edda

2014-01-01

Although considered as essential cofactors for a variety of enzymatic reactions and for important structural and functional roles in cell metabolism, metals at high concentrations are potent toxic pollutants and pose complex biochemical problems for cells. We report results of single dose acute toxicity testing in the model organism S. cerevisiae. The effects of moderate toxic concentrations of 10 different human health relevant metals, Ag(+), Al(3+), As(3+), Cd(2+), Co(2+), Hg(2+), Mn(2+), Ni(2+), V(3+), and Zn(2+), following short-term exposure were analyzed by transcription profiling to provide the identification of early-on target genes or pathways. In contrast to common acute toxicity tests where defined endpoints are monitored we focused on the entire genomic response. We provide evidence that the induction of central elements of the oxidative stress response by the majority of investigated metals is the basic detoxification process against short-term metal exposure. General detoxification mechanisms also comprised the induction of genes coding for chaperones and those for chelation of metal ions via siderophores and amino acids. Hierarchical clustering, transcription factor analyses, and gene ontology data further revealed activation of genes involved in metal-specific protein catabolism along with repression of growth-related processes such as protein synthesis. Metal ion group specific differences in the expression responses with shared transcriptional regulators for both, up-regulation and repression were also observed. Additionally, some processes unique for individual metals were evident as well. In view of current concerns regarding environmental pollution our results may support ongoing attempts to develop methods to monitor potentially hazardous areas or liquids and to establish standardized tests using suitable eukaryotic a model organism.

Suppressing the endocrine and autonomic stress systems does not impact the emotional stress experience after psychosocial stress.

PubMed

Ali, Nida; Nitschke, Jonas P; Cooperman, Cory; Pruessner, Jens C

2017-04-01

Acute psychosocial stress activates the physiological and endocrine stress systems and increases the subjective emotional experience of stress. While considerable efforts have been made to link changes in the activity of the biological stress systems with changes in the subjective emotional experience of stress, results so far have been mixed, at best. To investigate this association in a study employing experimental manipulation, we pharmacologically suppressed both the autonomic and the endocrine stress responses, and investigated the effects of acute psychosocial stress on the emotional stress experience. 22 healthy men and women received dexamethasone (2mg) the day before, and propranolol (80mg) one hour before psychosocial stress induction. A control group (n=24) received placebo pills on each occasion. Salivary cortisol, alpha-amylase and heart-rate responses to stress were assessed before, during and after stress induction. Subjective stress, mood, and state self-esteem assessments were made before and after stress. In the pharmacological manipulation group, subjects demonstrated no increase in autonomic or endocrine stress response, after exposure to psychosocial stress. Despite these effects, the emotional stress experience was intact in this group and identical to the control group. Participants in the experimental group showed an increase in subjective stress, greater mood dysregulation, and lower state self-esteem following stress exposure, with the response magnitude comparable to the control group. Our findings suggest that at least acutely, the physiological stress arousal systems and the emotional experience of stress are dissociated. This raises important questions about the efficacy of our measurement of subjective stress, and the unique contributions of the autonomic and endocrine responses in the subjective stress experience. Copyright © 2017 Elsevier Ltd. All rights reserved.

Virtual reality jogging as a novel exposure paradigm for the acute urge to be physically active in patients with eating disorders: Implications for treatment.

PubMed

Paslakis, Georgios; Fauck, Vanessa; Röder, Kathrin; Rauh, Elisabeth; Rauh, Manfred; Erim, Yesim

2017-11-01

The acute urge to be physically active is a relevant clinical phenomenon in patients suffering from eating disorders. In this study with n = 20 female patients with anorexia nervosa and n = 10 female patients with bulimia nervosa, a virtual reality (VR) jogging paradigm was applied as a novel highly immersive 3D exposure paradigm. Patients were asked to rate their acute urge to be physically active during the exposure procedure. A 10-item self-report questionnaire (smQ) was developed to capture the cognitive, emotional, and behavioral aspects of the acute urge to move. We hypothesized that exposure would lead to habituation of the urge to be physically active. We also hypothesized that leptin levels would be associated with the degree of the subjective urge to be physically active, while habituation would be associated with a decrease in stress hormones (α-amylase, cortisol, and cortisone in saliva). A statistically significant change in subjective scores in the smQ from baseline to postexposure was seen. Our novel VR paradigm may serve as a therapeutic tool for exposure and habituation of the urge of acutely engaging in physical activity in patients with eating disorders. © 2017 Wiley Periodicals, Inc.

Acute stress disorder in hospitalised victims of 26/11-terror attack on Mumbai, India.

PubMed

Balasinorwala, Vanshree Patil; Shah, Nilesh

2010-11-01

The 26/11 terror attacks on Mumbai have been internationally denounced. Acute stress disorder is common in victims of terror. To find out the prevalence and to correlate acute stress disorder, 70 hospitalised victims of terror were assessed for presence of the same using DSM-IV TR criteria. Demographic data and clinical variables were also collected. Acute stress disorder was found in 30% patients. On demographic profile and severity of injury, there were some interesting observations and differences between the victims who developed acute stress disorder and those who did not; though none of the differences reached the level of statistical significance. This study documents the occurrence of acute stress disorder in the victims of 26/11 terror attack.

The effects of acute stress on performance: implications for health professions education.

PubMed

LeBlanc, Vicki R

2009-10-01

This paper is a review of representative research on the impact of acute stressors on the clinical performance of individuals and teams. The Sciences Citation Index, Medline, and Psychinfo were used to search for articles up to and including 2008. The search terms were stress/tension/arousal/anxiety/cortisol/threat, cognition/skills/memory/attention/problem solving/decision making/performance, stress reduction/stress exposure/stress management/stress inoculation, and health professionals/medicine/medical students/residents/physicians/teams. The search was limited to papers in English from all developed countries. Secondary references were selected from primary papers. Elevated stress levels can impede performance on tasks that require divided attention, working memory, retrieval of information from memory, and decision making. These effects appear to be determined by the individual's appraisal of the demands and resources of a situation, the relationship between the stressor and the task, and factors such as coping styles, locus of control, and social supports. Given the potential negative impact of stress on performance, and the individualistic way in which people respond, medical educators might want to consider avenues for training learners in stress management. More research is needed to fully understand the contributions of personal factors such as coping style and locus of control, as well as the relationship of perceptions of stress to issues such as fatigue.

In vitro acute exposure to DEHP affects oocyte meiotic maturation, energy and oxidative stress parameters in a large animal model.

PubMed

Ambruosi, Barbara; Uranio, Manuel Filioli; Sardanelli, Anna Maria; Pocar, Paola; Martino, Nicola Antonio; Paternoster, Maria Stefania; Amati, Francesca; Dell'Aquila, Maria Elena

2011-01-01

Phthalates are ubiquitous environmental contaminants because of their use in plastics and other common consumer products. Di-(2-ethylhexyl) phthalate (DEHP) is the most abundant phthalate and it impairs fertility by acting as an endocrine disruptor. The aim of the present study was to analyze the effects of in vitro acute exposure to DEHP on oocyte maturation, energy and oxidative status in the horse, a large animal model. Cumulus cell (CC) apoptosis and oxidative status were also investigated. Cumulus-oocyte complexes from the ovaries of slaughtered mares were cultured in vitro in presence of 0.12, 12 and 1200 µM DEHP. After in vitro maturation (IVM), CCs were removed and evaluated for apoptosis (cytological assessment and TUNEL) and intracellular reactive oxygen species (ROS) levels. Oocytes were evaluated for nuclear chromatin configuration. Matured (Metaphase II stage; MII) oocytes were further evaluated for cytoplasmic energy and oxidative parameters. DEHP significantly inhibited oocyte maturation when added at low doses (0.12 µM; P<0.05). This effect was related to increased CC apoptosis (P<0.001) and reduced ROS levels (P<0.0001). At higher doses (12 and 1200 µM), DEHP induced apoptosis (P<0.0001) and ROS increase (P<0.0001) in CCs without affecting oocyte maturation. In DEHP-exposed MII oocytes, mitochondrial distribution patterns, apparent energy status (MitoTracker fluorescence intensity), intracellular ROS localization and levels, mt/ROS colocalization and total SOD activity did not vary, whereas increased ATP content (P<0.05), possibly of glycolytic origin, was found. Co-treatment with N-Acetyl-Cysteine reversed apoptosis and efficiently scavenged excessive ROS in DEHP-treated CCs without enhancing oocyte maturation. In conclusion, acute in vitro exposure to DEHP inhibits equine oocyte maturation without altering ooplasmic energy and oxidative stress parameters in matured oocytes which retain the potential to be fertilized and develop into embryos

In Vitro Acute Exposure to DEHP Affects Oocyte Meiotic Maturation, Energy and Oxidative Stress Parameters in a Large Animal Model

PubMed Central

Sardanelli, Anna Maria; Pocar, Paola; Martino, Nicola Antonio; Paternoster, Maria Stefania; Amati, Francesca; Dell'Aquila, Maria Elena

2011-01-01

Phthalates are ubiquitous environmental contaminants because of their use in plastics and other common consumer products. Di-(2-ethylhexyl) phthalate (DEHP) is the most abundant phthalate and it impairs fertility by acting as an endocrine disruptor. The aim of the present study was to analyze the effects of in vitro acute exposure to DEHP on oocyte maturation, energy and oxidative status in the horse, a large animal model. Cumulus cell (CC) apoptosis and oxidative status were also investigated. Cumulus-oocyte complexes from the ovaries of slaughtered mares were cultured in vitro in presence of 0.12, 12 and 1200 µM DEHP. After in vitro maturation (IVM), CCs were removed and evaluated for apoptosis (cytological assessment and TUNEL) and intracellular reactive oxygen species (ROS) levels. Oocytes were evaluated for nuclear chromatin configuration. Matured (Metaphase II stage; MII) oocytes were further evaluated for cytoplasmic energy and oxidative parameters. DEHP significantly inhibited oocyte maturation when added at low doses (0.12 µM; P<0.05). This effect was related to increased CC apoptosis (P<0.001) and reduced ROS levels (P<0.0001). At higher doses (12 and 1200 µM), DEHP induced apoptosis (P<0.0001) and ROS increase (P<0.0001) in CCs without affecting oocyte maturation. In DEHP-exposed MII oocytes, mitochondrial distribution patterns, apparent energy status (MitoTracker fluorescence intensity), intracellular ROS localization and levels, mt/ROS colocalization and total SOD activity did not vary, whereas increased ATP content (P<0.05), possibly of glycolytic origin, was found. Co-treatment with N-Acetyl-Cysteine reversed apoptosis and efficiently scavenged excessive ROS in DEHP-treated CCs without enhancing oocyte maturation. In conclusion, acute in vitro exposure to DEHP inhibits equine oocyte maturation without altering ooplasmic energy and oxidative stress parameters in matured oocytes which retain the potential to be fertilized and develop into embryos

Serum Response Factor (SRF) Ablation Interferes with Acute Stress-Associated Immediate and Long-Term Coping Mechanisms.

PubMed

Zimprich, Annemarie; Mroz, Gabi; Meyer Zu Reckendorf, Christopher; Anastasiadou, Sofia; Förstner, Philip; Garrett, Lillian; Hölter, Sabine M; Becker, Lore; Rozman, Jan; Prehn, Cornelia; Rathkolb, Birgit; Moreth, Kristin; Wurst, Wolfgang; Klopstock, Thomas; Klingenspor, Martin; Adamski, Jerzy; Wolf, Eckhard; Bekeredjian, Raffi; Fuchs, Helmut; Gailus-Durner, Valerie; de Angelis, Martin Hrabe; Knöll, Bernd

2017-12-01

Stress experience modulates behavior, metabolism, and energy expenditure of organisms. One molecular hallmark of an acute stress response is a rapid induction of immediate early genes (IEGs) such as c-Fos and Egr family members. IEG transcription in neurons is mediated by the neuronal activity-driven gene regulator serum response factor (SRF). We show a first role of SRF in immediate and long-lasting acute restraint stress (AS) responses. For this, we employed a standardized mouse phenotyping protocol at the German Mouse Clinic (GMC) including behavioral, metabolic, and cardiologic tests as well as gene expression profiling to analyze the consequences of forebrain-specific SRF deletion in mice exposed to AS. Adult mice with an SRF deletion in glutamatergic neurons (Srf; CaMKIIa-CreERT2 ) showed hyperactivity, decreased anxiety, and impaired working memory. In response to restraint AS, instant stress reactivity including locomotor behavior and corticosterone induction was impaired in Srf mutant mice. Interestingly, even several weeks after previous AS exposure, SRF-deficient mice showed long-lasting AS-associated changes including altered locomotion, metabolism, energy expenditure, and cardiovascular changes. This suggests a requirement of SRF for mediating long-term stress coping mechanisms in wild-type mice. SRF ablation decreased AS-mediated IEG induction and activity of the actin severing protein cofilin. In summary, our data suggest an SRF function in immediate AS reactions and long-term post-stress-associated coping mechanisms.

Recent life stress exposure is associated with poorer long-term memory, working memory, and self-reported memory.

PubMed

Shields, Grant S; Doty, Dominique; Shields, Rebecca H; Gower, Garrett; Slavich, George M; Yonelinas, Andrew P

2017-11-01

Although substantial research has examined the effects of stress on cognition, much of this research has focused on acute stress (e.g. manipulated in the laboratory) or chronic stress (e.g. persistent interpersonal or financial difficulties). In contrast, the effects of recent life stress on cognition have been relatively understudied. To address this issue, we examined how recent life stress is associated with long-term, working memory, and self-reported memory in a sample of 142 healthy young adults who were assessed at two time points over a two-week period. Recent life stress was measured using the newly-developed Stress and Adversity Inventory for Daily Stress (Daily STRAIN), which assesses the frequency of relatively common stressful life events and difficulties over the preceding two weeks. To assess memory performance, participants completed both long-term and working memory tasks. Participants also provided self-reports of memory problems. As hypothesized, greater recent life stress exposure was associated with worse performance on measures of long-term and working memory, as well as more self-reported memory problems. These associations were largely robust while controlling for possible confounds, including participants' age, sex, and negative affect. The findings indicate that recent life stress exposure is broadly associated with worse memory. Future studies should thus consider assessing recent life stress as a potential predictor, moderator, or covariate of memory performance.

Biological markers of stress in pediatric acute burn injury.

PubMed

Brown, Nadia J; Kimble, Roy M; Rodger, Sylvia; Ware, Robert S; McWhinney, Brett C; Ungerer, Jacobus P J; Cuttle, Leila

2014-08-01

Burns and their associated wound care procedures evoke significant stress and anxiety, particularly for children. Little is known about the body's physiological stress reactions throughout the stages of re-epithelialization following an acute burn injury. Previously, serum and urinary cortisol have been used to measure stress in burn patients, however these measures are not suitable for a pediatric burn outpatient setting. To assess the sensitivity of salivary cortisol and sAA in detecting stress during acute burn wound care procedures and to investigate the body's physiological stress reactions throughout burn re-epithelialization. Seventy-seven participants aged four to thirteen years who presented with an acute burn injury to the burn center at the Royal Children's Hospital, Brisbane, Australia, were recruited between August 2011 and August 2012. Both biomarkers were responsive to the stress of burn wound care procedures. sAA levels were on average 50.2 U/ml higher (p<0.001) at 10 min post-dressing removal compared to baseline levels. Salivary cortisol levels showed a blunted effect with average levels at ten minutes post dressing removal decreasing by 0.54 nmol/L (p<0.001) compared to baseline levels. sAA levels were associated with pain (p=0.021), no medication (p=0.047) and Child Trauma Screening Questionnaire scores at three months post re-epithelialization (p=0.008). Similarly, salivary cortisol was associated with no medication (p<0.001), pain scores (p=0.045) and total body surface area of the burn (p=0.010). Factors which support the use of sAA over salivary cortisol to assess stress during morning acute burn wound care procedures include; sensitivity, morning clinic times relative to cortisol's diurnal peaks, and relative cost. Copyright © 2013 Elsevier Ltd and ISBI. All rights reserved.

Effect of acute acoustic stress on anorectal function sensation in healthy human.

PubMed

Gonlachanvit, S; Rhee, J; Sun, W M; Chey, W D

2005-04-01

Little is known about the effects of acute acoustic stress on anorectal function. To determine the effects of acute acoustic stress on anorectal function and sensation in healthy volunteers. Ten healthy volunteers (7 M, 3 F, mean age 34 +/- 3 years) underwent anorectal manometry, testing of rectal compliance and sensation using a barostat with and without acute noise stress on separate days. Rectal perception was assessed using an ascending method of limits protocol and a 5-point Likert scale. Arousal and anxiety status were evaluated using a visual analogue scale. Acoustic stress significantly increased anxiety score (P < 0.05). Rectal compliance was significantly decreased with acoustic stress compared with control P (P < 0.000001). In addition, less intraballoon volume was needed to induce the sensation of severe urgency with acoustic stress (P < 0.05). Acoustic stress had no effect on hemodynamic parameters, anal sphincter pressure, threshold for first sensation, sensation of stool, or pain. Acute acoustic stimulation increased anxiety scores, decreased rectal compliance, and enhanced perception of severe urgency to balloon distention but did not affect anal sphincter pressure in healthy volunteers. These results may offer insight into the pathogenesis of stress-in-induced diarrhoea and faecal urgency.

Acute Stress Symptoms in Children: Results From an International Data Archive

ERIC Educational Resources Information Center

Kassam-Adams, Nancy; Palmieri, Patrick A.; Rork, Kristine; Delahanty, Douglas L.; Kenardy, Justin; Kohser, Kristen L.; Landolt, Markus A.; Le Brocque, Robyne; Marsac, Meghan L.; Meiser-Stedman, Richard; Nixon, Reginald D.V.; Bui, Eric; McGrath, Caitlin

2012-01-01

Objective: To describe the prevalence of acute stress disorder (ASD) symptoms and to examine proposed "DSM-5" symptom criteria in relation to concurrent functional impairment in children and adolescents. Method: From an international archive, datasets were identified that included assessment of acute traumatic stress reactions and…

The Relationship between Acute Stress Disorder and Posttraumatic Stress Disorder Following Cancer

ERIC Educational Resources Information Center

Kangas, Maria; Henry, Jane L.; Bryant, Richard A.

2005-01-01

In this study, the authors investigated the relationship between acute stress disorder (ASD) and posttraumatic stress disorder (PTSD) following cancer diagnosis. Patients who were recently diagnosed with 1st onset head and neck or lung malignancy (N = 82) were assessed for ASD within the initial month following their diagnosis and reassessed (n =…

Acute selenium selenite exposure effects on oxidative stress biomarkers and essential metals and trace-elements in the model organism zebrafish (Danio rerio).

PubMed

Hauser-Davis, R A; Silva, J A N; Rocha, Rafael C C; Saint'Pierre, Tatiana; Ziolli, R L; Arruda, M A Z

2016-01-01

Selenium (Se) is an essential trace-element that becomes toxic when present at high concentrations. Little is known regarding Se effects on parameters such as oxidative stress biomarkers. The aim of the present study was to investigate the effects of acute selenium exposure on oxidative stress biomarkers in a model organism, zebrafish (Danio rerio). Fish were exposed to selenium selenite at 1mgL(-1). Reduced glutathione (GSH), and metallothionein (MT) concentrations were determined in liver, kidney and brain, with MT also being determined in bile. Essential metals and trace-elements were also determined by inductively coupled mass spectrometry (ICP-MS) in order to verify possible metal homeostasis alterations. GSH concentrations in liver, kidney and brain increased significantly (1.05±0.03μmolg(-1) ww, 1.42±0.03μmolg(-1) ww and 1.64±0.03μmolg(-1) ww, respectively) in the Se-exposed group when compared to the controls (0.88±0.05μmolg(-1) ww, 0.80±0.04μmolg(-1) ww and 0.89±0.03μmolg(-1) ww for liver, kidney and brain, respectively). MT levels in Se-exposed liver (0.52±0.03μmolg(-1) ww) decreased significantly in comparison to the control group (0.64±0.02μmolg(-1) ww), while levels in bile increased, albeit non-significantly. This is in accordance with previous studies that indicate efficient biliary MT action, leading to a rapid metabolism and elimination of contaminants from the body. Levels in the brain increased significantly after Se-exposure (0.57±0.01μmolg(-1) ww) when compared to the control group (0.35±0.03μmolg(-1) ww) since this organ does not present a detoxification route as quick as the liver-gallbladder route. Several metal and trace-elements were altered with Se-exposure, indicating that excess of selenium results in metal dyshomeostasis. This is the first report on metal dyshomeostasis due to Se-exposure, which may be the first step in the mechanism of action of selenium toxicity, as is postulated to occur in certain major human

Negative Energy Balance Blocks Neural and Behavioral Responses to Acute Stress by “Silencing” Central Glucagon-Like Peptide 1 Signaling in Rats

PubMed Central

Maniscalco, James W.; Zheng, Huiyuan; Gordon, Patrick J.

2015-01-01

Previous reports indicate that caloric restriction attenuates anxiety and other behavioral responses to acute stress, and blunts the ability of stress to increase anterior pituitary release of adrenocorticotropic hormone. Since hindbrain glucagon-like peptide-1 (GLP-1) neurons and noradrenergic prolactin-releasing peptide (PrRP) neurons participate in behavioral and endocrine stress responses, and are sensitive to the metabolic state, we examined whether overnight food deprivation blunts stress-induced recruitment of these neurons and their downstream hypothalamic and limbic forebrain targets. A single overnight fast reduced anxiety-like behavior assessed in the elevated-plus maze and acoustic startle test, including marked attenuation of light-enhanced startle. Acute stress [i.e., 30 min restraint (RES) or 5 min elevated platform exposure] robustly activated c-Fos in GLP-1 and PrRP neurons in fed rats, but not in fasted rats. Fasting also significantly blunted the ability of acute stress to activate c-Fos expression within the anterior ventrolateral bed nucleus of the stria terminalis (vlBST). Acute RES stress suppressed dark-onset food intake in rats that were fed ad libitum, whereas central infusion of a GLP-1 receptor antagonist blocked RES-induced hypophagia, and reduced the ability of RES to activate PrRP and anterior vlBST neurons in ad libitum-fed rats. Thus, an overnight fast “silences” GLP-1 and PrRP neurons, and reduces both anxiety-like and hypophagic responses to acute stress. The partial mimicking of these fasting-induced effects in ad libitum-fed rats after GLP-1 receptor antagonism suggests a potential mechanism by which short-term negative energy balance attenuates neuroendocrine and behavioral responses to acute stress. SIGNIFICANCE STATEMENT The results from this study reveal a potential central mechanism for the “metabolic tuning” of stress responsiveness. A single overnight fast, which markedly reduces anxiety-like behavior in rats

Acute stress cardiomyopathy and deaths associated with electronic weapons.

PubMed

Cevik, Cihan; Otahbachi, Mohammad; Miller, Elizabeth; Bagdure, Satish; Nugent, Kenneth M

2009-03-06

Deaths associated with the use of electronic weapons almost always occur in young men involved in either civil disturbances or criminal activity. These situations are associated with high levels of circulating catecholamines and frequently associated with drug intoxication. The mechanism for these deaths is unclear. Clinical studies indicate that these high voltage electrical pulses do not cause cardiac arrhythmia. Acute stress cardiomyopathy provides an alternative explanation for deaths associated with electronic weapons and may provide a better explanation for the usual time course associated with taser deaths. Patients with acute stress cardiomyopathy usually have had an emotional or physical stress, have high circulating levels of catecholamines, present with an acute coronary syndrome but have normal coronary vessels without significant thrombus formation. They have unusual left ventricular dysfunction with so-called apical ballooning. This presentation has been attributed to the direct effects of catecholamines on myocardial cell function. Alternative explanations include vasospasm in the coronary microcirculation and/or acute thrombosis followed by rapid thrombolysis. Similar events could occur during the high stress situations associated with the use of electronic weapons. These events also likely explain restraint-related deaths which occur in independent of any use of electronic weapons. Forensic pathologists have the opportunity to provide important details about the pathogenesis of these deaths through histological studies and careful evaluation of coronary vessels.

Chronic voluntary wheel running facilitates corticosterone response habituation to repeated audiogenic stress exposure in male rats

PubMed Central

SASSE, SARAH K.; GREENWOOD, BENJAMIN N.; MASINI, CHER V.; NYHUIS, TARA J.; FLESHNER, MONIKA; DAY, HEIDI E. W.; CAMPEAU, SERGE

2008-01-01

Voluntary exercise is associated with the prevention and treatment of numerous physical and psychological illnesses, yet the mechanisms by which it confers this protection remain unclear. In contrast, stress, particularly under conditions of prolonged or repeated exposure when glucocorticoid levels are consistently elevated, can have a devastating impact on health. It has been suggested that the benefits of physical exercise may lie in an ability to reduce some of the more deleterious health effects of stress and stress hormones. The present series of experiments provides evidence that voluntary exercise facilitates habituation of corticosterone but not adrenocorticotropin hormone responses to repeated stress presentations. After 6 weeks of running wheel access or sedentary housing conditions, rats were exposed to 11 consecutive daily 30 min presentations of 98 dB noise stress. Similar corticosterone responses in exercised rats and sedentary controls were observed following the first, acute stress presentation. While both groups demonstrated habituation of corticosterone secretory responses with repeated noise stress exposures, the rate of habituation was significantly facilitated in exercised animals. These results suggest that voluntary exercise may reduce the negative impact of prolonged or repeated stress on health by enhancing habituation of hypothalamo-pituitary–adrenocortical axis responses at the level of the adrenal cortex, ultimately reducing the amount of glucocorticoids the body and brain are exposed to. PMID:19065456

Differential expression of heat shock transcription factors and heat shock proteins after acute and chronic heat stress in laying chickens (Gallus gallus).

PubMed

Xie, Jingjing; Tang, Li; Lu, Lin; Zhang, Liyang; Xi, Lin; Liu, Hsiao-Ching; Odle, Jack; Luo, Xugang

2014-01-01

Heat stress due to high environmental temperature negatively influences animal performances. To better understand the biological impact of heat stress, laying broiler breeder chickens were subjected either to acute (step-wisely increasing temperature from 21 to 35°C within 24 hours) or chronic (32°C for 8 weeks) high temperature exposure. High temperature challenges significantly elevated body temperature of experimental birds (P<0.05). However, oxidation status of lipid and protein and expression of heat shock transcription factors (HSFs) and heat shock proteins (HSPs) 70 and 90 were differently affected by acute and chronic treatment. Tissue-specific responses to thermal challenge were also found among heart, liver and muscle. In the heart, acute heat challenge affected lipid oxidation (P = 0.05) and gene expression of all 4 HSF gene expression was upregulated (P<0.05). During chronic heat treatment, the HSP 70 mRNA level was increased (P<0.05) and HSP 90 mRNA (P<0.05) was decreased. In the liver, oxidation of protein was alleviated during acute heat challenge (P<0.05), however, gene expression HSF2, 3 and 4 and HSP 70 were highly induced (P<0.05). HSP90 expression was increased by chronic thermal treatment (P<0.05). In the muscle, both types of heat stress increased protein oxidation, but HSFs and HSPs gene expression remained unaltered. Only tendencies to increase were observed in HSP 70 (P = 0.052) and 90 (P = 0.054) gene expression after acute heat stress. The differential expressions of HSF and HSP genes in different tissues of laying broiler breeder chickens suggested that anti-heat stress mechanisms might be provoked more profoundly in the heart, by which the muscle was least protected during heat stress. In addition to HSP, HSFs gene expression could be used as a marker during acute heat stress.

Self-reported acute health symptoms and exposure to companion animals

EPA Science Inventory

Background: In order to understand the etiological burden of disease associated with acute health symptoms (e.g. gastrointestinal [GI], respiratory, dermatological), it is important to understand how common exposures influence these symptoms. Exposures to familiar and unfamiliar ...

Pyrethroid insecticide lambda-cyhalothrin and its metabolites induce liver injury through the activation of oxidative stress and proinflammatory gene expression in rats following acute and subchronic exposure.

PubMed

Aouey, Bakhta; Derbali, Mohamed; Chtourou, Yassine; Bouchard, Michèle; Khabir, Abdelmajid; Fetoui, Hamadi

2017-02-01

Lambda-cyhalothrin (LTC) [α-cyano-3-phenoxybenzyl-3-(2-chloro-3,3,3-trifluoro-1-propenyl)-2,2-dimethylcyclo-propanecarboxylate] is a synthetic type II pyrethroid insecticide commonly used in residential and agricultural areas. The potential hepatotoxicity of pyrethroids remains unclear and could easily be assessed by measuring common clinical indicators of liver disease. To understand more about the potential risks for humans associated with LTC exposure, male adult rats were orally exposed to 6.2 and 31.1 mg/kg bw of LTC for 7, 30, 45, and 60 days. Histopathological changes and alterations of main parameters related to oxidative stress and inflammatory responses in the liver were evaluated. Further, lambda-cyhalothrin metabolites [3-(2-chloro-3,3,3-trifluoroprop-1-enyl)-2,2-dimethyl-cyclopropane carboxylic acid (CFMP), 4-hydroxyphenoxybenzoic acid (4-OH-3-PBA), and 3-phenoxybenzoic acid (3-PBA)] in the liver tissues were identified and quantified by ultra-high-performance liquid chromatography coupled to quadripole time-of-flight mass spectrometry (UHPLC-MS-Q-ToF). Results revealed that LTC exposure significantly increased markers of hepatic oxidative stress in a time-dependent and dose-dependent manner, and this was associated with an accumulation of CFMP and 3-PBA in the liver tissues. In addition, the levels of tumor necrosis factor-α (TNF-α) and interleukin (IL-6 and IL-1β) gene expressions were significantly increased in the liver of exposed rats compared to controls. Correlation analyses revealed that CFMP and 3-PBA metabolite levels in the liver tissues were significantly correlated with the indexes of oxidative stress, redox status, and inflammatory markers in rats exposed to lambda-cyhalothin. Overall, this study provided novel evidence that hepatic damage is likely due to increased oxidative stress and inflammation under the condition of acute and subchronic exposure to lambda-cyhalothrin and that LTC metabolites (CFMP and 3-PBA) could be used as

Acute stress shifts the balance between controlled and automatic processes in prospective memory.

PubMed

Möschl, Marcus; Walser, Moritz; Plessow, Franziska; Goschke, Thomas; Fischer, Rico

2017-10-01

In everyday life we frequently rely on our abilities to postpone intentions until later occasions (prospective memory; PM) and to deactivate completed intentions even in stressful situations. Yet, little is known about the effects of acute stress on these abilities. In the present work we investigated the impact of acute stress on PM functioning under high task demands. (1) Different from previous studies, in which intention deactivation required mostly low processing demands, we used salient focal PM cues to induce high processing demands during intention-deactivation phases. (2) We systematically manipulated PM-monitoring demands in a nonfocal PM task that required participants to monitor for either one or six specific syllables that could occur in ongoing-task words. Eighty participants underwent the Trier Social Stress Test, a standardized stress induction protocol, or a standardized control situation, before performing a computerized PM task. Our primary interests were whether PM performance, PM-monitoring costs, aftereffects of completed intentions and/or commission-error risk would differ between stressed and non-stressed individuals and whether these effects would differ under varying task demands. Results revealed that PM performance and aftereffects of completed intentions during subsequent performance were not affected by acute stress induction, replicating previous findings. Under high demands on intention deactivation (focal condition), however, acute stress produced a nominal increase in erroneous PM responses after intention completion (commission errors). Most importantly, under high demands on PM monitoring (nonfocal condition), acute stress led to a substantial reduction in PM-monitoring costs. These findings support ideas of selective and demand-dependent effects of acute stress on cognitive functioning. Under high task demands, acute stress might induce a shift in processing strategy towards resource-saving behavior, which seems to increase the

Expedited patient-specific assessment of contact stress exposure in the ankle joint following definitive articular fracture reduction.

PubMed

Kern, Andrew M; Anderson, Donald D

2015-09-18

Acute injury severity, altered joint kinematics, and joint incongruity are three important mechanical factors linked to post-traumatic osteoarthritis (PTOA). Finite element analysis (FEA) was previously used to assess the influence of increased contact stress due to joint incongruity on PTOA development. While promising agreement with PTOA development was seen, the inherent complexities of contact FEA limited the numbers of subjects that could be analyzed. Discrete element analysis (DEA) is a simplified methodology for contact stress computation, which idealizes contact surfaces as a bed of independent linear springs. In this study, DEA was explored as an expedited alternative to FEA contact stress exposure computation. DEA was compared to FEA using results from a previously completed validation study of two cadaveric human ankles, as well as a previous study of post-operative contact stress exposure in 11 patients with tibial plafond fracture. DEA-computed maximum contact stresses were within 19% of those experimentally measured, with 90% of the contact area having computed contact stress values within 1MPa of those measured. In the 11 fractured ankles, maximum contact stress and contact area differences between DEA and FEA were 0.85 ± 0.64 MPa and 22.5 ± 11.5mm(2). As a predictive measure for PTOA development, both DEA and FEA had 100% concordance with presence of OA (KL grade ≥ 2) and >95% concordance with KL grade at 2 years. These results support DEA as a reasonable alternative to FEA for computing contact stress exposures following surgical reduction of a tibial plafond fracture. Copyright © 2015 Elsevier Ltd. All rights reserved.

Differential influence of the 5-HTTLPR genotype, neuroticism and real-life acute stress exposure on appetite and energy intake.

PubMed

Capello, Aimée E M; Markus, C Rob

2014-06-01

Stress or negative mood often promotes energy intake and overeating. Since the serotonin transporter-linked polymorphic region (5-HTTLPR) is found to mediate stress vulnerability as well as to influence energy intake, this gene may also influence the negative effects of stress exposure on overeating. Moreover, since stress proneness also reflects cognitive stress vulnerability - as often defined by trait neuroticism - this may additionally predispose for stress-induced overeating. In the present study it was investigated whether the 5-HTTLPR genotype interacted with neuroticism on changes in mood, appetite and energy intake following exposure to a real-life academic examination stressor. In a balanced-experimental design, homozygous S-allele and L-allele carriers (N = 94) with the lowest and highest neuroticism scores were selected from a large database of 5-HTTLPR genotyped students. Mood, appetite and energy intake were measured before and after a 2-hour academic examination and compared with a control day. Examination influenced appetite for particular sweet snacks differently depending on 5-HTTLPR genotype and neuroticism. S/S compared with L/L subjects reported greater examination stress, and this was accompanied by a more profound post-stress increase in appetite for sweet snacks. Data also revealed a 5-HTTLPR genotype by trait neuroticism interaction on energy intake, regardless of examination. These results consolidate previous assumptions of 5-HTTLPR involvement in stress vulnerability and suggest 5-HTTLPR and neuroticism may influence stress-induced overeating depending on the type of food available. These findings furthermore link previous findings of increased risk for weight gain in S/S-allele carriers, particularly with high scores on trait neuroticism, to increased energy intake. Copyright © 2014 Elsevier Ltd. All rights reserved.

Rigid patterns of effortful choice behavior after acute stress in rats.

PubMed

Hart, Evan E; Stolyarova, Alexandra; Conoscenti, Michael A; Minor, Thomas R; Izquierdo, Alicia

2017-01-01

Physical effort is a common cost of acquiring rewards, and decreased effort is a feature of many neuropsychiatric disorders. Stress affects performance on several tests of cognition and decision making in both humans and nonhumans. Only a few recent reports show impairing effects of stress in operant tasks involving effort and cognitive flexibility. Brain regions affected by stress, such as the medial prefrontal cortex and amygdala, are also implicated in mediating effortful choices. Here, we assessed effort-based decision making after an acute stress procedure known to induce persistent impairment in shuttle escape and elevated plasma corticosterone. In these animals, we also probed levels of polysialyted neural cell adhesion molecule (PSA-NCAM), a marker of structural plasticity, in medial frontal cortex and amygdala. We found that animals that consistently worked for high magnitude rewards continued to do so, even after acute shock stress. We also found that PSA-NCAM was increased in both regions after effortful choice experience but not after shock stress alone. These findings are discussed with reference to the existing broad literature on cognitive effects of stress and in the context of how acute stress may bias effortful decisions to a rigid pattern of responding.

Effects of acute cigarette smoking on total blood count and markers of oxidative stress in active and passive smokers.

PubMed

Lymperaki, E; Makedou, K; Iliadis, S; Vagdatli, E

2015-01-01

Free radicals, as a product of cigarette smoke, are considered to have deleterious effects causing oxidative stress. Acute active smoking seems to be followed by transient leukocytosis and delayed increase in neutrophil activation. The aim of the present study was to investigate the oxidative status of smokers and passive non-smokers, as well as the impact that acute cigarette smoking has on hematological parameters. Thirty-two healthy volunteers, 16 active smokers (Group A) aged 20-23 years and 16 age-matched, non-smokers (Group B), 18 women and 14 men in total, participated voluntarily in the study. All subjects did not have any food, drink, or cigarette smoking for eight hours before the study. Each time, two active smokers and two non-smokers were exposed simultaneously for half an hour to the smoke of two cigarettes smoked consecutively by the smokers. Blood was drawn before and after the exposure to cigarette smoke. Whole blood was analyzed immediately for total blood count parameters and serum was stored in -70(◦)C until serum levels of malondialdehyde (MDA) and vitamin E (VitE), and total antioxidant capacity (TAC) were determined. No statistical significant difference was observed in the values of white blood cells and their subpopulations between the two groups and within the same group before and after exposure to cigarette smoke. In the group of smokers, granulocyte/lymphocyte ratio increased significantly, MDA levels showed significant elevation and protective VitE serum levels decreased significantly, whereas TAC was reduced, but not significantly, after the exposure. In the group of passive, non-smokers the results of the blood count parameters, MDA and VitE were similar to Group A, and there was a significant decrease in TAC, as well. Between the two groups, only hematocrit values and MDA levels differed significantly before the exposure to smoke, and no other significant difference was detected before or after the exposure, between active and

An enriched environment reduces the stress level and locomotor activity induced by acute morphine treatment and by saline after chronic morphine treatment in mice.

PubMed

Xu, Jia; Sun, Jinling; Xue, Zhaoxia; Li, Xinwang

2014-06-18

This study investigated the relationships among an enriched environment, stress levels, and drug addiction. Mice were divided randomly into four treatment groups (n=12 each): enriched environment without restraint stress (EN), standard environment without restraint stress (SN), enriched environment with restraint stress (ES), and standard environment with restraint stress (SS). Mice were reared in the respective environment for 45 days. Then, the ES and SS groups were subjected to restraint stress daily (2 h/day) for 14 days, whereas the EN and SN groups were not subjected to restraint stress during this stage. The stress levels of all mice were tested in the elevated plus maze immediately after exposure to restraint stress. After the 2-week stress testing period, mice were administered acute or chronic morphine (5 mg/kg) treatment for 7 days. Then, after a 7-day withdrawal period, the mice were injected with saline (1 ml/kg) or morphine (5 mg/kg) daily for 2 days to observe locomotor activity. The results indicated that the enriched environment reduced the stress and locomotor activity induced by acute morphine administration or saline after chronic morphine treatment. However, the enriched environment did not significantly inhibit locomotor activity induced by morphine challenge. In addition, the stress level did not mediate the effect of the enriched environment on drug-induced locomotor activity after acute or chronic morphine treatment.

Chronic intermittent psychosocial stress (social defeat/overcrowding) in mice increases the severity of an acute DSS-induced colitis and impairs regeneration.

PubMed

Reber, S O; Obermeier, F; Straub, R H; Straub, H R; Falk, W; Neumann, I D

2006-10-01

Ulcerative colitis is a multifactorial disease, with immunological, genetic, and environmental factors playing an important role in its pathogenesis. Here we investigated the consequences of exposure to chronic psychosocial stress on the severity of a dextran sulfate sodium (DSS)-induced colitis in male C57BL/6 mice. Chronic stress was induced by repeated exposure to social defeat (SD, 2 h) and overcrowding (OC, 24 h) during 19 consecutive days. SD/OC mice showed a diminished body weight gain, thymus-atrophy, and adrenal hypertrophy, but similar light-phase plasma corticosterone concentrations, compared with unstressed mice. In contrast, the rise in dark-phase corticosterone concentration was significantly attenuated in SD/OC mice, whereas plasma ACTH concentrations and hypothalamic CRH mRNA expression did not differ between stressed and nonstressed groups. Additionally, adrenal cells from SD/OC mice showed a decreased in vitro response to ACTH stimulation. Subsequent treatment with 1% DSS for 7 d resulted in a more severe intestinal inflammation in SD/OC mice, as reflected by an increase in body weight loss, histological damage scores, and secretion of IL-6, TNFalpha, and interferon-gamma from mesenteric lymph node cells and by decreased colon length. The impaired health status of stressed mice was also reflected by a significantly lower survival rate after termination of the DSS treatment. In conclusion, the present findings demonstrate that chronic intermittent exposure to a psychosocial stressor before the induction of acute DSS-colitis results in adrenal insufficiency, increases in the severity of the acute inflammation, and impairs the healing phase.

Acute stress enhances learning and memory by activating acid-sensing ion channels in rats.

PubMed

Ye, Shunjie; Yang, Rong; Xiong, Qiuju; Yang, Youhua; Zhou, Lianying; Gong, Yeli; Li, Changlei; Ding, Zhenhan; Ye, Guohai; Xiong, Zhe

2018-04-15

Acute stress has been shown to enhance learning and memory ability, predominantly through the action of corticosteroid stress hormones. However, the valuable targets for promoting learning and memory induced by acute stress and the underlying molecular mechanisms remain unclear. Acid-sensing ion channels (ASICs) play an important role in central neuronal systems and involves in depression, synaptic plasticity and learning and memory. In the current study, we used a combination of electrophysiological and behavioral approaches in an effort to explore the effects of acute stress on ASICs. We found that corticosterone (CORT) induced by acute stress caused a potentiation of ASICs current via glucocorticoid receptors (GRs) not mineralocorticoid receptors (MRs). Meanwhile, CORT did not produce an increase of ASICs current by pretreated with GF109203X, an antagonist of protein kinase C (PKC), whereas CORT did result in a markedly enhancement of ASICs current by bryostatin 1, an agonist of PKC, suggesting that potentiation of ASICs function may be depended on PKC activating. More importantly, an antagonist of ASICs, amiloride (10 μM) reduced the performance of learning and memory induced by acute stress, which is further suggesting that ASICs as the key components involves in cognitive processes induced by acute stress. These results indicate that acute stress causes the enhancement of ASICs function by activating PKC signaling pathway, which leads to potentiated learning and memory. Copyright © 2018 Elsevier Inc. All rights reserved.

Dysfunction of serotoninergic and dopaminergic neuronal systems in the antidepressant-resistant impairment of social behaviors induced by social defeat stress exposure as juveniles.

PubMed

Hasegawa, Sho; Miyake, Yuriko; Yoshimi, Akira; Mouri, Akihiro; Hida, Hirotake; Yamada, Kiyofumi; Ozaki, Norio; Nabeshima, Toshitaka; Noda, Yukihiro

2018-03-29

Extensive studies have been performed on the role of monoaminergic neuronal systems in rodents exposed to social defeat stress as adults. In the present study, we investigated the role of monoaminergic neuronal systems in the impairment of social behaviors induced by social defeat stress exposure as juveniles. Juvenile, male C57BL/6J mice were exposed to social defeat stress for 10 consecutive days. From 1 day after the last stress exposure, desipramine, sertraline, and aripiprazole, were administered for 15 days. Social behaviors were assessed at 1 and 15 days after the last stress exposure. Monoamine turnover was determined in specific regions of the brain in the mice exposed to the stress. Stress exposure as juveniles induced the impairment of social behaviors in adolescent mice. In mice that showed the impairment of social behaviors, turnover of the serotonin and dopamine, but not noradrenaline was decreased in specific brain regions. Acute and repeated administration of desipramine, sertraline, and aripiprazole failed to attenuate the impairment of social behaviors, whereas repeated administration of a combination of sertraline and aripiprazole showed additive attenuating effects. These findings suggest that social defeat stress exposure as juveniles induces the treatment-resistant impairment of social behaviors in adolescents through dysfunction in the serotoninergic and dopaminergic neuronal systems. The combination of sertraline and aripiprazole may be used as a new treatment strategy for treatment-resistant stress-related psychiatric disorders in adolescents with adverse juvenile experiences.

Posttraumatic stress disorder in disaster relief workers following direct and indirect trauma exposure to Ground Zero.

PubMed

Zimering, Rose; Gulliver, Suzy B; Knight, Jeffrey; Munroe, James; Keane, Terence M

2006-08-01

The present study compared rates of posttraumatic stress disorder (PTSD) in relief workers at the World Trade Center collapse from two sources: direct exposure to the disaster site and indirect exposure through survivor narratives. Standardized clinical interviews for PTSD were conducted with 109 relief workers 6-8 months after the September 11th terrorist attacks. Rates of acute PTSD from direct and indirect exposure to traumatic stressors were 6.4% and 4.6%, respectively. The findings suggest that indirect exposures can lead to PTSD even when Criterion A1 of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-Text Revision (DSM-IV-TR; American Psychiatric Association, 2000, p. 463), i.e., "experienced by a family member or other close associate" is not met. Further research is necessary to define precisely the parameters of indirect traumatic exposure that may be linked to the development of PTSD.

Exposure to ammonia and acute respiratory effects in a urea fertilizer factory.

PubMed

Rahman, Md Hamidur; Bråtveit, Magne; Moen, Bente E

2007-01-01

Personal exposures to ammonia and acute respiratory effects were determined in workers at a urea fertilizer factory in Bangladesh. Full-shift personal exposure to ammonia was measured using a PAC III direct reading instrument and Drager diffusion tubes. Respiratory symptoms were elicited by a questionnaire study (n = 113), and preshift and postshift lung function (FVC, FEV1, and PEFR) were tested using spirometry (n = 88). Urea plant workers had higher mean exposure to ammonia and prevalence of acute respiratory symptoms than did workers in the ammonia plant. The symptoms with highest prevalence in the urea plant were chest tightness (33%) and cough (28%). FVC and FEV1 decreased significantly across the work shift among urea plant workers. The higher level of exposure to ammonia in the urea plant was associated with an increased prevalence of respiratory symptoms and an acute decline in lung function.

Concomitant stress potentiates the preference for, and consumption of, ethanol induced by chronic pre-exposure to ethanol.

PubMed

Morais-Silva, G; Fernandes-Santos, J; Moreira-Silva, D; Marin, M T

2016-01-01

Ethanol abuse is linked to several acute and chronic injuries that can lead to health problems. Ethanol addiction is one of the most severe diseases linked to the abuse of this drug. Symptoms of ethanol addiction include compulsive substance intake and withdrawal syndrome. Stress exposure has an important role in addictive behavior for many drugs of abuse (including ethanol), but the consequences of stress and ethanol in the organism when these factors are concomitant results in a complex interaction. We investigated the effects of concomitant, chronic administration of ethanol and stress exposure on the withdrawal and consumption of, as well as the preference for, ethanol in mice. Male Swiss mice (30-35 g, 8-10 per group) were exposed to an ethanol liquid diet as the only source of food for 15 days. In the final 5 days, they were exposed to forced swimming stress. Twelve hours after removal of the ethanol liquid diet, animals were evaluated for ethanol withdrawal by measuring anxiety-related behaviors and locomotor activity. Twenty-four hours after evaluation of ethanol withdrawal, they were evaluated for voluntary consumption of ethanol in a "three-bottle choice" paradigm. Mice exposed to chronic consumption of ethanol had decreased locomotor activity during withdrawal. Contrary to our expectations, a concomitant forced swimming stress did not aggravate ethanol withdrawal. Nevertheless, simultaneous ethanol administration and stress exposure increased voluntary consumption of ethanol, mainly solutions containing high concentrations of ethanol. These results showed that stressful situations during ethanol intake may aggravate specific addiction-related behaviors.

Surgeons' and surgical trainees' acute stress in real operations or simulation: A systematic review.

PubMed

Georgiou, Konstantinos; Larentzakis, Andreas; Papavassiliou, Athanasios G

2017-12-01

Acute stress in surgery is ubiquitous and has an immediate impact on surgical performance and patient safety. Surgeons react with several coping strategies; however, they recognise the necessity of formal stress management training. Thus, stress assessment is a direct need. Surgical simulation is a validated standardised training milieu designed to replicate real-life situations. It replicates stress, prevents biases, and provides objective metrics. The complexity of stress mechanisms makes stress measurement difficult to quantify and interpret. This systematic review aims to identify studies that have used acute stress estimation measurements in surgeons or surgical trainees during real operations or surgical simulation, and to collectively present the rationale of these tools, with special emphasis in salivary markers. A search strategy was implemented to retrieve relevant articles from MEDLINE and SCOPUS databases. The 738 articles retrieved were reviewed for further evaluation according to the predetermined inclusion/exclusion criteria. Thirty-three studies were included in this systematic review. The methods for acute stress assessment varied greatly among studies with the non-invasive techniques being the most commonly used. Subjective and objective tests for surgeons' acute stress assessment are being presented. There is a broad spectrum of acute mental stress assessment tools in the surgical field and simulation and salivary biomarkers have recently gained popularity. There is a need to maintain a consistent methodology in future research, towards a deeper understanding of acute stress in the surgical field. Copyright © 2017 Royal College of Surgeons of Edinburgh (Scottish charity number SC005317) and Royal College of Surgeons in Ireland. Published by Elsevier Ltd. All rights reserved.

Effects of emotional exposure on state anxiety after acute exercise.

PubMed

Smith, J Carson

2013-02-01

Despite the well-known anxiolytic effect of acute exercise, it is unknown if anxiety reductions after acute exercise conditions survive in the face of a subsequently experienced arousing emotional exposure. The purpose of this study was to compare the effects of moderate-intensity cycle ergometer exercise to a seated rest control condition on state anxiety symptoms after exposure to a variety of highly arousing pleasant and unpleasant stimuli. Thirty-seven healthy and normally physically active young adults completed two conditions on separate days: 1) 30 min of seated rest and 2) 30 min of moderate-intensity cycle ergometer exercise (RPE = 13; "somewhat hard"). After each condition, participants viewed 90 arousing pleasant, unpleasant, and neutral pictures from the International Affective Picture System for 30 min. State anxiety was measured before and 15 min after each condition, and again after exposure to the affective pictures. State anxiety significantly decreased from baseline to after the exercise and seated rest conditions (P = 0.003). After the emotional picture-viewing period, state anxiety significantly increased to baseline values after the seated rest condition (P = 0.001) but remained reduced after the exercise condition. These findings suggest that the anxiolytic effects of acute exercise may be resistant to the potentially detrimental effects on mood after exposure to arousing emotional stimuli.

Acute and chronic respiratory effects of sodium borate particulate exposures.

PubMed Central

Wegman, D H; Eisen, E A; Hu, X; Woskie, S R; Smith, R G; Garabrant, D H

1994-01-01

This study examined work-related chronic abnormality in pulmonary function and work-related acute irritant symptoms associated with exposure to borate dust in mining and processing operations. Chronic effects were examined by pulmonary function at the beginning and end of a 7-year interval. Time-specific estimates of sodium borate particulate exposures were used to estimate cumulative exposure during the study interval. Change in pulmonary function over the 7 years was found unrelated to the estimate of cumulative exposure during that interval. Exposure-response associations also were examined with respect to short-term peak exposures and incidence of five symptoms of acute respiratory irritation. Hourly measures of health outcome and continuous measures of particulate exposure were made on each subject throughout the day. Whenever a subject reported one of the irritant symptoms, a symptom intensity score was also recorded along with the approximate time of onset. The findings indicated that exposure-response relationships were present for each of the specific symptoms at several symptom intensity levels. The associations were present when exposure was estimated by both day-long and short-term (15-min) time-weighted average exposures. Associations persisted after taking account of smoking, age, and the presence of a common cold. No significant difference in response rate was found between workers exposed to different types of sodium borate dusts. PMID:7889871

Acute phase response, inflammation and metabolic syndrome biomarkers of Libby asbestos exposure

DOE Office of Scientific and Technical Information (OSTI.GOV)

Shannahan, Jonathan H.; Alzate, Oscar; Winnik, Witold M.

Identification of biomarkers assists in the diagnosis of disease and the assessment of health risks from environmental exposures. We hypothesized that rats exposed to Libby amphibole (LA) would present with a unique serum proteomic profile which could help elucidate epidemiologically-relevant biomarkers. In four experiments spanning varied protocols and temporality, healthy (Wistar Kyoto, WKY; and F344) and cardiovascular compromised (CVD) rat models (spontaneously hypertensive, SH; and SH heart failure, SHHF) were intratracheally instilled with saline (control) or LA. Serum biomarkers of cancer, inflammation, metabolic syndrome (MetS), and the acute phase response (APR) were analyzed. All rat strains exhibited acute increases inmore » α-2-macroglobulin, and α1-acid glycoprotein. Among markers of inflammation, lipocalin-2 was induced in WKY, SH and SHHF and osteopontin only in WKY after LA exposure. While rat strain- and age-related changes were apparent in MetS biomarkers, no LA effects were evident. The cancer marker mesothelin was increased only slightly at 1 month in WKY in one of the studies. Quantitative Intact Proteomic profiling of WKY serum at 1 day or 4 weeks after 4 weekly LA instillations indicated no oxidative protein modifications, however APR proteins were significantly increased. Those included serine protease inhibitor, apolipoprotein E, α-2-HS-glycoprotein, t-kininogen 1 and 2, ceruloplasmin, vitamin D binding protein, serum amyloid P, and more 1 day after last LA exposure. All changes were reversible after a short recovery regardless of the acute or long-term exposures. Thus, LA exposure induces an APR and systemic inflammatory biomarkers that could have implications in systemic and pulmonary disease in individuals exposed to LA. -- Highlights: ► Biomarkers of asbestos exposure are required for disease diagnosis. ► Libby amphibole exposure is associated with increased human mortality. ► Libby amphibole increases circulating proteins

Acute restraint stress induces endothelial dysfunction: role of vasoconstrictor prostanoids and oxidative stress.

PubMed

Carda, Ana P P; Marchi, Katia C; Rizzi, Elen; Mecawi, André S; Antunes-Rodrigues, José; Padovan, Claudia M; Tirapelli, Carlos R

2015-01-01

We hypothesized that acute stress would induce endothelial dysfunction. Male Wistar rats were restrained for 2 h within wire mesh. Functional and biochemical analyses were conducted 24 h after the 2-h period of restraint. Stressed rats showed decreased exploration on the open arms of an elevated-plus maze (EPM) and increased plasma corticosterone concentration. Acute restraint stress did not alter systolic blood pressure, whereas it increased the in vitro contractile response to phenylephrine and serotonin in endothelium-intact rat aortas. NG-nitro-l-arginine methyl ester (l-NAME; nitric oxide synthase, NOS, inhibitor) did not alter the contraction induced by phenylephrine in aortic rings from stressed rats. Tiron, indomethacin and SQ29548 reversed the increase in the contractile response to phenylephrine induced by restraint stress. Increased systemic and vascular oxidative stress was evident in stressed rats. Restraint stress decreased plasma and vascular nitrate/nitrite (NOx) concentration and increased aortic expression of inducible (i) NOS, but not endothelial (e) NOS. Reduced expression of cyclooxygenase (COX)-1, but not COX-2, was observed in aortas from stressed rats. Restraint stress increased thromboxane (TX)B(2) (stable TXA(2) metabolite) concentration but did not affect prostaglandin (PG)F2α concentration in the aorta. Restraint reduced superoxide dismutase (SOD) activity, whereas concentrations of hydrogen peroxide (H(2)O(2)) and reduced glutathione (GSH) were not affected. The major new finding of our study is that restraint stress increases vascular contraction by an endothelium-dependent mechanism that involves increased oxidative stress and the generation of COX-derived vasoconstrictor prostanoids. Such stress-induced endothelial dysfunction could predispose to the development of cardiovascular diseases.

Acute decrease in HDL cholesterol associated with exposure to welding fumes.

PubMed

Rice, Mary Berlik; Cavallari, Jenn; Fang, Shona; Christiani, David

2011-01-01

To investigate acute changes in circulating lipids after exposure to relatively high levels of particulate matter through welding. Using a repeated measures panel study, lipid levels before and after welding and personal exposures to fine particulate matter (PM2.5) were measured in 36 male welders over 63 exposure and/or control days. There was a trend toward decrease in HDL (-2.3 mg/dL, P = 0.08) 18 hours after welding. This effect became significant (-2.6 mg/dL, P = 0.05) after adjustment for possible confounders. The effect was strongest (-4.3 mg/dL, P = 0.02) among welders who did not weld the day before the study. There were no significant changes in other lipids associated with welding or PM2.5 exposure. Welding exposure was associated with an acute decrease in circulating HDL, which may relate to the inflammatory and proatherosclerotic effects of fine particle exposure.

Acute Decrease in HDL Cholesterol Associated With Exposure to Welding Fumes

PubMed Central

Rice, Mary Berlik; Cavallari, Jenn; Fang, Shona; Christiani, David

2011-01-01

Objective To investigate acute changes in circulating lipids after exposure to relatively high levels of particulate matter through welding. Methods Using a repeated measures panel study, lipid levels before and after welding and personal exposures to fine particulate matter (PM2.5) were measured in 36 male welders over 63 exposure and/or control days. Results There was a trend toward decrease in HDL (−2.3 mg/dL, P = 0.08) 18 hours after welding. This effect became significant (−2.6 mg/dL, P = 0.05) after adjustment for possible confounders. The effect was strongest (−4.3 mg/dL, P = 0.02) among welders who did not weld the day before the study. There were no significant changes in other lipids associated with welding or PM2.5 exposure. Conclusion Welding exposure was associated with an acute decrease in circulating HDL, which may relate to the inflammatory and proatherosclerotic effects of fine particle exposure. PMID:21187793

Acute exposure to waterpipe tobacco smoke induces changes in the oxidative and inflammatory markers in mouse lung

PubMed Central

Khabour, Omar F.; Alzoubi, Karem H.; Bani-Ahmad, Mohammed; Dodin, Arwa; Eissenberg, Thomas; Shihadeh, Alan

2013-01-01

Context Tobacco smoking represents a global public health threat, claiming approximately 5 million lives a year. Waterpipe tobacco use has become popular particularly among youth in the past decade, buttressed by the perception that the waterpipe “filters” the smoke, rendering it less harmful than cigarette smoke. Objective In this study, we examined the acute exposure of waterpipe smoking on lung inflammation and oxidative stress in mice, and compared that to cigarette smoking. Materials and methods Mice were divided into three groups; fresh air control, cigarette and waterpipe. Animals were exposed to fresh air, cigarette, or waterpipe smoke using whole body exposure system one hour daily for 7 days. Results Both cigarette and waterpipe smoke exposure resulted in elevation of total white blood cell count, as well as absolute count of neutrophils, macrophages, and lymphocytes (P < 0.01). Both exposures also elevated proinflammatory markers such as TNF-α and IL-6 in BALF (P < 0.05), and oxidative stress markers including GPx activity in lungs (P < 0.05). Moreover, waterpipe smoke increased catalase activity in the lung (P < 0.05). However, none of the treatments altered IL-10 levels. Discussion and conclusion Results of cigarette smoking confirmed previous finding. Waterpipe results indicate that, similar to cigarettes, exposure to waterpipe tobacco smoke is harmful to the lungs. PMID:22906173

Juvenile social defeat stress exposure persistently impairs social behaviors and neurogenesis.

PubMed

Mouri, Akihiro; Ukai, Mayu; Uchida, Mizuki; Hasegawa, Sho; Taniguchi, Masayuki; Ito, Takahiro; Hida, Hirotake; Yoshimi, Akira; Yamada, Kiyofumi; Kunimoto, Shohko; Ozaki, Norio; Nabeshima, Toshitaka; Noda, Yukihiro

2018-05-01

Adverse juvenile experiences, including physical abuse, often have negative health consequences later in life. We investigated the influence of social defeat stress exposure as juveniles on neuropsychological behaviors, and the causal role of glucocorticoids in abnormal behaviors and impairment of neurogenesis in mice exposed to the stress. The juvenile (24-day-old) and adult (70-day-old) male C57BL/6J mice were exposed to social defeat stress induced by an aggressive ICR mouse. Social defeat stress exposure as juveniles, even for 1 day, induced persistent social avoidance to the unfamiliar ICR mouse in the social interaction test, but that was not observed in mice exposed to the stress as adults. Social avoidance by the stress exposure as juveniles for 10 consecutive days was observed, when the target mouse was not only unfamiliar ICR but also another C57BL/J mouse, but not an absent or an anesthetized ICR mouse. The stress exposure did not induce anxiety- and depression-like behaviors in spontaneous locomotor activity, elevated plus-maze test, marble-burying test, forced swimming test, or sucrose preference test. Serum corticosterone levels increased immediately after the stress exposure. The hippocampal neurogenesis was suppressed 1 day and 4 weeks after the stress exposure. Administration of mifepristone, a glucocorticoid receptor antagonist, prior to each stress exposure, blocked the persistent social avoidance and suppression of neurogenesis. In conclusion, social avoidance induced by social defeat stress exposure as juveniles are more persistent than that as adults. These social avoidances are associated with suppression of hippocampal neurogenesis via glucocorticoid receptors. Copyright © 2018 Elsevier Ltd. All rights reserved.

Olive oil-supplemented diet alleviates acute heat stress-induced mitochondrial ROS production in chicken skeletal muscle.

PubMed

Mujahid, Ahmad; Akiba, Yukio; Toyomizu, Masaaki

2009-09-01

We have previously shown that avian uncoupling protein (avUCP) is downregulated on exposure to acute heat stress, stimulating mitochondrial reactive oxygen species (ROS) production and oxidative damage. In this study, we investigated whether upregulation of avUCP could attenuate oxidative damage caused by acute heat stress. Broiler chickens (Gallus gallus) were fed either a control diet or an olive oil-supplemented diet (6.7%), which has been shown to increase the expression of UCP3 in mammals, for 8 days and then exposed either to heat stress (34 degrees C, 12 h) or kept at a thermoneutral temperature (25 degrees C). Skeletal muscle mitochondrial ROS (measured as H(2)O(2)) production, avUCP expression, oxidative damage, mitochondrial membrane potential, and oxygen consumption were studied. We confirmed that heat stress increased mitochondrial ROS production and malondialdehyde levels and decreased the amount of avUCP. As expected, feeding birds an olive oil-supplemented diet increased the expression of avUCP in skeletal muscle mitochondria and decreased ROS production and oxidative damage. Studies on mitochondrial function showed that heat stress increased membrane potential in state 4, which was reversed by feeding birds an olive oil-supplemented diet, although no differences in basal proton leak were observed between control and heat-stressed groups. These results show that under heat stress, mitochondrial ROS production and olive oil-induced reduction of ROS production may occur due to changes in respiratory chain activity as well as avUCP expression in skeletal muscle mitochondria.

Oxidative stress, inflammation, and DNA damage in multiple organs of mice acutely exposed to amorphous silica nanoparticles.

PubMed

Nemmar, Abderrahim; Yuvaraju, Priya; Beegam, Sumaya; Yasin, Javed; Kazzam, Elsadig E; Ali, Badreldin H

2016-01-01

The use of amorphous silica (SiO2) in biopharmaceutical and industrial fields can lead to human exposure by injection, skin penetration, ingestion, or inhalation. However, the in vivo acute toxicity of amorphous SiO2 nanoparticles (SiNPs) on multiple organs and the mechanisms underlying these effects are not well understood. Presently, we investigated the acute (24 hours) effects of intraperitoneally administered 50 nm SiNPs (0.25 mg/kg) on systemic toxicity, oxidative stress, inflammation, and DNA damage in the lung, heart, liver, kidney, and brain of mice. Lipid peroxidation was significantly increased by SiNPs in the lung, liver, kidney, and brain, but was not changed in the heart. Similarly, superoxide dismutase and catalase activities were significantly affected by SiNPs in all organs studied. While the concentration of tumor necrosis factor α was insignificantly increased in the liver and brain, its increase was statistically significant in the lung, heart, and kidney. SiNPs induced a significant elevation in pulmonary and renal interleukin 6 and interleukin-1 beta in the lung, liver, and brain. Moreover, SiNPs caused a significant increase in DNA damage, assessed by comet assay, in all the organs studied. SiNPs caused leukocytosis and increased the plasma activities of lactate dehydrogenase, creatine kinase, alanine aminotranferase, and aspartate aminotransferase. These results indicate that acute systemic exposure to SiNPs causes oxidative stress, inflammation, and DNA damage in several major organs, and highlight the need for thorough evaluation of SiNPs before they can be safely used in human beings.

Nerve growth factor (NGF) immunoreactive neurons in the juvenile rat hippocampus: response to acute and long-term high-light open-field (HL-OF) or forced swim (FS) stress stimulation.

PubMed

Badowska-Szalewska, E; Spodnik, E; Ludkiewicz, B; Klejbor, I; Moryś, J

2011-12-29

This study aimed at examining and comparing the influence of two different stress stimuli on the density (number of cells/mm²) of nerve growth factor (NGF) containing neurons in the hippocampal CA1 and CA3 pyramidal cell layers and the dentate gyrus (DG) granule cell layer in juvenile rats (P28; P-postnatal day). The high-light open-field (HL-OF) test and forced swim (FS) test were employed to investigate the effects of a single, 15-min acute exposure and repeated (15 min daily for 21 days) long-term exposure to stress. In order to detect NGF-ir neurons, immunohistochemical (-ir) techniques were used. In comparison with nonstressed animals, acute and long-term HL-OF or FS stimulation resulted in a marked increase (P<0.001) in the density of NGF-ir containing cells in all the hippocampal structures. The frequency of stress application (acute vs. long-term), however, did not have a substantial impact on the studied parameter, with the exception of the CA3 sector, where a decreased density (P<0.001) of NGF-ir neurons was observed after long-term exposure to FS. It may be concluded that a rise in the density of NGF-ir neurons in the juvenile rat hippocampus after exposure to HL-OF or FS stressors could have affected the activity of the hypothalamic-pituitary-adrenocortical (HPA) stress axis. Prolonged HL-OF or FS stress was probably aggravating enough not to trigger the habituation process. The type of stressor applied (HL-OF vs. FS) was not essentially a factor determining the density of NGF-ir cells in the hippocampus. Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.

Good Stress, Bad Stress and Oxidative Stress: Insights from Anticipatory Cortisol Reactivity

PubMed Central

Aschbacher, Kirstin; O'Donovan, Aoife; Wolkowitz, Owen M.; Dhabhar, Firdaus S.; Su, Yali; Epel, Elissa

2014-01-01

Chronic psychological stress appears to accelerate biological aging, and oxidative damage is an important potential mediator of this process. However, the mechanisms by which psychological stress promotes oxidative damage are poorly understood. This study investigates the theory that cortisol increases in response to an acutely stressful event have the potential to either enhance or undermine psychobiological resilience to oxidative damage, depending on the body's prior exposure to chronic psychological stress. In order to achieve a range of chronic stress exposure, forty-eight post-menopausal women were recruited in a case-control design that matched women caring for spouses with dementia (a chronic stress model) with similarly aged control women whose spouses were healthy. Participants completed a questionnaire assessing perceived stress over the previous month and provided fasting blood. Three markers of oxidative damage were assessed: 8-iso-prostaglandin F2α (IsoP), lipid peroxidation, 8-hydroxyguanosine (8-OxoG) and 8-hydroxy-2′-deoxyguanosine (8-OHdG), reflecting oxidative damage to RNA/DNA respectively. Within approximately one week, participants completed a standardized acute laboratory stress task while salivary cortisol responses were measured. The increase from 0 to 30 min was defined as “peak” cortisol reactivity, while the increase from 0 to 15 min was defined as “anticipatory” cortisol reactivity, representing a cortisol response that began while preparing for the stress task. Women under chronic stress had higher 8-oxoG, oxidative damage to RNA (p<.01). A moderated mediation model was tested, in which it was hypothesized that heightened anticipatory cortisol reactivity would mediate the relationship between perceived stress and elevated oxidative stress damage, but only among women under chronic stress. Consistent with this model, bootstrapped path analysis found significant indirect paths from perceived stress to 8-OxoG and IsoP (but not

Good stress, bad stress and oxidative stress: insights from anticipatory cortisol reactivity.

PubMed

Aschbacher, Kirstin; O'Donovan, Aoife; Wolkowitz, Owen M; Dhabhar, Firdaus S; Su, Yali; Epel, Elissa

2013-09-01

Chronic psychological stress appears to accelerate biological aging, and oxidative damage is an important potential mediator of this process. However, the mechanisms by which psychological stress promotes oxidative damage are poorly understood. This study investigates the theory that cortisol increases in response to an acutely stressful event have the potential to either enhance or undermine psychobiological resilience to oxidative damage, depending on the body's prior exposure to chronic psychological stress. In order to achieve a range of chronic stress exposure, forty-eight post-menopausal women were recruited in a case-control design that matched women caring for spouses with dementia (a chronic stress model) with similarly aged control women whose spouses were healthy. Participants completed a questionnaire assessing perceived stress over the previous month and provided fasting blood. Three markers of oxidative damage were assessed: 8-iso-prostaglandin F(2α) (IsoP), lipid peroxidation, 8-hydroxyguanosine (8-oxoG) and 8-hydroxy-2'-deoxyguanosine (8-OHdG), reflecting oxidative damage to RNA/DNA respectively. Within approximately one week, participants completed a standardized acute laboratory stress task while salivary cortisol responses were measured. The increase from 0 to 30 min was defined as "peak" cortisol reactivity, while the increase from 0 to 15 min was defined as "anticipatory" cortisol reactivity, representing a cortisol response that began while preparing for the stress task. Women under chronic stress had higher 8-oxoG, oxidative damage to RNA (p<.01). A moderated mediation model was tested, in which it was hypothesized that heightened anticipatory cortisol reactivity would mediate the relationship between perceived stress and elevated oxidative stress damage, but only among women under chronic stress. Consistent with this model, bootstrapped path analysis found significant indirect paths from perceived stress to 8-oxoG and IsoP (but not 8-OHd

Self-esteem levels and cardiovascular and inflammatory responses to acute stress.

PubMed

O'Donnell, Katie; Brydon, Lena; Wright, Caroline E; Steptoe, Andrew

2008-11-01

Acute mental stress tests have helped to clarify the pathways through which psychosocial factors are linked to disease risk. This methodology is now being used to investigate potentially protective psychosocial factors. We investigated whether global self-esteem might buffer cardiovascular and inflammatory responses to acute stress. One hundred and one students completed the Rosenberg Self-Esteem Scale. Heart rate and heart rate variability (HRV) were recorded for 5 min periods at baseline, during two mental stress tasks, (a speech and a color-word task) and 10, 25 and 40 min into a recovery period. Plasma levels of tumor-necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-1 receptor antagonist (IL-1Ra) were assessed at baseline, immediately post-stress and after 45 min recovery. Repeated measures analysis of variance demonstrated that heart rate levels were lower across all time points in those with high self-esteem, although heart rate reactivity to stress was not related to self-esteem. There were no differences in baseline HRV, TNF-alpha, IL-6 or IL-1Ra. Multiple linear regressions revealed that greater self-esteem was associated with a smaller reduction in heart rate variability during the speech task, but not the color-word task. Greater self-esteem was associated with smaller TNF-alpha and IL-1Ra responses immediately following acute stress and smaller IL-1Ra responses at 45 min post-stress. In conclusion, global self-esteem is associated with lower heart rate and attenuated HRV and inflammatory responses to acute stress. These responses could be processes through which self-esteem protects against the development of disease.

Genome-wide Gene Expression Profiling of Acute Metal Exposures in Male Zebrafish

DTIC Science & Technology

2014-10-23

Data in Brief Genome-wide gene expression profiling of acute metal exposures in male zebrafish Christine E. Baer a,⁎, Danielle L. Ippolito b, Naissan... Zebrafish Whole organism Nickel Chromium Cobalt Toxicogenomics To capture global responses to metal poisoning and mechanistic insights into metal...toxicity, gene expression changes were evaluated in whole adult male zebrafish following acute 24 h high dose exposure to three metals with known human

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

PubMed

Qi, Mingming; Gao, Heming; Liu, Guangyuan

2017-04-14

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. Copyright © 2017 Elsevier B.V. All rights reserved.

Endoplasmic reticulum stress-mediated neuronal apoptosis by acrylamide exposure

DOE Office of Scientific and Technical Information (OSTI.GOV)

Komoike, Yuta, E-mail: komoike@research.twmu.ac.jp

Acrylamide (AA) is a well-known neurotoxic compound in humans and experimental animals. However, intracellular stress signaling pathways responsible for the neurotoxicity of AA are still not clear. In this study, we explored the involvement of the endoplasmic reticulum (ER) stress response in AA-induced neuronal damage in vitro and in vivo. Exposure of SH-SY5Y human neuroblastoma cells to AA increased the levels of phosphorylated form of eukaryotic translation initiation factor 2α (eIF2α) and its downstream effector, activating transcription factor 4 (ATF4), indicating the induction of the unfolded protein response (UPR) by AA exposure. Furthermore, AA exposure increased the mRNA level ofmore » c/EBP homologous protein (CHOP), the ER stress-dependent apoptotic factor, and caused the accumulation of reactive oxygen species (ROS) in SH-SY5Y cells. Treatments of SH-SY5Y cells with the chemical chaperone, 4-phenylbutyric acid and the ROS scavenger, N-acetyl-cysteine reduced the AA-induced expression of ATF4 protein and CHOP mRNA, and resulted in the suppression of apoptosis. In addition, AA-induced eIF2α phosphorylation was also suppressed by NAC treatment. In consistent with in vitro study, exposure of zebrafish larvae at 6-day post fertilization to AA induced the expression of chop mRNA and apoptotic cell death in the brain, and also caused the disruption of brain structure. These findings suggest that AA exposure induces apoptotic neuronal cell death through the ER stress and subsequent eIF2α–ATF4–CHOP signaling cascade. The accumulation of ROS by AA exposure appears to be responsible for this ER stress-mediated apoptotic pathway. - Highlights: • Exposure of SH-SY5Y cells to AA activates the eIF2α–ATF4 pathway of the UPR. • Exposure of SH-SY5Y cells to AA induces the CHOP expression and apoptosis. • Exposure of zebrafish to AA induces the chop expression and apoptosis in the brain. • AA possibly induces apoptotic neuronal cell death through the

Modification of hippocampal markers of synaptic plasticity by memantine in animal models of acute and repeated restraint stress: implications for memory and behavior.

PubMed

Amin, Shaimaa Nasr; El-Aidi, Ahmed Amro; Ali, Mohamed Mostafa; Attia, Yasser Mahmoud; Rashed, Laila Ahmed

2015-06-01

Stress is any condition that impairs the balance of the organism physiologically or psychologically. The response to stress involves several neurohormonal consequences. Glutamate is the primary excitatory neurotransmitter in the central nervous system, and its release is increased by stress that predisposes to excitotoxicity in the brain. Memantine is an uncompetitive N-methyl D-aspartate glutamatergic receptors antagonist and has shown beneficial effect on cognitive function especially in Alzheimer's disease. The aim of the work was to investigate memantine effect on memory and behavior in animal models of acute and repeated restraint stress with the evaluation of serum markers of stress and the expression of hippocampal markers of synaptic plasticity. Forty-two male rats were divided into seven groups (six rats/group): control, acute restraint stress, acute restraint stress with Memantine, repeated restraint stress, repeated restraint stress with Memantine and Memantine groups (two subgroups as positive control). Spatial working memory and behavior were assessed by performance in Y-maze. We evaluated serum cortisol, tumor necrotic factor, interleukin-6 and hippocampal expression of brain-derived neurotrophic factor, synaptophysin and calcium-/calmodulin-dependent protein kinase II. Our results revealed that Memantine improved spatial working memory in repeated stress, decreased serum level of stress markers and modified the hippocampal synaptic plasticity markers in both patterns of stress exposure; in ARS, Memantine upregulated the expression of synaptophysin and brain-derived neurotrophic factor and downregulated the expression of calcium-/calmodulin-dependent protein kinase II, and in repeated restraint stress, it upregulated the expression of synaptophysin and downregulated calcium-/calmodulin-dependent protein kinase II expression.

Chronic and Acute Stress Promote Overexploitation in Serial Decision Making.

PubMed

Lenow, Jennifer K; Constantino, Sara M; Daw, Nathaniel D; Phelps, Elizabeth A

2017-06-07

Many decisions that humans make resemble foraging problems in which a currently available, known option must be weighed against an unknown alternative option. In such foraging decisions, the quality of the overall environment can be used as a proxy for estimating the value of future unknown options against which current prospects are compared. We hypothesized that such foraging-like decisions would be characteristically sensitive to stress, a physiological response that tracks biologically relevant changes in environmental context. Specifically, we hypothesized that stress would lead to more exploitative foraging behavior. To test this, we investigated how acute and chronic stress, as measured by changes in cortisol in response to an acute stress manipulation and subjective scores on a questionnaire assessing recent chronic stress, relate to performance in a virtual sequential foraging task. We found that both types of stress bias human decision makers toward overexploiting current options relative to an optimal policy. These findings suggest a possible computational role of stress in decision making in which stress biases judgments of environmental quality. SIGNIFICANCE STATEMENT Many of the most biologically relevant decisions that we make are foraging-like decisions about whether to stay with a current option or search the environment for a potentially better one. In the current study, we found that both acute physiological and chronic subjective stress are associated with greater overexploitation or staying at current options for longer than is optimal. These results suggest a domain-general way in which stress might bias foraging decisions through changing one's appraisal of the overall quality of the environment. These novel findings not only have implications for understanding how this important class of foraging decisions might be biologically implemented, but also for understanding the computational role of stress in behavior and cognition more broadly

Chronic and Acute Stress Promote Overexploitation in Serial Decision Making

PubMed Central

Lenow, Jennifer K.; Constantino, Sara M.

2017-01-01

Many decisions that humans make resemble foraging problems in which a currently available, known option must be weighed against an unknown alternative option. In such foraging decisions, the quality of the overall environment can be used as a proxy for estimating the value of future unknown options against which current prospects are compared. We hypothesized that such foraging-like decisions would be characteristically sensitive to stress, a physiological response that tracks biologically relevant changes in environmental context. Specifically, we hypothesized that stress would lead to more exploitative foraging behavior. To test this, we investigated how acute and chronic stress, as measured by changes in cortisol in response to an acute stress manipulation and subjective scores on a questionnaire assessing recent chronic stress, relate to performance in a virtual sequential foraging task. We found that both types of stress bias human decision makers toward overexploiting current options relative to an optimal policy. These findings suggest a possible computational role of stress in decision making in which stress biases judgments of environmental quality. SIGNIFICANCE STATEMENT Many of the most biologically relevant decisions that we make are foraging-like decisions about whether to stay with a current option or search the environment for a potentially better one. In the current study, we found that both acute physiological and chronic subjective stress are associated with greater overexploitation or staying at current options for longer than is optimal. These results suggest a domain-general way in which stress might bias foraging decisions through changing one's appraisal of the overall quality of the environment. These novel findings not only have implications for understanding how this important class of foraging decisions might be biologically implemented, but also for understanding the computational role of stress in behavior and cognition more broadly

The dynamic interplay between acute psychosocial stress, emotion and autobiographical memory.

PubMed

Sheldon, Signy; Chu, Sonja; Nitschke, Jonas P; Pruessner, Jens C; Bartz, Jennifer A

2018-06-06

Although acute psychosocial stress can impact autobiographical memory retrieval, the nature of this effect is not entirely clear. One reason for this ambiguity is because stress can have opposing effects on the different stages of autobiographical memory retrieval. We addressed this issue by testing how acute stress affects three stages of the autobiographical memory retrieval - accessing, recollecting and reconsolidating a memory. We also investigate the influence of emotion valence on this effect. In a between-subjects design, participants were first exposed to an acute psychosocial stressor or a control task. Next, the participants were shown positive, negative or neutral retrieval cues and asked to access and describe autobiographical memories. After a three to four day delay, participants returned for a second session in which they described these autobiographical memories. During initial retrieval, stressed participants were slower to access memories than were control participants; moreover, cortisol levels were positively associated with response times to access positively-cued memories. There were no effects of stress on the amount of details used to describe memories during initial retrieval, but stress did influence memory detail during session two. During session two, stressed participants recovered significantly more details, particularly emotional ones, from the remembered events than control participants. Our results indicate that the presence of stress impairs the ability to access consolidated autobiographical memories; moreover, although stress has no effect on memory recollection, stress alters how recollected experiences are reconsolidated back into memory traces.

The Prosodic Evolution of West Slavic in the Context of the Neo-Acute Stress

ERIC Educational Resources Information Center

Feldstein, Ronald F.

1975-01-01

Because of neo-acute stress--or transferred acute stress--long vowel prosody in West Slavic had a special evolution. Two kinds of long vowel evolution are examined. The nature of transitionality across Slavic territory from tonal opposition to distinctive stress placement is pointed out. (SC)

Chronic vs. Short-Term Acute O 3 Exposure Effects on Nocturnal Transpiration in Two Californian Oaks

Treesearch

Nancy Grulke; E. Paoletti; R. L. Heath

2007-01-01

We tested the effect of daytime chronic moderate ozone (O3) exposure, short-term acute exposure, and both chronic and acute O3 exposure combined on nocturnal transpiration in California black oak and blue oak seedlings. Chronic O3 exposure (70 ppb for 8 h/day) was implemented in open-top chambers for...

Striatal dopamine dynamics in mice following acute and repeated toluene exposure.

PubMed

Apawu, Aaron K; Mathews, Tiffany A; Bowen, Scott E

2015-01-01

The abused inhalant toluene has potent behavioral effects, but only recently has progress been made in understanding the neurochemical actions that mediate the action of toluene in the brain. Available evidence suggests that toluene inhalation alters dopamine (DA) neurotransmission, but toluene's mechanism of action is unknown. The present study evaluated the effect of acute and repeated toluene inhalation (0, 2,000, or 4,000 ppm) on locomotor activity as well as striatal DA release and uptake using slice fast-scan cyclic voltammetry. Acutely, 2,000 and 4,000 ppm toluene increased locomotor activity, while neurochemically only 4,000 ppm toluene potentiated electrically evoked DA release across the caudate-putamen and the nucleus accumbens. Repeated administration of toluene resulted in sensitization to toluene's locomotor activity effects. Brain slices obtained from mice repeatedly exposed to toluene demonstrated no difference in stimulated DA release in the caudate-putamen as compared to control animals. Repeated exposure to 2,000 and 4,000 ppm toluene caused a concentration-dependent decrease of 25-50 % in evoked DA release in the nucleus accumbens core and shell relative to air-exposed mice. These voltammetric neurochemical findings following repeated toluene exposure suggest that there may be a compensatory downregulation of the DA system. Acute or repeated toluene exposure had no effect on the DA uptake kinetics. Taken together, these results demonstrate that acute toluene inhalation potentiates DA release, while repeated toluene exposure attenuates DA release in the nucleus accumbens only.

Acute social stress increases biochemical and self report markers of stress without altering spatial learning in humans.

PubMed

Klopp, Christine; Garcia, Carlos; Schulman, Allan H; Ward, Christopher P; Tartar, Jaime L

2012-01-01

Spatial learning is shown to be influenced by acute stress in both human and other animals. However, the intricacies of this relationship are unclear. Based on prior findings we hypothesized that compared to a control condition, a social stress condition would not affect spatial learning performance despite elevated biochemical markers of stress. The present study tested the effects of social stress in human males and females on a subsequent spatial learning task. Social stress induction consisted of evaluative stress (the Trier Social Stress Test, TSST) compared to a placebo social stress. Compared to the placebo condition, the TSST resulted in significantly elevated cortisol and alpha amylase levels at multiple time points following stress induction. In accord, cognitive appraisal measures also showed that participants in the TSST group experienced greater perceived stress compared to the placebo group. However, there were no group differences in performance on a spatial learning task. Our findings suggest that unlike physiological stress, social stress does not result in alterations in spatial learning in humans. It is possible that moderate social evaluative stress in humans works to prevent acute stress-mediated alterations in hippocampal learning processes..

[Acute Stress and Broken Heart Syndrome. A Case Report].

PubMed

Vergel, Juliana; Tamayo-Orozco, Sebastián; Vallejo-Gómez, Andrés Felipe; Posada, María Teresa; Restrepo, Diana

Stress has been associated with an acute heart failure syndrome of important morbidity and mortality. Case report and non-systematic review of the relevant literature. A 65-year-old woman with a history of an untreated generalized anxiety disorder, whom after the violent death of her son presented with oppressive chest pain irradiated to neck and left superior extremity, lasting for more than 30minutes, initial clinical suspect suggests acute coronary syndrome. Tako-tsubo cardiomyopathy is characterized by a reversible left ventricular dysfunction and wall movement abnormalities, without any compromise of the coronary arteries, associated to high plasma levels of catecholamines which in most cases correlates with an acute stress of emotional or physical type. Tako-tsubo cardiomyopathy has to be considered by physicians among the differential diagnosis when facing a patient with suspected acute coronary syndrome, especially in post-menopausal women with a history of psychiatric comorbidities such as a generalized anxiety disorder. Copyright © 2016 Asociación Colombiana de Psiquiatría. Publicado por Elsevier España. All rights reserved.

Emotional Stress and Cardiovascular Complications in Animal Models: A Review of the Influence of Stress Type

PubMed Central

Crestani, Carlos C.

2016-01-01

Emotional stress has been recognized as a modifiable risk factor for cardiovascular diseases. The impact of stress on physiological and psychological processes is determined by characteristics of the stress stimulus. For example, distinct responses are induced by acute vs. chronic aversive stimuli. Additionally, the magnitude of stress responses has been reported to be inversely related to the degree of predictability of the aversive stimulus. Therefore, the purpose of the present review was to discuss experimental research in animal models describing the influence of stressor stimulus characteristics, such as chronicity and predictability, in cardiovascular dysfunctions induced by emotional stress. Regarding chronicity, the importance of cardiovascular and autonomic adjustments during acute stress sessions and cardiovascular consequences of frequent stress response activation during repeated exposure to aversive threats (i.e., chronic stress) is discussed. Evidence of the cardiovascular and autonomic changes induced by chronic stressors involving daily exposure to the same stressor (predictable) vs. different stressors (unpredictable) is reviewed and discussed in terms of the impact of predictability in cardiovascular dysfunctions induced by stress. PMID:27445843

Cancer, acute stress disorder, and repressive coping.

PubMed

Pedersen, Anette Fischer; Zachariae, Robert

2010-02-01

The purpose of this study was to investigate the association between repressive coping style and Acute Stress Disorder (ASD) in a sample of cancer patients. A total of 112 cancer patients recently diagnosed with cancer participated in the study. ASD was assessed by the Stanford Acute Stress Reaction Questionnaire, and repressive coping was assessed by a combination of scores from the Marlowe-Crowne Social Desirability Scale, and the Bendig version of the Taylor Manifest Anxiety Scale. Significantly fewer patients classified as "repressors" were diagnosed with ASD compared to patients classified as "non-repressors". However, further investigations revealed that the lower incidence of ASD in repressors apparently was caused by a low score on anxiety and not by an interaction effect between anxiety and defensiveness. Future studies have to investigate whether different psychological mechanisms are responsible for the lower incidence of ASD in repressors and true low-anxious patients.

Leptin concentrations in response to acute stress predict subsequent intake of comfort foods

PubMed Central

Tomiyama, A. Janet; Schamarek, Imke; Lustig, Robert H.; Kirschbaum, Clemens; Puterman, Eli; Havel, Peter J.; Epel, Elissa S.

2012-01-01

Both animals and humans show a tendency toward eating more “comfort food” (high fat, sweet food) after acute stress. Such stress eating may be contributing to the obesity epidemic, and it is important to understand the underlying psychobiological mechanisms. Prior investigations have studied what makes individuals eat more after stress; this study investigates what might make individuals eat less. Leptin has been shown to increase following a laboratory stressor, and is known to affect eating behavior. This study examined whether leptin reactivity accounts for individual differences in stress eating. To test this, we exposed forty women to standardized acute psychological laboratory stress (Trier Social Stress Test) while blood was sampled repeatedly for measurements of plasma leptin. We then measured food intake after the stressor in 29 of these women. Increasing leptin during the stressor predicted lower intake of comfort food. These initial findings suggest that acute changes in leptin may be one of the factors modulating down the consumption of comfort food following stress. PMID:22579988

Psychosocial stress factors, including the relationship with the coach, and their influence on acute and overuse injury risk in elite female football players

PubMed Central

Pensgaard, Anne Marte; Ivarsson, Andreas; Nilstad, Agnethe; Solstad, Bård Erlend; Steffen, Kathrin

2018-01-01

Background The relationship between specific types of stressors (eg, teammates, coach) and acute versus overuse injuries is not well understood. Objective To examine the roles of different types of stressors as well as the effect of motivational climate on the occurrence of acute and overuse injuries. Methods Players in the Norwegian elite female football league (n=193 players from 12 teams) participated in baseline screening tests prior to the 2009 competitive football season. As part of the screening, we included the Life Event Survey for Collegiate Athletes and the Perceived Motivational Climate in Sport Questionnaire (Norwegian short version). Acute and overuse time-loss injuries and exposure to training and matches were recorded prospectively in the football season using weekly text messaging. Data were analysed with Bayesian logistic regression analyses. Results Using Bayesian logistic regression analyses, we showed that perceived negative life event stress from teammates was associated with an increased risk of acute injuries (OR=1.23, 95% credibility interval (1.01 to 1.48)). There was a credible positive association between perceived negative life event stress from the coach and the risk of overuse injuries (OR=1.21, 95% credibility interval (1.01 to 1.45)). Conclusions Players who report teammates as a source of stress have a greater risk of sustaining an acute injury, while players reporting the coach as a source of stress are at greater risk of sustaining an overuse injury. Motivational climate did not relate to increased injury occurrence. PMID:29629182

Psychosocial stress factors, including the relationship with the coach, and their influence on acute and overuse injury risk in elite female football players.

PubMed

Pensgaard, Anne Marte; Ivarsson, Andreas; Nilstad, Agnethe; Solstad, Bård Erlend; Steffen, Kathrin

2018-01-01

The relationship between specific types of stressors (eg, teammates, coach) and acute versus overuse injuries is not well understood. To examine the roles of different types of stressors as well as the effect of motivational climate on the occurrence of acute and overuse injuries. Players in the Norwegian elite female football league (n=193 players from 12 teams) participated in baseline screening tests prior to the 2009 competitive football season. As part of the screening, we included the Life Event Survey for Collegiate Athletes and the Perceived Motivational Climate in Sport Questionnaire (Norwegian short version). Acute and overuse time-loss injuries and exposure to training and matches were recorded prospectively in the football season using weekly text messaging. Data were analysed with Bayesian logistic regression analyses. Using Bayesian logistic regression analyses, we showed that perceived negative life event stress from teammates was associated with an increased risk of acute injuries (OR=1.23, 95% credibility interval (1.01 to 1.48)). There was a credible positive association between perceived negative life event stress from the coach and the risk of overuse injuries (OR=1.21, 95% credibility interval (1.01 to 1.45)). Players who report teammates as a source of stress have a greater risk of sustaining an acute injury, while players reporting the coach as a source of stress are at greater risk of sustaining an overuse injury. Motivational climate did not relate to increased injury occurrence.

Developmental Exposure to Mild Variable Stress: Adult ...

EPA Pesticide Factsheets

In utero exposure to mild variable stress has been reported to influence learning and memory formation in offspring. Our research aims to examine whether nonchemical environmental stressors will exacerbate effects to chemical exposure. This study utilized a varying stress paradigm to simulate human psychosocial stress incurred during and after pregnancy to identify phenotypic learning changes in adult offspring that are potential stress markers. We additionally wanted to compare these behavioral outcomes to rat performance induced by perinatal exposure to manganese (Mn), a neurotoxic environmental element, at 2 or 5 g/l in drinking water throughout gestation and lactation. Pregnant Long Evans rats were exposed to an unpredictable series of mild stressful events which had previously been shown to increase maternal corticosterone levels. Nonchemical stressors were presented from GD 13 through GD 21 and included varying noise, light, housing, and confinement during both sleep and wake cycles. A subgroup of offspring was also exposed to periods of maternal separation. Starting at PND 97 offspring were trained with a trace fear conditioning protocol whereby rats were exposed to a compound cue (light and tone) followed by 30 seconds (trace period) and a mild foot shock (1mA, 0.5 seconds). Five paired training sessions occurred on the first day. The following day, context and cue learning were assessed by measuring motor activity. Preliminary data suggests adu

Exposure of Lactating Dairy Cows to Acute Pre-Ovulatory Heat Stress Affects Granulosa Cell-Specific Gene Expression Profiles in Dominant Follicles

PubMed Central

Vanselow, Jens; Vernunft, Andreas; Koczan, Dirk; Spitschak, Marion; Kuhla, Björn

2016-01-01

High environmental temperatures induce detrimental effects on various reproductive processes in cattle. According to the predicted global warming the number of days with unfavorable ambient temperatures will further increase. The objective of this study was to investigate effects of acute heat stress during the late pre-ovulatory phase on morphological, physiological and molecular parameters of dominant follicles in cycling cows during lactation. Eight German Holstein cows in established lactation were exposed to heat stress (28°C) or thermoneutral conditions (15°C) with pair-feeding for four days. After hormonal heat induction growth of the respective dominant follicles was monitored by ultrasonography for two days, then an ovulatory GnRH dose was given and follicular steroid hormones and granulosa cell-specific gene expression profiles were determined 23 hrs thereafter. The data showed that the pre-ovulatory growth of dominant follicles and the estradiol, but not the progesterone concentrations tended to be slightly affected. mRNA microarray and hierarchical cluster analysis revealed distinct expression profiles in granulosa cells derived from heat stressed compared to pair-fed animals. Among the 255 affected genes heatstress-, stress- or apoptosis associated genes were not present. But instead, we found up-regulation of genes essentially involved in G-protein coupled signaling pathways, extracellular matrix composition, and several members of the solute carrier family as well as up-regulation of FST encoding follistatin. In summary, the data of the present study show that acute pre-ovulatory heat stress can specifically alter gene expression profiles in granulosa cells, however without inducing stress related genes and pathways and suggestively can impair follicular growth due to affecting the activin-inhibin-follistatin system. PMID:27532452

Exposure of Lactating Dairy Cows to Acute Pre-Ovulatory Heat Stress Affects Granulosa Cell-Specific Gene Expression Profiles in Dominant Follicles.

PubMed

Vanselow, Jens; Vernunft, Andreas; Koczan, Dirk; Spitschak, Marion; Kuhla, Björn

2016-01-01

High environmental temperatures induce detrimental effects on various reproductive processes in cattle. According to the predicted global warming the number of days with unfavorable ambient temperatures will further increase. The objective of this study was to investigate effects of acute heat stress during the late pre-ovulatory phase on morphological, physiological and molecular parameters of dominant follicles in cycling cows during lactation. Eight German Holstein cows in established lactation were exposed to heat stress (28°C) or thermoneutral conditions (15°C) with pair-feeding for four days. After hormonal heat induction growth of the respective dominant follicles was monitored by ultrasonography for two days, then an ovulatory GnRH dose was given and follicular steroid hormones and granulosa cell-specific gene expression profiles were determined 23 hrs thereafter. The data showed that the pre-ovulatory growth of dominant follicles and the estradiol, but not the progesterone concentrations tended to be slightly affected. mRNA microarray and hierarchical cluster analysis revealed distinct expression profiles in granulosa cells derived from heat stressed compared to pair-fed animals. Among the 255 affected genes heatstress-, stress- or apoptosis associated genes were not present. But instead, we found up-regulation of genes essentially involved in G-protein coupled signaling pathways, extracellular matrix composition, and several members of the solute carrier family as well as up-regulation of FST encoding follistatin. In summary, the data of the present study show that acute pre-ovulatory heat stress can specifically alter gene expression profiles in granulosa cells, however without inducing stress related genes and pathways and suggestively can impair follicular growth due to affecting the activin-inhibin-follistatin system.

Effects of topiramate and other anti-glutamatergic drugs on the acute intoxicating actions of ethanol in mice: modulation by genetic strain and stress

PubMed Central

Chen, Yi-Chyan; Holmes, Andrew

2008-01-01

Compounds with anti-glutamatergic properties currently in clinical use for various indications (e.g., Alzheimer's disease, epilepsy, psychosis, mood disorders) have potential utility as novel treatments for alcoholism. Enhanced sensitivity to certain acute intoxicating effects (ataxia, sedative) of alcohol may be one mechanism by which anti-glutamatergic drugs modulate alcohol use. We examined the effects of six compounds (memantine, dextromethorphan, haloperidol, lamotrigine, oxcarbazepine, topiramate) on sensitivity to acute intoxicating effects of ethanol (ataxia, hypothermia, sedation/hypnosis) in C57BL/6J mice. Analysis of topiramate was extended to determine the influence of genetic background (via comparison of the 129S1, BALB/cJ, C57BL/6J, DBA/2J inbred strains) and prior stress history (via chronic exposure of C57BL/6J to swim stress) on topiramate's effects on ethanol-induced sedation/hypnosis. Results showed that one N-methyl-D-aspartate receptor (NMDAR) antagonist, memantine, but not another, dextromethorphan, potentiated the ataxic but not hypothermic or sedative/hypnotic effects of ethanol. Haloperidol increased ethanol-induced ataxia and sedation/hypnosis to a similar extent as the prototypical NMDAR antagonist MK-801. Of the anticonvulsants tested, lamotrigine accentuated ethanol-induced sedation/hypnosis, while oxcarbazepine was without effect. Topiramate was without effect per se under baseline conditions in C57BL/6J, but had a synergistic effect with MK-801 on ethanol-induced sedation/hypnosis. Comparing inbred strains, topiramate was found to significantly potentiated ethanol's sedative/hypnotic effects in BALB/cJ, but not 129S1, C57BL/6J or DBA/2J strains. Topiramate also increased ethanol-induced sedation/hypnosis in C57BL/6J after exposure to chronic stress exposure. Current data demonstrate that, with the exception of MK-801 and haloperidol, the compounds tested had either no significant or assay-selective effects on sensitivity to acute

Involvement of glucocorticoid-mediated Zn2+ signaling in attenuation of hippocampal CA1 LTP by acute stress.

PubMed

Takeda, Atsushi; Suzuki, Miki; Tamano, Haruna; Takada, Shunsuke; Ide, Kazuki; Oku, Naoto

2012-03-01

Glucocorticoid-glutamatergic interactions have been proposed as a potential model to explain stress-mediated impairment of cognition. However, it is unknown whether glucocorticoid-zincergic interactions are involved in this impairment. Histochemically reactive zinc (Zn(2+)) is co-released with glutamate from zincergic neurons. In the present study, involvement of synaptic Zn(2+) in stress-induced attenuation of CA1 LTP was examined in hippocampal slices from young rats after exposure to tail suspension stress for 30s, which significantly increased serum corticosterone. Stress-induced attenuation of CA1 LTP was ameliorated by administration of clioquinol, a membrane permeable zinc chelator, to rats prior to exposure to stress, implying that the reduction of synaptic Zn(2+) by clioquinol participates in this amelioration. To pursue the involvement of corticosterone-mediated Zn(2+) signal in the attenuated CA1 LTP by stress, dynamics of synaptic Zn(2+) was checked in hippocampal slices exposed to corticosterone. Corticosterone increased extracellular Zn(2+) levels measured with ZnAF-2 dose-dependently, as well as the intracellular Ca(2+) levels measured with calcium orange AM, suggesting that corticosterone excites zincergic neurons in the hippocampus and increases Zn(2+) release from the neuron terminals. Intracellular Zn(2+) levels measured with ZnAF-2DA were also increased dose-dependently, but not in the coexistence of CaEDTA, a membrane-impermeable zinc chelator, suggesting that intracellular Zn(2+) levels is increased by the influx of extracellular Zn(2+). Furthermore, corticosterone-induced attenuation of CA1 LTP was abolished in the coexistence of CaEDTA. The present study suggests that corticosterone-mediated increase in postsynaptic Zn(2+) signal in the cytosolic compartment is involved in the attenuation of CA1 LTP after exposure to acute stress. Copyright © 2012 Elsevier Ltd. All rights reserved.

Preadaptation to Cold Stress in Salmonella enterica Serovar Typhimurium Increases Survival during Subsequent Acid Stress Exposure

PubMed Central

Shah, Jigna; Desai, Prerak T.; Chen, Dong; Stevens, John R.

2013-01-01

Salmonella is an important cause of bacterial food-borne gastroenteritis. Salmonella encounters multiple abiotic stresses during pathogen elimination methods used in food processing, and these stresses may influence its subsequent survivability within the host or in the environment. Upon ingestion, Salmonella is exposed to gastrointestinal acidity, a first line of the host innate defense system. This study tested the hypothesis that abiotic stresses encountered during food processing alter the metabolic mechanisms in Salmonella that enable survival and persistence during subsequent exposure to the host gastrointestinal acidic environment. Out of the four different abiotic stresses tested, viz., cold, peroxide, osmotic, and acid, preadaptation of the log-phase culture to cold stress (5°C for 5 h) significantly enhanced survival during subsequent acid stress (pH 4.0 for 90 min). The gene expression profile of Salmonella preadapted to cold stress revealed induction of multiple genes associated with amino acid metabolism, oxidative stress, and DNA repair, while only a few of the genes in the above-mentioned stress response and repair pathways were induced upon exposure to acid stress alone. Preadaptation to cold stress decreased the NAD+/NADH ratio and hydroxyl (OH·) radical formation compared with those achieved with the exposure to acid stress alone, indicating alteration of aerobic respiration and the oxidative state of the bacteria. The results from this study suggest that preadaptation to cold stress rescues Salmonella from the deleterious effect of subsequent acid stress exposure by induction of genes involved in stress response and repair pathways, by modification of aerobic respiration, and by redox modulation. PMID:24056458

Corticosterone release in oxytocin gene deletion mice following exposure to psychogenic versus non-psychogenic stress.

PubMed

Amico, Janet A; Cai, Hou-ming; Vollmer, Regis R

2008-09-19

Both anxiety-related behavior [J.A. Amico, R.C. Mantella, R.R. Vollmer, X. Li, Anxiety and stress responses in female oxytocin deficient mice, J. Neuroendocrinol. 16 (2004) 1-6; R.C. Mantella, R.R. Vollmer, X. Li, J.A. Amico, Female oxytocin-deficient mice display enhanced anxiety-related behavior, Endocrinology 144 (2003) 2291-2296] and the release of corticosterone following a psychogenic stress such as exposure to platform shaker was greater in female [J.A. Amico, R.C. Mantella, R.R. Vollmer, X. Li, Anxiety and stress responses in female oxytocin deficient mice, J. Neuroendocrinol. 16 (2004) 1-6; R.C. Mantella, R.R. Vollmer, L. Rinaman, X. Li, J.A. Amico, Enhanced corticosterone concentrations and attenuated Fos expression in the medial amygdala of female oxytocin knockout mice exposed to psychogenic stress, Am. J. Physiol. Regul. Integr. Comp. Physiol. 287 (2004) R1494-R1504], but not male [R.C. Mantella, R.R. Vollmer, J.A. Amico, Corticosterone release is heightened in food or water deprived oxytocin deficient male mice, Brain Res. 1058 (2005) 56-61], oxytocin gene deletion (OTKO) mice compared to wild type (WT) cohorts. In the present study we exposed OTKO and WT female mice to another psychogenic stress, inserting a rectal probe to record body temperature followed by brief confinement in a metabolic cage, and measured plasma corticosterone following the stress. OTKO mice released more corticosterone than WT mice (P<0.03) following exposure to this stress. In contrast, if OTKO and WT female and male mice were administered insulin-induced hypoglycemia, an acute physical stress, corticosterone release was not different between genotypes. The absence of central OT signaling pathways in female mice heightens the neuroendocrine (e.g., corticosterone) response to psychogenic stress, but not to the physical stress of insulin-induced hypoglycemia.

mRNA Transcript Abundance during Plant Growth and the Influence of Li + Exposure

DOE PAGES

Duff, M. C.; Kuhne, W. W.; Halverson, N. V.; ...

2014-10-23

Lithium (Li) toxicity in plants is, at a minimum, a function of Li + concentration, exposure time, species and growth conditions. Most plant studies with Li + focus on short-term acute exposures. This study examines short- and long-term effects of Li + exposure in Arabidopsis with Li + uptake studies and measured shoot mRNA transcript abundance levels in treated and control plants. Stress, pathogen-response and arabinogalactan protein genes were typically more up-regulated in older (chronic, low level) Li +-treatment plants and in the much younger plants from acute high-level exposures. The gene regulation behavior of high-level Li + resembled priormore » studies due to its influence on: inositol synthesis, 1-aminocyclopropane-1-carboxylate synthases and membrane ion transport. In contrast, chronically-exposed plants had gene regulation responses that were indicative of pathogen, cold, and heavy-metal stress, cell wall degradation, ethylene production, signal transduction, and calcium-release modulation. Acute Li + exposure phenocopies magnesium-deficiency symptoms and is associated with elevated expression of stress response genes that could lead to consumption of metabolic and transcriptional energy reserves and the dedication of more resources to cell development. In contrast, chronic Li + exposure increases expression signal transduction genes. The identification of new Li +-sensitive genes and a gene-based “response plan” for acute and chronic Li + exposure are delineated.« less

mRNA Transcript abundance during plant growth and the influence of Li(+) exposure.

PubMed

Duff, M C; Kuhne, W W; Halverson, N V; Chang, C-S; Kitamura, E; Hawthorn, L; Martinez, N E; Stafford, C; Milliken, C E; Caldwell, E F; Stieve-Caldwell, E

2014-12-01

Lithium (Li) toxicity in plants is, at a minimum, a function of Li(+) concentration, exposure time, species and growth conditions. Most plant studies with Li(+) focus on short-term acute exposures. This study examines short- and long-term effects of Li(+) exposure in Arabidopsis with Li(+) uptake studies and measured shoot mRNA transcript abundance levels in treated and control plants. Stress, pathogen-response and arabinogalactan protein genes were typically more up-regulated in older (chronic, low level) Li(+)-treatment plants and in the much younger plants from acute high-level exposures. The gene regulation behavior of high-level Li(+) resembled prior studies due to its influence on: inositol synthesis, 1-aminocyclopropane-1-carboxylate synthases and membrane ion transport. In contrast, chronically-exposed plants had gene regulation responses that were indicative of pathogen, cold, and heavy-metal stress, cell wall degradation, ethylene production, signal transduction, and calcium-release modulation. Acute Li(+) exposure phenocopies magnesium-deficiency symptoms and is associated with elevated expression of stress response genes that could lead to consumption of metabolic and transcriptional energy reserves and the dedication of more resources to cell development. In contrast, chronic Li(+) exposure increases expression signal transduction genes. The identification of new Li(+)-sensitive genes and a gene-based "response plan" for acute and chronic Li(+) exposure are delineated. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

Oxidative stress response to acute hypobaric hypoxia and its association with indirect measurement of increased intracranial pressure: a field study

PubMed Central

Strapazzon, Giacomo; Malacrida, Sandro; Vezzoli, Alessandra; Dal Cappello, Tomas; Falla, Marika; Lochner, Piergiorgio; Moretti, Sarah; Procter, Emily; Brugger, Hermann; Mrakic-Sposta, Simona

2016-01-01

High altitude is the most intriguing natural laboratory to study human physiological response to hypoxic conditions. In this study, we investigated changes in reactive oxygen species (ROS) and oxidative stress biomarkers during exposure to hypobaric hypoxia in 16 lowlanders. Moreover, we looked at the potential relationship between ROS related cellular damage and optic nerve sheath diameter (ONSD) as an indirect measurement of intracranial pressure. Baseline measurement of clinical signs and symptoms, biological samples and ultrasonography were assessed at 262 m and after passive ascent to 3830 m (9, 24 and 72 h). After 24 h the imbalance between ROS production (+141%) and scavenging (−41%) reflected an increase in oxidative stress related damage of 50–85%. ONSD concurrently increased, but regression analysis did not infer a causal relationship between oxidative stress biomarkers and changes in ONSD. These results provide new insight regarding ROS homeostasis and potential pathophysiological mechanisms of acute exposure to hypobaric hypoxia, plus other disease states associated with oxidative-stress damage as a result of tissue hypoxia. PMID:27579527

Acute respiratory symptoms and evacuation-related behavior after exposure to chlorine gas leakage.

PubMed

Han, Sung-Woo; Choi, Won-Jun; Yi, Min-Kee; Song, Seng-Ho; Lee, Dong-Hoon; Han, Sang-Hwan

2016-01-01

A study was performed on the accidental chlorine gas leakage that occurred in a factory of printed circuit boards manufactured without chlorine. Health examination was performed for all 52 workers suspected of exposure to chlorine gas, and their evacuation-related behaviors were observed in addition to analyzing the factors that affected the duration of their acute respiratory symptoms. Behavioral characteristics during the incidence of the accidental chlorine gas leakage, the estimated time of exposure, and the duration of subjective acute respiratory symptoms were investigated. In addition, clinical examination, chest radiography, and dental erosion test were performed. As variables that affected the duration of respiratory symptoms, dose group, body weight, age, sex, smoking, work period, and wearing a protective gear were included and analyzed by using the Cox proportional hazard model. Of 47 workers exposed to chlorine gas, 36 (77 %) developed more than one subjective symptom. The duration of the subjective symptoms according to exposure level significantly differed, with a median of 1 day (range, 0-5 days) in the low-exposure group and 2 days (range, 0-25 days) in the high-exposure group. Among the variables that affected the duration of the acute respiratory symptoms, which were analyzed by using the Cox proportional hazard model, only exposure level was significant (hazard ratio 2.087, 95 % CI = 1.119, 3.890). Regarding the evacuation-related behaviors, 22 workers (47 %) voluntarily evacuated to a safety zone immediately after recognizing the accidental exposure, but 25 workers (43 %) delayed evacuation until the start of mandatory evacuation (min 5, max 25 min). The duration of the subjective acute respiratory symptoms significantly differed between the low- and high-exposure groups. Among the 27 workers in the high-exposure group, 17 misjudged the toxicity after being aware of the gas leakage, which is a relatively high number.

Changes in the levels of p-ERK, p-CREB, and c-fos in rat mesocorticolimbic dopaminergic system after morphine-induced conditioned place preference: the role of acute and subchronic stress.

PubMed

Haghparast, Abbas; Fatahi, Zahra; Alamdary, Shabnam Zeighamy; Reisi, Zahra; Khodagholi, Fariba

2014-03-01

ERK pathway plays a critical role in the cellular adaptive responses to environmental changes. Stressful conditions can induce the activation of activate ERK, and its downstream targets, CREB and c-fos, in neural cells. Exposure to opioids has the same effect. In this study, we investigated the effects of morphine-induced conditioned place preference (CPP) on p-ERK/ERK ratio, p-CREB/CREB ratio and c-fos level in the mesocorticolimbic dopaminergic system including the nucleus accumbens (NAc), amygdala (AMY), striatum (Str), and prefrontal cortex (PFC).Our aim was to determine if acute and subchronic stress would affect these alterations. Male Wistar rats were divided into two saline- and morphine-treated groups. Each group contained of control, acute stress, and subchronic stress subgroups. The CPP procedure was performed for all of the rats. We dissected out the NAc, AMY, Str, and PFC regions and measured the mentioned ratios and c-fos level by Western blot analysis. The results revealed that in saline-treated animals, all factors enhanced significantly after performing acute and subchronic stress while there was an exception in p-ERK/ERK ratio in the Str and PFC; the changes were not significant during acute stress. Conditioning score decreased after applying the subchronic but not acute stress. In morphine-treated animals, all factors were increased after application of acute and subchronic stress, and conditioning scores also decreased after stress. Our findings suggest that in saline- or morphine-treated animals, acute and subchronic stress increases p-ERK, p-CREB, and c-fos levels in the mesocorticolimbic system. It has been shown that morphine induces the enhancement of the mentioned factors; on the other hand, our result demonstrates that stress can amplify these changes.

Acute stress differentially affects spatial configuration learning in high and low cortisol-responding healthy adults

PubMed Central

Meyer, Thomas; Smeets, Tom; Giesbrecht, Timo; Quaedflieg, Conny W. E. M.; Merckelbach, Harald

2013-01-01

Background Stress and stress hormones modulate memory formation in various ways that are relevant to our understanding of stress-related psychopathology, such as posttraumatic stress disorder (PTSD). Particular relevance is attributed to efficient memory formation sustained by the hippocampus and parahippocampus. This process is thought to reduce the occurrence of intrusions and flashbacks following trauma, but may be negatively affected by acute stress. Moreover, recent evidence suggests that the efficiency of visuo-spatial processing and learning based on the hippocampal area is related to PTSD symptoms. Objective The current study investigated the effect of acute stress on spatial configuration learning using a spatial contextual cueing task (SCCT) known to heavily rely on structures in the parahippocampus. Method Acute stress was induced by subjecting participants (N = 34) to the Maastricht Acute Stress Test (MAST). Following a counterbalanced within-subject approach, the effects of stress and the ensuing hormonal (i.e., cortisol) activity on subsequent SCCT performance were compared to SCCT performance following a no-stress control condition. Results Acute stress did not impact SCCT learning overall, but opposing effects emerged for high versus low cortisol responders to the MAST. Learning scores following stress were reduced in low cortisol responders, while high cortisol-responding participants showed improved learning. Conclusions The effects of stress on spatial configuration learning were moderated by the magnitude of endogenous cortisol secretion. These findings suggest a possible mechanism by which cortisol responses serve an adaptive function during stress and trauma, and this may prove to be a promising route for future research in this area. PMID:23671762

Acute stressor exposure modifies plasma exosome-associated heat shock protein 72 (Hsp72) and microRNA (miR-142-5p and miR-203).

PubMed

Beninson, Lida A; Brown, Peter N; Loughridge, Alice B; Saludes, Jonel P; Maslanik, Thomas; Hills, Abigail K; Woodworth, Tyler; Craig, Wendy; Yin, Hang; Fleshner, Monika

2014-01-01

Exosomes, biologically active nanoparticles (40-100 nm) released by hematopoietic and non-hematopoietic cells, contain a variety of proteins and small, non-coding RNA known as microRNA (miRNA). Exposure to various pathogens and disease states modifies the composition and function of exosomes, but there are no studies examining in vivo exosomal changes evoked by the acute stress response. The present study reveals that exposing male Fisher 344 rats to an acute stressor modulates the protein and miRNA profile of circulating plasma exosomes, specifically increasing surface heat shock protein 72 (Hsp72) and decreasing miR-142-5p and -203. The selected miRNAs and Hsp72 are associated with immunomodulatory functions and are likely a critical component of stress-evoked modulation of immunity. Further, we demonstrate that some of these stress-induced modifications in plasma exosomes are mediated by sympathetic nervous system (SNS) activation of alpha-1 adrenergic receptors (ADRs), since drug-mediated blockade of the receptors significantly attenuates the stress-induced modifications of exosomal Hsp72 and miR-142-5p. Together, these findings demonstrate that activation of the acute stress response modifies the proteomic and miRNA profile of exosomes released into the circulation.

Gene networks and toxicity pathways induced by acute cadmium exposure in adult largemouth bass (Micropterus salmoides).

PubMed

Mehinto, Alvine C; Prucha, Melinda S; Colli-Dula, Reyna C; Kroll, Kevin J; Lavelle, Candice M; Barber, David S; Vulpe, Christopher D; Denslow, Nancy D

2014-07-01

Cadmium is a heavy metal that can accumulate to toxic levels in the environment leading to detrimental effects in animals and humans including kidney, liver and lung injuries. Using a transcriptomics approach, genes and cellular pathways affected by a low dose of cadmium were investigated. Adult largemouth bass were intraperitoneally injected with 20μg/kg of cadmium chloride (mean exposure level - 2.6μg of cadmium per fish) and microarray analyses were conducted in the liver and testis 48h after injection. Transcriptomic profiles identified in response to cadmium exposure were tissue-specific with the most differential expression changes found in the liver tissues, which also contained much higher levels of cadmium than the testis. Acute exposure to a low dose of cadmium induced oxidative stress response and oxidative damage pathways in the liver. The mRNA levels of antioxidants such as catalase increased and numerous transcripts related to DNA damage and DNA repair were significantly altered. Hepatic mRNA levels of metallothionein, a molecular marker of metal exposure, did not increase significantly after 48h exposure. Carbohydrate metabolic pathways were also disrupted with hepatic transcripts such as UDP-glucose, pyrophosphorylase 2, and sorbitol dehydrogenase highly induced. Both tissues exhibited a disruption of steroid signaling pathways. In the testis, estrogen receptor beta and transcripts linked to cholesterol metabolism were suppressed. On the contrary, genes involved in cholesterol metabolism were highly increased in the liver including genes encoding for the rate limiting steroidogenic acute regulatory protein and the catalytic enzyme 7-dehydrocholesterol reductase. Integration of the transcriptomic data using functional enrichment analyses revealed a number of enriched gene networks associated with previously reported adverse outcomes of cadmium exposure such as liver toxicity and impaired reproduction. Copyright © 2014 Elsevier B.V. All rights

Stressful life events and acute kidney injury in intensive and semi-intensive care unities.

PubMed

Diniz, Denise Para; Marques, Daniella Aparecida; Blay, Sérgio Luis; Schor, Nestor

2012-03-01

Several studies point out that pathophysiological changes related to stress may influence renal function and are associated with disease onset and evolution. However, we have not found any studies about the influence of stress on renal function and acute kidney injury. To evaluate the association between stressful life events and acute kidney injury diagnosis, specifying the most stressful classes of events for these patients in the past 12 months. Case-control study. The study was carried out at Hospital São Paulo, in Universidade Federal de São Paulo and at Hospital dos Servidores do Estado de São Paulo, in Brazil. Patients with acute kidney injury and no chronic disease, admitted to the intensive or semi-intensive care units were included. Controls included patients in the same intensive care units with other acute diseases, except for the acute kidney injury, and also with no chronic disease. Out of the 579 patients initially identified, 475 answered to the Social Readjustment Rating Scale (SRRS) questionnaire and 398 were paired by age and gender (199 cases and 199 controls). The rate of stressful life events was statistically similar between cases and controls. The logistic regression analysis to detect associated effects of the independent variables to the stressful events showed that: increasing age and economic classes A and B in one of the hospitals (Hospital São Paulo - UNIFESP) increased the chance of a stressful life event (SLE). This study did not show association between the Acute Kidney Injury Group with a higher frequency of stressful life events, but that old age, higher income, and type of clinical center were associated.

Effects of acute thermal stress on the survival, predator avoidance, and physiology of juvenile fall Chinook salmon

USGS Publications Warehouse

Mesa, M.G.; Weiland, L.K.; Wagner, P.

2002-01-01

We subjected juvenile fall chinook salmon from the Hanford Reach of the Columbia River to acute thermal stressors in the laboratory that were derived from field data. We assessed the effects of thermal stress on: (1) the extent of direct mortality; (2) the vulnerability of fish to predation by smallmouth bass; and (3) some general physiological stress responses and synthesis of heat shock protein 70 (hsp70). Thermally-stressed fish showed little direct mortality and no increases in vulnerability to predation. However, these fish showed transient increases in plasma concentrations of cortisol, glucose, and lactate, and a dramatic (25-fold higher than controls) and persistent (lasting 2 wk) increase in levels of liver hsp70. Our results indicate that exposure of Hanford Reach juvenile fall chinook salmon to such stressors did not lead to significant increases in direct mortality or vulnerability to predation, but did alter physiological homeostasis, which should be of concern to those managing this resource. Because our fish received only a single exposure to one of the stressors we examined, we are also concerned about the consequences of exposing fish to multiple, cumulative stressors - a likely scenario for fish in the wild.

Exposure to Solute Stress Affects Genome-Wide Expression but Not the Polycyclic Aromatic Hydrocarbon-Degrading Activity of Sphingomonas sp. Strain LH128 in Biofilms

PubMed Central

Fida, Tekle Tafese; Breugelmans, Philip; Lavigne, Rob; Coronado, Edith; Johnson, David R.; van der Meer, Jan Roelof; Mayer, Antonia P.; Heipieper, Hermann J.; Hofkens, Johan

2012-01-01

Members of the genus Sphingomonas are important catalysts for removal of polycyclic aromatic hydrocarbons (PAHs) in soil, but their activity can be affected by various stress factors. This study examines the physiological and genome-wide transcription response of the phenanthrene-degrading Sphingomonas sp. strain LH128 in biofilms to solute stress (invoked by 450 mM NaCl solution), either as an acute (4-h) or a chronic (3-day) exposure. The degree of membrane fatty acid saturation was increased as a response to chronic stress. Oxygen consumption in the biofilms and phenanthrene mineralization activities of biofilm cells were, however, not significantly affected after imposing either acute or chronic stress. This finding was in agreement with the transcriptomic data, since genes involved in PAH degradation were not differentially expressed in stressed conditions compared to nonstressed conditions. The transcriptomic data suggest that LH128 adapts to NaCl stress by (i) increasing the expression of genes coping with osmolytic and ionic stress such as biosynthesis of compatible solutes and regulation of ion homeostasis, (ii) increasing the expression of genes involved in general stress response, (iii) changing the expression of general and specific regulatory functions, and (iv) decreasing the expression of protein synthesis such as proteins involved in motility. Differences in gene expression between cells under acute and chronic stress suggest that LH128 goes through changes in genome-wide expression to fully adapt to NaCl stress, without significantly changing phenanthrene degrading activity. PMID:23001650

Differences of acute versus chronic ethanol exposure on anxiety-like behavioral responses in zebrafish.

PubMed

Mathur, Priya; Guo, Su

2011-06-01

Zebrafish, a vertebrate model organism amenable to high throughput screening, is an attractive system to model and study the mechanisms underlying human diseases. Alcoholism and alcoholic medical disorders are among the most debilitating diseases, yet the mechanisms by which ethanol inflicts the disease states are not well understood. In recent years zebrafish behavior assays have been used to study learning and memory, fear and anxiety, and social behavior. It is important to characterize the effects of ethanol on zebrafish behavioral repertoires in order to successfully harvest the strength of zebrafish for alcohol research. One prominent effect of alcohol in humans is its effect on anxiety, with acute intermediate doses relieving anxiety and withdrawal from chronic exposure increasing anxiety, both of which have significant contributions to alcohol dependence. In this study, we assess the effects of both acute and chronic ethanol exposure on anxiety-like behaviors in zebrafish, using two behavioral paradigms, the Novel Tank Diving Test and the Light/Dark Choice Assay. Acute ethanol exposure exerted significant dose-dependent anxiolytic effects. However, withdrawal from repeated intermittent ethanol exposure disabled recovery from heightened anxiety. These results demonstrate that zebrafish exhibit different anxiety-like behavioral responses to acute and chronic ethanol exposure, which are remarkably similar to these effects of alcohol in humans. Because of the accessibility of zebrafish to high throughput screening, our results suggest that genes and small molecules identified in zebrafish will be of relevance to understand how acute versus chronic alcohol exposure have opposing effects on the state of anxiety in humans. Copyright © 2011 Elsevier B.V. All rights reserved.

Disordered eating behaviour is associated with blunted cortisol and cardiovascular reactions to acute psychological stress.

PubMed

Ginty, Annie T; Phillips, Anna C; Higgs, Suzanne; Heaney, Jennifer L J; Carroll, Douglas

2012-05-01

Research suggests a potential dysregulation of the stress response in individuals with bulimia nervosa. This study measured both cardiovascular and cortisol reactions to a standardised laboratory stress task in individuals identified as showing disordered eating behaviour to determine whether dysregulation of the stress response is characteristic of the two branches of the stress response system. Female students (N=455) were screened using two validated eating disorder questionnaires. Twelve women with disordered eating, including self-induced vomiting, and 12 healthy controls were selected for laboratory stress testing. Salivary cortisol and cardiovascular activity, via Doppler imaging and semi-automatic blood pressure monitoring, were measured at resting baseline and during and after exposure to a 10-min mental arithmetic stress task. Compared to controls the disordered eating group showed blunted cortisol, cardiac output, heart rate, and stroke volume reactions to the acute stress, as well as an attenuated vasodilatory reaction. These effects could not be accounted for in terms of group differences in stress task performance, subjective task impact/engagement, age, BMI, neuroticism, cardio-respiratory fitness, or co-morbid exercise dependence. Our findings suggest that disordered eating is characterised by a dysregulation of the autonomic stress-response system. As such, they add further weight to the general contention that blunted stress reactivity is characteristic of a number of maladaptive behaviours and states. Copyright © 2011 Elsevier Ltd. All rights reserved.

A preclinical model of binge eating elicited by yo-yo dieting and stressful exposure to food: effect of sibutramine, fluoxetine, topiramate, and midazolam.

PubMed

Cifani, Carlo; Polidori, Carlo; Melotto, Sergio; Ciccocioppo, Roberto; Massi, Maurizio

2009-05-01

Preclinical models are needed to investigate the neurobiology and psychobiology of binge eating and to identify innovative pharmacotherapeutic strategies. A modification of the model based on the combination of cyclic caloric restrictions and acute stress was developed to further increase its face validity and reliability and, for the first time, to assess its predictive value. Four groups of female rats were employed: group 1 was normally fed and not stressed on the test day (25th); group 2 was fed normally but was exposed to an acute stress on day 25; group 3 was exposed to three cycles (4 days 66% of chow intake + 4 days food ad libitum) of yo-yo dieting but not stressed; and group 4 was exposed to cyclic yo-yo dieting and then stressed. All groups were fed highly palatable food (HPF) for 2 h on days 5-6 and 13-14. Acute stress was elicited by exposing rats to HPF, but preventing them from access to it for 15 min. The combination of cyclic food restriction and stressful exposure to food markedly increased HPF intake. Sibutramine and fluoxetine inhibited food intake in all conditions. Topiramate selectively inhibited compulsive HPF intake in rats submitted to caloric restriction and stress. Midazolam increased HPF intake. Pharmacological results suggest that this model, in addition to face validity as an isomorphic model of human binge eating, is endowed with good predictive validity.

Stress exposure prior to fear acquisition interacts with estradiol status to alter recall of fear extinction in humans.

PubMed

Antov, Martin I; Stockhorst, Ursula

2014-11-01

Classical fear acquisition and extinction are important models for the etiology and treatment of anxiety disorders such as posttraumatic stress disorder (PTSD). Women are at a higher risk for PTSD than men. Levels of circulating 17-β estradiol (E2) in women have been linked to deficits in fear extinction and extinction recall. In PTSD, fear learning coincides with acute traumatic stress. However, little is known about the possible interaction between stress exposure and hormone status on fear acquisition and extinction learning. In a 2-day, 2×3 between-subjects design with healthy participants, we examined the effects of stress (psychosocial stressor vs. control, placed 45 min prior to conditioning) and natural E2-status on differential fear conditioning, covering fear acquisition, immediate extinction (Day 1), and 24h-delayed extinction recall (Day 2). To operationalize E2-status, we compared women in the early follicular phase (EF) of their menstrual cycle (low E2, low progesterone plasma levels), women in the midcycle phase (MC, high E2, low progesterone), and men. Conditioning was indicated by differential skin conductance responses. We found an interaction between stress exposure and natural E2-status in women only: In MC-women, extinction recall on Day 2 (24h after initial extinction training) was better when fear acquisition had been preceded by stress. In EF-women, the inverse was true. We show that extinction recall of conditioned fear acquired after stress depends on estrogen status in women. Therefore, extinction-based exposure therapy in free-cycling female anxiety patients should take cycle status into account. Copyright © 2014 Elsevier Ltd. All rights reserved.

Acute stress does not impair long-term memory retrieval in older people.

PubMed

Pulopulos, Matias M; Almela, Mercedes; Hidalgo, Vanesa; Villada, Carolina; Puig-Perez, Sara; Salvador, Alicia

2013-09-01

Previous studies have shown that stress-induced cortisol increases impair memory retrieval in young people. This effect has not been studied in older people; however, some findings suggest that age-related changes in the brain can affect the relationships between acute stress, cortisol and memory in older people. Our aim was to investigate the effects of acute stress on long-term memory retrieval in healthy older people. To this end, 76 participants from 56 to 76 years old (38 men and 38 women) were exposed to an acute psychosocial stressor or a control task. After the stress/control task, the recall of pictures, words and stories learned the previous day was assessed. There were no differences in memory retrieval between the stress and control groups on any of the memory tasks. In addition, stress-induced cortisol response was not associated with memory retrieval. An age-related decrease in cortisol receptors and functional changes in the amygdala and hippocampus could underlie the differences observed between the results from this study and those found in studies performed with young people. Copyright © 2013 Elsevier Inc. All rights reserved.

S-Nitroso-Proteome in Poplar Leaves in Response to Acute Ozone Stress

PubMed Central

Vanzo, Elisa; Ghirardo, Andrea; Merl-Pham, Juliane; Lindermayr, Christian; Heller, Werner; Hauck, Stefanie M.; Durner, Jörg; Schnitzler, Jörg-Peter

2014-01-01

Protein S-nitrosylation, the covalent binding of nitric oxide (NO) to protein cysteine residues, is one of the main mechanisms of NO signaling in plant and animal cells. Using a combination of the biotin switch assay and label-free LC-MS/MS analysis, we revealed the S-nitroso-proteome of the woody model plant Populus x canescens. Under normal conditions, constitutively S-nitrosylated proteins in poplar leaves and calli comprise all aspects of primary and secondary metabolism. Acute ozone fumigation was applied to elicit ROS-mediated changes of the S-nitroso-proteome. This treatment changed the total nitrite and nitrosothiol contents of poplar leaves and affected the homeostasis of 32 S-nitrosylated proteins. Multivariate data analysis revealed that ozone exposure negatively affected the S-nitrosylation status of leaf proteins: 23 proteins were de-nitrosylated and 9 proteins had increased S-nitrosylation content compared to the control. Phenylalanine ammonia-lyase 2 (log2[ozone/control] = −3.6) and caffeic acid O-methyltransferase (−3.4), key enzymes catalyzing important steps in the phenylpropanoid and subsequent lignin biosynthetic pathways, respectively, were de-nitrosylated upon ozone stress. Measuring the in vivo and in vitro phenylalanine ammonia-lyase activity indicated that the increase of the phenylalanine ammonia-lyase activity in response to acute ozone is partly regulated by de-nitrosylation, which might favor a higher metabolic flux through the phenylpropanoid pathway within minutes after ozone exposure. PMID:25192423

The effect of acute exposure to hyperbaric oxygen on respiratory system mechanics in the rat.

PubMed

Rubini, Alessandro; Porzionato, Andrea; Zara, Susi; Cataldi, Amelia; Garetto, Giacomo; Bosco, Gerardo

2013-10-01

This study was designed to investigate the possible effects of acute hyperbaric hyperoxia on respiratory mechanics of anaesthetised, positive-pressure ventilated rats. We measured respiratory mechanics by the end-inflation occlusion method in nine rats previously acutely exposed to hyperbaric hyperoxia in a standard fashion. The method allows the measurements of respiratory system elastance and of both the "ohmic" and of the viscoelastic components of airway resistance, which respectively depend on the newtonian pressure dissipation due to the ohmic airway resistance to air flow, and on the viscoelastic pressure dissipation caused by respiratory system tissues stress-relaxation. The activities of inducible and endothelial NO-synthase in the lung's tissues (iNOS and eNOS respectively) also were investigated. Data were compared with those obtained in control animals. We found that the exposure to hyperbaric hyperoxia increased respiratory system elastance and both the "ohmic" and viscoelastic components of inspiratory resistances. These changes were accompanied by increased iNOS but not eNOS activities. Hyperbaric hyperoxia was shown to acutely induce detrimental effects on respiratory mechanics. A possible causative role was suggested for increased nitrogen reactive species production because of increased iNOS activity.

Ability to Discriminate Between Sustainable and Unsustainable Heat Stress Exposures-Part 1: WBGT Exposure Limits.