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Acute Stress (acute + stress)
Selected AbstractsRelationship Between Interindividual Differences and Physiological Indexes of Acute Stress in RatsJOURNAL OF APPLIED BIOBEHAVIORAL RESEARCH, Issue 4 2005Mitsuo Nagane We used in vivo microdialysis to examine interindividual differences in the effects of acute immobilization stress and diazepam treatment on monoamine turnover in the hippocampus of male rats as an index of stress. Immobilization significantly increased the concentrations of 3,4-dihydroxyphenyl-aceticacid (DOPAC), homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA). This effect was attenuated by injection of diazepam, Interindividual differences in reactivity to stressors caused differential changes in different metabolic products of monoamines. In our study, stress-induced changes in DOPAC levels were relatively great, and there was a similar change in the concentration of HVA. We conclude that at least 2 indexes of stress should be measured to take into account interindividual differences in the changes in stress indexes. [source] Anticipation of Acute Stress in Isoprenaline-Sensitive and , Resistant Rats: Strain and Gender DifferencesBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2000Anna Yamamotová The effect of stress anticipation was studied in two inbred Wistar rat strains with high and low sensitivity to isoprenaline. The animals were exposed to tail-flick and 4-hr water immersion restraint stress on two consecutive days. On the first day stress was applied to one group and the next day to the anticipation group. The changes in adrenal, heart and spleen weights, tail-flick latency, incidence of gastric ulcers, and the antioxidant defense system in the sensorimotor cortex were compared with two non-stressed control groups. Anticipatory stress decreased adrenal weights. The content of thiobarbituric acid reactive substances (TBARS) was increased both in acute and anticipatory stress; superoxide dismutase, glutathione peroxidase, and antioxidative capacity were increased in anticipatory stress only. Stress anticipation decreased the pain threshold in the isoprenaline-sensitive and increased in the isoprenaline-resistant rats and led to more frequent gastric ulcers in the isoprenaline-resistant group. Significant sex differences were observed both in adrenal weights and TBARS content. The relative adrenal weights were negatively correlated with the TBARS content. We suggest that the outcome of anticipatory stress may depend upon the relation between the hormonal and antioxidant functions of the adrenals and that anticipation-induced activation of antioxidant enzymes may ameliorate the acute stress response. Anticipation itself was found to be a stronger stressor than physical acute stress. [source] Possible involvement of GABAergic modulation in the protective effect of gabapentin against immobilization stress-induced behavior alterations and oxidative damage in miceFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 6 2007Anil Kumar Abstract Introduction Acute stress may be experienced in response to an immediate physical, emotional or psychological stimulus. Stress has been known to affect several brain activities and promote long-term changes in multiple neural systems. In the present study, we investigated the possible involvement of GABAergic modulation in the protective effect of gabapentin in acute immobilization-induced behavioral alterations and oxidative damage in mice. Materials and methods Mice were immobilized for periods of 6 h. Animals were divided into different groups, consisting of six in each. Various GABAergic modulators were administered either alone or in their combinations, 30 min before subjecting the animals for immobilization stress. Various behavioral tests (mirror chamber, actophotometer) followed by oxidative parameters (malondialdehyde level, glutathione, catalase, nitrite and protein) were assessed in animals. Results Six hours acute immobilization stress caused significant locomotor impairment, anxiety-like behavior in mice. Biochemical analyses also revealed an increase malondialdehyde, nitrite level and depletion of glutathione and catalase activity in 6 h stressed brains. Pretreatment with gabapentin (50 and 100 mg/kg, i.p.) significantly improved ambulatory movements, anti-anxiety effect (decreased time latency to enter in mirror chamber, increased number of entries and duration in mirror chamber) and antioxidative activity in stressed mice (P < 0.05). Further, picrotoxin (1.0 mg/kg) blocked and muscimol (0.05 mg/kg) potentiated the protective action of gabapentin (50 mg/kg). Results of both behavior as well as biochemical alterations in combination studies were significant as compared to their effect per se (P < 0.05). Conclusion Results of present study suggest GABAergic modulation might be involved in the protective effect of gabapentin against immobilization-induced behavior alteration and oxidative damage in mice. [source] Stress and GABAA receptorsJOURNAL OF NEUROCHEMISTRY, Issue 5 2010Kelly J. Skilbeck J. Neurochem. (2010) 112, 1115,1130. Abstract GABAA receptors are sensitive to subtle changes in the environment in both early-life and adulthood. These neurochemical responses to stress in adulthood are sex-dependent. Acute stress induces rapid changes in GABAA receptors in experimental animals, with the direction of the changes varying according to the sex of the animals and the stress-paradigm studied. These rapid alterations are of particular interest as they provide an example of fast neurotransmitter system plasticity that may be mediated by stress-induced increases in neurosteroids, perhaps via effects on phosphorylation and/or receptor trafficking. Interestingly, some studies have also provided evidence for long-lasting changes in GABAA receptors as a result of exposure to stressors in early-life. The short- and long-term stress sensitivity of the GABAergic system implicates GABAA receptors in the non-genetic etiology of psychiatric illnesses such as depression and schizophrenia in which stress may be an important factor. [source] APJ Receptor mRNA Expression in the Rat Hypothalamic Paraventricular Nucleus: Regulation By Stress and GlucocorticoidsJOURNAL OF NEUROENDOCRINOLOGY, Issue 11 2003A.-M. O'Carroll Abstract The apelin receptor (APJ receptor, APJR) has recently come to prominence following the isolation and identification of its endogenous ligand, apelin, from bovine stomach tissue extracts. Investigation of APJR mRNA expression has revealed a hypothalamic distribution similar to that of vasopressin suggesting that the apelin,APJR system may be involved in the regulation of the hypothalamic-adrenal-pituitary (HPA) stress axis. To investigate whether APJR is involved in the regulation of hypothalamic function during stress, APJR mRNA expression levels were measured by in situ hybridization in the hypothalamus of rats subjected to acute and repeated restraint stress. Acute stress caused an increase in APJR mRNA expression in the hypothalamic parvocellular paraventricular nucleus (pPVN) while repeated restraint stress induced a sustained up-regulation of pPVN APJR mRNA expression in intact rats. Removal of endogenous glucocorticoids by adrenalectomy also resulted in an increased expression of APJR mRNA in the PVN, suggesting a negative regulation of APJR mRNA expression by glucocorticoids. The role of glucocorticoids in mediating these stress-induced changes was investigated by analysing the effects of acute and repeated restraint stress on APJR mRNA levels in adrenalectomized rats. In these rats, APJR mRNA expression levels did not change above the already elevated levels of adrenalectomized-control rats. These data suggest that acute and repeated stress exert a stimulatory influence on APJR mRNA expression at the hypothalamic level that may be dependent on basal levels of circulating glucocorticoids, and further suggest a role for APJR in the regulation of hypothalamic function. [source] Amitriptyline modifies the visceral hypersensitivity response to acute stress in the irritable bowel syndromeALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 5 2009N. M. THOUA Summary Background, Acute physical stress causes alteration in gut autonomic function and visceral hypersensitivity in patients with irritable bowel syndrome (IBS). We have developed a model to measure this stress response. Aim, To assess whether treatment with a drug effective in treating IBS (amitriptyline) alters the response to acute stress in IBS patients. Methods, Nineteen patients with IBS were given amitriptyline 25,50 mg. Patients underwent physical stress (cold pressor) test at baseline and after 3 months of treatment. Physiological parameters measured were: stress perception; systemic autonomic tone [heart rate (HR) and blood pressure (BP)]; gut specific autonomic innervation [rectal mucosal blood flow (RMBF)] and visceral sensitivity (rectal electrosensitivity). Results, Fourteen of 19 (74%) patients improved symptomatically after 3 months of amitriptyline. Acute stress induced increased perception of stress and systemic autonomic tone and reduced RMBF in symptomatic responders and nonresponders (P > 0.05 for all). All nonresponders but only 3 of 14 responders continued to exhibit stress-induced reduced pain threshold at 3 months (change from baseline ,31% vs. +2%, P < 0.03 respectively). Conclusion, In this open study, amitriptyline appears to decrease stress-induced electrical hypersensitivity; this effect is independent of autonomic tone. The gut response to acute stress deserves further study as a model to study drug efficacy in IBS. [source] Effects of psychological stress on the cerebral processing of visceral stimuli in healthy womenNEUROGASTROENTEROLOGY & MOTILITY, Issue 7 2009C. Rosenberger Abstract, The aim of the study was to analyse effects of psychological stress on the neural processing of visceral stimuli in healthy women. The brain functional magnetic resonance imaging blood oxygen level-dependent response to non-painful and painful rectal distensions was recorded from 14 healthy women during acute psychological stress and a control condition. Acute stress was induced with a modified public speaking stress paradigm. State anxiety was assessed with the State-Trait-Anxiety Inventory; chronic stress was measured with the Perceived Stress Questionnaire. During non-painful distensions, activation was observed in the right posterior insular cortex (IC) and right S1. Painful stimuli revealed activation of the bilateral anterior IC, right S1, and right pregenual anterior cingulate cortex. Chronic stress score was correlated with activation of the bilateral amygdala, right posterior IC (post-IC), left periaqueductal grey (PAG), and right dorsal posterior cingulate gyrus (dPCC) during non-painful stimulation, and with activation of the right post-IC, right PAG, left thalamus (THA), and right dPCC during painful distensions. During acute stress, state anxiety was significantly higher and the acute stress , control contrast revealed activation of the right dPCC, left THA and right S1 during painful stimulation. This is the first study to demonstrate effects of acute stress on cerebral activation patterns during visceral pain in healthy women. Together with our finding that chronic stress was correlated wit the neural response to visceral stimuli, these results provide a framework for further studies addressing the role of chronic stress and emotional disturbances in the pathophysiology of visceral hyperalgesia. [source] Acute stress enhances contact dermatitis by promoting nuclear factor-,B DNA-binding activity and interleukin-18 expression in miceTHE JOURNAL OF DERMATOLOGY, Issue 6 2010Jing ZHANG Abstract Psychological stress adversely affects the immune system, and aggravates various skin diseases, such as psoriasis, alopecia areata and atopic dermatitis. However, the precise underlying mechanisms remain to be elucidated. The goal of this study was to use a murine restraint stress model to determine the mechanisms by which psychological stress modulates immune response in contact dermatitis. In the present study, mice were sensitized and challenged on the skin with 2,4-dinitrofluorobenzene. Acute restraint stress was administrated to healthy or sensitized mice before challenge, and nuclear factor (NF)-,B DNA-binding activation of nuclear protein and expression of interleukin (IL)-18 mRNA in murine spleen lymphocytes was detected. Chemical sympathectomy was performed using the neurotoxin 6-hydroxy-dopamine to determine the effect of the sympathetic nervous system. The experiment showed that restraint stress induced a series of changes which include increasing of NF-,B DNA-binding activity and IL-18 mRNA expression in spleen lymphocytes and enhancement of contact hypersensitivity response, and these changes may be mediated by the sympathetic nervous system. These findings provide new insights into the roles of the nervous system in the aggravation of skin diseases. [source] Flow cytometric measurement of circulating endothelial cells: The effect of age and peripheral arterial disease on baseline levels of mature and progenitor populationsCYTOMETRY, Issue 2 2006Rebecca Gusic Shaffer Abstract Background: Age and cardiovascular disease status appear to alter numbers and function of circulating endothelial progenitor cells (EPCs). Despite no universal phenotypic definition, numerous studies have implicated progenitors with apparent endothelial potential in local responses to vascular injury and with cardiovascular disease in general. To further define the role of this lineage in peripheral artery disease (PAD), we developed a multiparameter flow cytometry assay to analyze multiple phenotypic definitions of progenitor cells (PCs), EPCs, and mature endothelial cells (ECs) and evaluate effects of age and PAD on baseline levels of each subset. Methods: Blood was collected from young healthy subjects (N = 9, mean age 33 ± 8 years), older healthy subjects (N = 13, mean age 66 ± 8 years), and older subjects with PAD (N = 15, mean age 69 ± 8 years). After ammonium chloride lysis, cells were stained and analyzed on a Becton-Dickinson LSR II with a 5-color antibody panel: FITC-anti-CD31, PE-anti-CD146, PE-anti-CD133, PerCP-Cy5.5-anti-CD3,-CD19,-CD33 (lineage panel), PE-Cy7-anti-CD34, and APC-anti-VEGF-R2. Viability was assessed by propidium iodide exclusion, and only viable, low to medium side scatter lineage-negative singlets were analyzed. In some studies, cells were sorted for morphological studies. Subsets were defined as indicated later. Results: Our results, using a comprehensive flow cytometric panel, indicate that CD133+, CD34+, and CD133+/CD34+ PCs are elevated in younger healthy individuals compared to older individuals, both healthy and with PAD. However, the number of EPCs and mature ECs did not significantly differ among the three groups. Assessment of endothelial colony forming units and dual acLDL-lectin staining supported the flow cytometric findings. Conclusions: We describe a comprehensive flow cytometric method to detect circulating mature and progenitor endothelial populations confirmed by conventional morphological and functional assays. Our findings suggest that aging may influence circulating levels of PCs, but not EPCs or ECs; PAD had no effect on baseline levels of any populations investigated. This study provides the basis for evaluating the potential effects of acute stress and therapeutic intervention on circulating progenitor and endothelial populations as a biomarker for cardiovascular status. © 2005 International Society for Analytical Cytology [source] Influence of isolation on the recovery of pond mesocosms from the application of an insecticide.ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 6 2007Abstract The immediate response and recovery of the macrobenthic communities of nonisolated and isolated freshwater outdoor 9 m3 mesocosms following an acute stress caused by the addition of deltamethrin were studied over a 14-month period. To discriminate between internal and external recovery mechanisms, half of the treated ponds were covered by 1-mm mesh lids that restricted aerial recolonization. Both structural (abundance of the different taxonomic groups) and functional (litter breakdown) parameters were monitored. Insects were broadly reduced in numbers by deltamethrin addition. In general, noninsect groups were not affected or increased in abundance in deltamethrin-treated ponds, probably because of relative insensitivity to deltamethrin, reduced predation, and lower competition for food. No major change in litter breakdown rates were seen, probably because of functional redundancy among the macrobenthic community. Chironominae larvae recovered in open, treated mesocosms 62 d after deltamethrin addition and most insect groups recovered 84 d after the treatment date. However, the presence of lids significantly reduced insect recovery rate, suggesting that it largely depends on the immigration of winged forms (i.e., external recovery) from surrounding non- or less affected systems. These results indicate that the recovery time of macrobenthic communities in an affected natural pond would depend on spatial characteristics of the landscape and also the season that exposure occurs. Isolated ecosystems would display posttreatment insect recovery dynamics very different from highly connected ones, evolving toward alternate pseudoequilibrium states, possibly with lower biodiversity but with preserved functionality. Consequences for higher tier risk assessment of pesticides are discussed. [source] Immediate,early gene induction in hippocampus and cortex as a result of novel experience is not directly related to the stressfulness of that experienceEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2005Thaddeus W. W. Pace Abstract The stressful quality of an experience, as perceived by rats, is believed to be largely represented by the magnitude of a hypothalamic,pituitary,adrenal (HPA) axis response. The hippocampus may be especially important for assessing the stressfulness of psychological stressors such as novel experience. If such is the case then experience-dependent immediate,early gene expression levels within the hippocampus may parallel relative levels of HPA axis activity. We examined this prospect in rats that were placed in four different novel environments (empty housing tub, circular arena, elevated pedestal or restraint tube). Restraint and pedestal produced the largest magnitude of increased ACTH and corticosterone secretion, arena an intermediate level (Experiment 2) and tub the least magnitude of increase. We saw a very similar experience-dependent pattern of relative Fos protein, c-fos mRNA and zif268 mRNA expression in the paraventricular nucleus of the hypothalamus. However, in hippocampus (and select regions of cortex), immediate,early gene expression was associated with the exploratory potential of the novel experience rather than level of HPA axis activity; pedestal and arena elicited the greatest immediate,early gene expression, tub an intermediate level and restraint the least amount of expression. We conclude that the stressfulness of psychological stressors is not represented by the amount of immediate,early gene induction elicited in hippocampus and cortex, nor does there appear to be a general enhancing or depressive influence of acute stress on immediate,early gene induction in those brain regions. [source] Synergistic regulation of neuropeptide levels by internal and external stimuliEXPERIMENTAL DERMATOLOGY, Issue 9 2004J. Hosoi The skin is the most peripheral organ confronting the external environment. We found that the level of substance P is regulated by both internal and external stimuli. Mock interview induced the acute stress in human assessed by the measurement of serum cortisol. The serum level of substance P increased within 1 h after the mock interview. Interestingly, the increase was suppressed by inhalation of 1,3-dimethoxy-5-methylbenzene. Similar regulation was observed in mice. Furthermore, restraint or the intravenous administration of substance P induced the activation of cutaneous mast cells. Housing under the condition of lower humidity (about 30%) for 24 h caused the increase in the substance P level both in peripheral blood and in the skin. Restraint for 2 h during the housing under the condition of lower humidity increased the substance P level further. The activation of cutaneous mast cells under the dry condition was reported. These data suggest that cutaneous neuropeptide level is regulated by both psychological and environmental mechanisms. The regulation may cause the downregulation of the threshold of the induction of itch and inflammation. [source] Early transcriptional response of Saccharomyces cerevisiae to stress imposed by the herbicide 2,4-dichlorophenoxyacetic acidFEMS YEAST RESEARCH, Issue 2 2006Miguel Cacho Teixeira Abstract The global gene transcription pattern of the eukaryotic experimental model Saccharomyces cerevisiae in response to sudden aggression with the widely used herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) was analysed. Under acute stress, 14% of the yeast transcripts suffered a greater than twofold change. The yeastract database was used to predict the transcription factors mediating the response registered in this microarray analysis. Most of the up-regulated genes in response to 2,4-D are known targets of Msn2p, Msn4p, Yap1p, Pdr1p, Pdr3p, Stp1p, Stp2p and Rpn4p. The major regulator of ribosomal protein genes, Sfp1p, is known to control 60% of the down-regulated genes, in particular many involved in the transcriptional and translational machinery and in cell division. The yeast response to the herbicide includes the increased expression of genes involved in the oxidative stress response, the recovery or degradation of damaged proteins, cell wall remodelling and multiple drug resistance. Although the protective role of TPO1 and PDR5 genes was confirmed, the majority of the responsive genes encoding multidrug resistance do not confer resistance to 2,4-D. The increased expression of genes involved in alternative carbon and nitrogen source metabolism, fatty acid ,-oxidation and autophagy was also registered, suggesting that acute herbicide stress leads to nutrient limitation. [source] Prenatal stress modifies hippocampal synaptic plasticity and spatial learning in young rat offspringHIPPOCAMPUS, Issue 5 2006Jianli Yang Abstract Clinical studies demonstrate that prenatal stress causes cognitive deficits and increases vulnerability to affective disorders in children and adolescents. The underlying mechanisms are not yet fully understood. Here, we reported that prenatal stress (10 unpredictable, 1 s, 0.8 mA foot shocks per day during gestational days 13,19) impaired long-term potentiation (LTP) but facilitated long-term depression (LTD) in hippocampal CA1 region in slices of the prenatal stressed offspring (5 weeks old). Cross-fostering neonate offspring by the prenatal stressed or control mothers did not change the effects of prenatal stress on the hippocampal LTP and LTD. Furthermore, prenatal stress enhanced the effects of acute stress on the hippocampal LTP and LTD and impaired spatial learning and memory in the Morris water maze in the young rat offspring. Therefore, prenatal stress alters synaptic plasticity and enhances the effects of acute stress on synaptic plasticity in the hippocampus, which may be the mechanism for the impaired spatial learning and memory in young rat offspring. © 2006 Wiley-Liss, Inc. [source] Methylenedioxymethamphetamine (MDMA, ,Ecstasy'): a stressor on the immune systemIMMUNOLOGY, Issue 4 2004Thomas J. Connor Summary Drug abuse is a global problem of considerable concern to health. One such health concern stems from the fact that many drugs of abuse have immunosuppressive actions and consequently have the potential to increase susceptibility to infectious disease. This article is focused on the impact of the amphetamine derivative, methylenedioxymethamphetamine (MDMA; ,Ecstasy') on immunity. Research conducted over the last 5 years, in both laboratory animals and humans, has demonstrated that MDMA has immunosuppressive actions. Specifically, MDMA suppresses neutrophil phagocytosis, suppresses production of the pro-inflammatory cytokines tumour necrosis factor-, (TNF-,) and interleukin (IL)-1,, and increases production of the endogenous immunosuppressive cytokine (IL-10), thereby promoting an immunosuppressive cytokine phenotype. MDMA also suppresses circulating lymphocyte numbers, with CD4+ T cells being particularly affected, and alters T-cell function as indicated by reduced mitogen-stimulated T-cell proliferation, and a skewing of T-cell cytokine production in a T helper 2 (Th2) direction. For the most part, the aforementioned effects of MDMA are not the result of a direct action of the drug on immune cells, but rather caused by the release of endogenous immunomodulatory substances. Consequently, the physiological mechanisms that are thought to underlie the immunosuppressive effects of MDMA will be discussed. As many of the physiological changes elicited by MDMA closely resemble those induced by acute stress, it is suggested that exposure to MDMA could be regarded as a ,chemical stressor' on the immune system. Finally, the potential of MDMA-induced immunosuppression to translate into significant health risks for abusers of the drug will be discussed. [source] Repressive Coping and Blood Measures of Disease Risk: Lipids and Endocrine and Immunological Responses to a Laboratory Stressor,JOURNAL OF APPLIED SOCIAL PSYCHOLOGY, Issue 8 2000Steven D. Barger Relations between repressive coping and a variety of health-related variahles including insulin, lipids, catecholamines, and cellular immune components, were investigated in a laboratory study of acute stress among a sample of healthy male college students (N - 83). Compared to nonrepressors, at baseline, repressors had fewer numbers of circulating CD4 (T-helper) cells, greater numbers of natural killer (NK) cells. lower high-density lipoprotein (HDL), a higher total/HDL cholesterol ratio, and higher fasting insulin levels. In response to an acute laboratory stressor (Stroop Color Word Conflict Test). repressors demonstrated an attenuated increase in the number of circulating NK cells compared to nonrepressors. Confounds such as physical activity, age, and smoking were unrelated to the dependent measures. [source] Short-term dietary restriction and fasting precondition against ischemia reperfusion injury in miceAGING CELL, Issue 1 2010James R. Mitchell Summary Dietary restriction (DR) extends lifespan and increases resistance to multiple forms of stress, including ischemia reperfusion injury to the brain and heart in rodents. While maximal effects on lifespan require long-term restriction, the kinetics of onset of benefits against acute stress is not known. Here, we show that 2,4 weeks of 30% DR improved survival and kidney function following renal ischemia reperfusion injury in mice. Brief periods of water-only fasting were similarly effective at protecting against ischemic damage. Significant protection occurred within 1 day, persisted for several days beyond the fasting period and extended to another organ, the liver. Protection by both short-term DR and fasting correlated with improved insulin sensitivity, increased expression of markers of antioxidant defense and reduced expression of markers of inflammation and insulin/insulin-like growth factor-1 signaling. Unbiased transcriptional profiling of kidneys from mice subject to short-term DR or fasting revealed a significant enrichment of signature genes of long-term DR. These data demonstrate that brief periods of reduced food intake, including short-term daily restriction and fasting, can increase resistance to ischemia reperfusion injury in rodents and suggest a rapid onset of benefits of DR in mammals. [source] Congenital DNA repair deficiency results in protection against renal ischemia reperfusion injury in miceAGING CELL, Issue 2 2009Denis Susa Summary Cockayne syndrome and other segmental progerias with inborn defects in DNA repair mechanisms are thought to be due in part to hypersensitivity to endogenous oxidative DNA damage. The accelerated aging-like symptoms of this disorder include dysmyelination within the central nervous system, progressive sensineuronal hearing loss and retinal degeneration. We tested the effects of congenital nucleotide excision DNA repair deficiency on acute oxidative stress sensitivity in vivo. Surprisingly, we found mouse models of Cockayne syndrome less susceptible than wild type animals to surgically induced renal ischemia reperfusion injury, a multifactorial injury mediated in part by oxidative damage. Renal failure-related mortality was significantly reduced in Csb,/, mice, kidney function was improved and proliferation was significantly higher in the regenerative phase following ischemic injury. Protection from ischemic damage correlated with improved baseline glucose tolerance and insulin sensitivity and a reduced inflammatory response following injury. Protection was further associated with genetic ablation of a different Cockayne syndrome-associated gene, Csa. Our data provide the first functional in vivo evidence that congenital DNA repair deficiency can induce protection from acute stress in at least one organ. This suggests that while specific types of unrepaired endogenous DNA damage may lead to detrimental effects in certain tissues, they may at the same time elicit beneficial adaptive changes in others and thus contribute to the tissue specificity of disease symptoms. [source] Maternal Genotype Influences Stress Reactivity of Vasopressin-Deficient Brattleboro RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 12 2003D. Zelena Abstract The role of vasopressin, cosecreted with corticotropin-releasing hormone (CRH), in stress is debated, because both normal as well as reduced adrenocorticotropin hormone (ACTH) rise to an acute challenge has been reported in Brattleboro rats genetically lacking vasopressin (di/di). Because di/di pups could be born either from di/+ (heterozygous) or from di/di mothers, and maternal influence is known to modify adult responsiveness, we investigated whether the influence of maternal genotype could explain the variability. Adult rats from mothers with different genotypes were stressed with 60 min restraint and trunk blood was collected for measuring hormone content by radioimmunoassay at the end of stress. All offspring of di/+ mothers had similar ACTH responses to restraint, while the di/di rats born to, and raised by di/di mothers showed reduced ACTH reactivity to restraint. The di/di rats showed elevated water turnover and required a daily cage cleaning every day, which meant frequent handling. To offset the role of handling, all rats had daily cage cleaning in the next series, but the results were the same as in the first series. To investigate whether lactation, the behaviour of the mother or some other factor during the pregnancy is responsible for the differences, pups from di/+ dams were raised by di/di foster mothers and vice versa. We found that the genotype of parental mother is more important than that of the foster mother. The corticosterone and prolactin elevation normally seen after acute stress was unchanged by family history, maternal or personal genotype. Furthermore, in studies with mutant animals, the rearing conditions should be controlled by the experimenter. In experiments with Brattleboro rats, the use of homozygous and heterozygous rats from the same litters of di/+ dams and di/di males is recommended. Our results suggest that vasopressin is not indispensable for ACTH release, and that the di/di genotype of the parental mother can decrease the stress reactivity of the di/di Brattleboro rats. [source] Reproduction and Resistance to Stress: When and HowJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2003J. C. Wingfield Abstract Environmental and social stresses have deleterious effects on reproductive function in vertebrates. Global climate change, human disturbance and endocrine disruption from pollutants are increasingly likely to pose additional stresses that could have a major impact on human society. Nonetheless, some populations of vertebrates (from fish to mammals) are able to temporarily resist environmental and social stresses, and breed successfully. A classical trade-off of reproductive success for potential survival is involved. We define five examples. (i) Aged individuals with minimal future reproductive success that should attempt to breed despite potential acute stressors. (ii) Seasonal breeders when time for actual breeding is so short that acute stress should be resisted in favour of reproductive success. (iii) If both members of a breeding pair provide parental care, then loss of a mate should be compensated for by the remaining individual. (iv) Semelparous species in which there is only one breeding period followed by programmed death. (v) Species where, because of the transience of dominance status in a social group, individuals may only have a short window of opportunity for mating. We suggest four mechanisms underlying resistance of the gonadal axis to stress. (i) Blockade at the central nervous system level, i.e. an individual no longer perceives the perturbation as stressful. (ii) Blockade at the level of the hypothalamic-pituitary-adrenal axis (i.e. failure to increase secretion of glucocorticosteroids). (iii) Blockade at the level of the hypothalamic-pituitary-gonad axis (i.e. resistance of the reproductive system to the actions of glucocorticosteroids). (iv) Compensatory stimulation of the gonadal axis to counteract inhibitory glucocorticosteroid actions. Although these mechanisms are likely genetically determined, their expression may depend upon a complex interaction with environmental factors. Future research will provide valuable information on the biology of stress and how organisms cope. Such mechanisms would be particularly insightful as the spectre of global change continues to unfold. [source] "Juvenile stress" alters maturation-related changes in expression of the neural cell adhesion molecule L1 in the limbic system: Relevance for stress-related psychopathologiesJOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2010M.M. Tsoory Abstract L1 is critically involved in neural development and maturation, activity-dependent synaptic plasticity, and learning processes. Among adult rats, chronic stress protocols that affect L1 functioning also induce impaired cognitive and neural functioning and heightened anxiety reminiscent of stress-induced mood and anxiety disorders. Epidemiological studies indicate that childhood trauma is related predominantly to higher rates of both mood and anxiety disorders in adulthood and is associated with altered limbic system functioning. Exposing rats to stress during the juvenile period ("juvenile stress") has comparable effects and was suggested as a model of induced predisposition for these disorders. This study examined the effects of juvenile stress on rats aversive learning and on L1 expression soon after exposure and in adulthood, both following additional exposure to acute stress and in its absence. Adult juvenile-stressed rats exhibited enhanced cued fear conditioning, reduced novel-setting exploration, and impaired avoidance learning. Furthermore, juvenile stress increased L1 expression in the BLA, CA1, DG, and EC both soon after the stressful experience and during adulthood. It appears that juvenile stress affects the normative maturational decrease in L1 expression. The results support previous indications that juvenile stress alters the maturation of the limbic system and further support a role for L1 regulation in the mechanisms that underlie the predisposition to exhibit mood and/or anxiety disorders in adulthood. Furthermore, the findings support the "network hypothesis," which postulates that information-processing problems within relevant neural networks might underlie stress-induced mood and anxiety disorders. © 2009 Wiley-Liss, Inc. [source] Effect of oral melatonin on the procoagulant response to acute psychosocial stress in healthy men: a randomized placebo-controlled studyJOURNAL OF PINEAL RESEARCH, Issue 4 2008Petra H. Wirtz Abstract:, Acute mental stress is a potent trigger of acute coronary syndromes. Catecholamine-induced hypercoagulability with acute stress contributes to thrombus growth after coronary plaque rupture. Melatonin may diminish catecholamine activity. We hypothesized that melatonin mitigates the acute procoagulant stress response and that this effect is accompanied by a decrease in the stress-induced catecholamine surge. Forty-five healthy young men received a single oral dose of either 3 mg melatonin (n = 24) or placebo medication (n = 21). One hour thereafter, they underwent a standardized short-term psychosocial stressor. Plasma levels of clotting factor VII activity (FVII:C), FVIII:C, fibrinogen, D-dimer, and catecholamines were measured at rest, immediately after stress, and 20 min and 60 min post-stress. The integrated change in D-dimer levels from rest to 60 min post-stress differed between medication groups controlling for demographic and metabolic factors (P = 0.047, = 0.195). Compared with the melatonin group, the placebo group showed a greater increase in absolute D-dimer levels from rest to immediately post-stress (P = 0.13; = 0.060) and significant recovery of D-dimer levels from immediately post-stress to 60 min thereafter (P = 0.007; = 0.174). Stress-induced changes in FVII:C, FVIII:C, fibrinogen, and catecholamines did not significantly differ between groups. Oral melatonin attenuated the stress-induced elevation in the sensitive coagulation activation marker D-dimer without affecting catecholamine activity. The finding provides preliminary support for a protective effect of melatonin in reducing the atherothrombotic risk with acute mental stress. [source] Effect of Chronic Ethanol Ingestion on Alveolar Type II Cell: Glutathione and Inflammatory Mediator-Induced ApoptosisALCOHOLISM, Issue 7 2001Lou Ann S. Brown Background : In septic patients, chronic alcohol abuse increases the incidence of the acute respiratory distress syndrome, a syndrome that requires alveolar type II cell proliferation and differentiation for repair of the damaged alveolar epithelium. We previously showed in a rat model that chronic ethanol ingestion decreased the antioxidant glutathione (GSH) in type II cells and exacerbated endotoxin-mediated acute lung injury. We hypothesized that this GSH depletion by ethanol, particularly mitochondrial GSH, predisposed type II cells to inflammatory mediator-induced apoptosis. Methods: Adult male rats were fed the Lieber-DeCarli diet for 2, 6, or 16 weeks. Alveolar type II cells were then isolated and treated with hydrogen peroxide or TNF-,. The effect on glutathione (cytosolic and mitochondrial), apoptotic events, and necrosis were determined. In other studies, rats were fed ethanol for 6 weeks and were treated with endotoxin and apoptosis of type II cells determined by the TUNEL method. Results: Chronic ethanol ingestion alone resulted in a progressive decrease in mitochondrial GSH and a progressive increase in the basal apoptosis and necrosis rate (p, 0.05). Furthermore, there was a progressive increase in the sensitivity of the cells to H2O2 or TNF-, induced cytochrome c release, caspase 3 activation, apoptosis, and necrosis (p, 0.05). Finally, there was a 2-fold increase in apoptotic type II cells in vivo when chronic ethanol ingestion was superimposed on endotoxemia. Conclusions: These results suggested that chronic ethanol ingestion resulted in a progressive depletion of mitochondrial GSH and sensitization of type II cells to inflammatory mediator-induced apoptosis and necrosis. These effects may be particularly relevant during acute stress when proliferation and differentiation of these cells are critical to repair of the damaged alveolar epithelium and may have important ramifications for the treatment of acute respiratory distress syndrome in patients with a history of alcohol abuse. [source] The role of panic attacks in acute stress disorder in children,JOURNAL OF TRAUMATIC STRESS, Issue 6 2007Emma Sinclair This study examined the role of peritraumatic panic symptoms during trauma in childhood acute stress. Children (N = 60) who had suffered traumatic injury were administered the Child Acute Stress Reaction Questionnaire, the Child Depression Inventory, and the Physical Reactions Scale to index panic attacks that occurred during the trauma. Panic attacks were experienced during their trauma by 100% of participants with acute stress reactions and 24% of participants without stress reactions. Panic attacks during trauma accounted for 28% of the variance of acute stress reactions, with an additional variance accounted for by age, time since the accident, and dysphoria. These findings are discussed in terms of fear conditioning models of posttraumatic stress. [source] Posttraumatic stress after a motor vehicle accident: A six-month follow-up study utilizing latent growth modelingJOURNAL OF TRAUMATIC STRESS, Issue 6 2006Kitty K. Wu Features of posttraumatic stress disorder (PTSD) for 596 survivors of motor vehicle accidents were examined by self-report measures at 1 week, 1 month, 3 months, and 6 months after the motor vehicle accident (MVA). Latent growth modeling was utilized to study the trend and predictors of the level of distress. Results indicated that 5,20% of the participants reported to have a significant level of posttraumatic stress in one, two, or three of the PTSD symptom clusters within the period studied. Survivors with significant acute stress 1 week after the MVA had a higher risk for developing chronic posttraumatic stress. Although the severity of intrusive and hyperarousal symptoms decreased over time, the severity of avoidance symptoms remained unchanged. Factors predicting the course of PTSD after an MVA are identified. [source] Acute Stress Hyperglycemia in Cats Is Associated with Struggling and Increased Concentrations of Lactate and NorepinephrineJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2002Jacqueline S. Rand We characterized the changes in blood glucose concentrations in healthy cats exposed to a short stressor and determined the associations between glucose concentrations, behavioral indicators of stress, and blood variables implicated in stress hyperglycemia (plasma glucose, lactate, insulin, glucagon, cortisol, epinephrine, and norepinephrine concentrations). Twenty healthy adult cats with normal glucose tolerance had a 5-minute spray bath. Struggling and vocalization were the most frequent behavioral responses. There was a strong relationship between struggling and concentrations of glucose and lactate. Glucose and lactate concentrations increased rapidly and significantly in all cats in response to bathing, with peak concentrations occurring at the end of the bath (glucose baseline 83 mg/dL, mean peak 162 mg/dL; lactate baseline 6.3 mg/dL, mean peak 64.0 mg/dL). Glucose response resolved within 90 minutes in 12 of the 20 cats. Changes in mean glucose concentrations were strongly correlated with changes in mean lactate (r= .84; P <.001) and mean norepinephrine concentrations (r= .81; P < .001). There was no significant correlation between changes in mean glucose concentrations and changes in mean insulin, glucagon, cortisol, or epinephrine concentrations. Struggling and lactate concentrations were predictive of hyperglycemia. Gluconeogenesis stimulated by lactate release is the likely mechanism for hyperglycemia in healthy cats in this model of acute stress. Careful handling techniques that minimize struggling associated with blood collection may reduce the incidence of stress hyperglycemia in cats. [source] Amitriptyline modifies the visceral hypersensitivity response to acute stress in the irritable bowel syndromeALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 5 2009N. M. THOUA Summary Background, Acute physical stress causes alteration in gut autonomic function and visceral hypersensitivity in patients with irritable bowel syndrome (IBS). We have developed a model to measure this stress response. Aim, To assess whether treatment with a drug effective in treating IBS (amitriptyline) alters the response to acute stress in IBS patients. Methods, Nineteen patients with IBS were given amitriptyline 25,50 mg. Patients underwent physical stress (cold pressor) test at baseline and after 3 months of treatment. Physiological parameters measured were: stress perception; systemic autonomic tone [heart rate (HR) and blood pressure (BP)]; gut specific autonomic innervation [rectal mucosal blood flow (RMBF)] and visceral sensitivity (rectal electrosensitivity). Results, Fourteen of 19 (74%) patients improved symptomatically after 3 months of amitriptyline. Acute stress induced increased perception of stress and systemic autonomic tone and reduced RMBF in symptomatic responders and nonresponders (P > 0.05 for all). All nonresponders but only 3 of 14 responders continued to exhibit stress-induced reduced pain threshold at 3 months (change from baseline ,31% vs. +2%, P < 0.03 respectively). Conclusion, In this open study, amitriptyline appears to decrease stress-induced electrical hypersensitivity; this effect is independent of autonomic tone. The gut response to acute stress deserves further study as a model to study drug efficacy in IBS. [source] The cellular level of the recognition factor RssB is rate-limiting for ,S proteolysis: implications for RssB regulation and signal transduction in ,S turnover in Escherichia coliMOLECULAR MICROBIOLOGY, Issue 6 2002Mihaela Pruteanu Summary Degradation of the general stress sigma factor ,S of Escherichia coli is a prime example of regulated proteolysis in prokaryotes. Whereas exponentially growing cells rapidly degrade ,S, various stress conditions result in stabilization and, therefore, rapid accumulation of ,S. Proteolysis of ,S requires the response regulator RssB, a direct recognition factor with phosphorylation-dependent affinity for ,S, which targets ,S to the ClpXP protease. Here, we demonstrate that a sudden increase in ,S synthesis results in ,S stabilization, indicating titration of an essential proteolytic component. Evidence is provided that RssB is the overall rate-limiting factor for ,S proteolysis. As a consequence, the cell has to continuously adjust the expression of RssB to ,S in order to maintain ,S proteolysis in growing cells, despite variations in the rate of ,S synthesis. Such homeostatic feedback-coupling is provided by rssB transcription being dependent on the ,S -controlled rssAB operon promoter. However, strong and rapid increases in ,S synthesis, in re-sponse to acute stress, exceed the compensatory potential of this feedback loop with the result that ,S is stabilized because of RssB titration. We propose that RssB control of ,S proteolysis functions as a genetic switch, in which (i) the ,off' state (low ,S levels caused by proteolysis) is stabilized by a homeostatic negative feedback, and (ii) the threshold for switching to the ,on' state (high levels of stable ,S) is dependent on the cellular level of active, i.e. phosphorylated RssB. [source] Effects of psychological stress on the cerebral processing of visceral stimuli in healthy womenNEUROGASTROENTEROLOGY & MOTILITY, Issue 7 2009C. Rosenberger Abstract, The aim of the study was to analyse effects of psychological stress on the neural processing of visceral stimuli in healthy women. The brain functional magnetic resonance imaging blood oxygen level-dependent response to non-painful and painful rectal distensions was recorded from 14 healthy women during acute psychological stress and a control condition. Acute stress was induced with a modified public speaking stress paradigm. State anxiety was assessed with the State-Trait-Anxiety Inventory; chronic stress was measured with the Perceived Stress Questionnaire. During non-painful distensions, activation was observed in the right posterior insular cortex (IC) and right S1. Painful stimuli revealed activation of the bilateral anterior IC, right S1, and right pregenual anterior cingulate cortex. Chronic stress score was correlated with activation of the bilateral amygdala, right posterior IC (post-IC), left periaqueductal grey (PAG), and right dorsal posterior cingulate gyrus (dPCC) during non-painful stimulation, and with activation of the right post-IC, right PAG, left thalamus (THA), and right dPCC during painful distensions. During acute stress, state anxiety was significantly higher and the acute stress , control contrast revealed activation of the right dPCC, left THA and right S1 during painful stimulation. This is the first study to demonstrate effects of acute stress on cerebral activation patterns during visceral pain in healthy women. Together with our finding that chronic stress was correlated wit the neural response to visceral stimuli, these results provide a framework for further studies addressing the role of chronic stress and emotional disturbances in the pathophysiology of visceral hyperalgesia. [source] Life events and hemodynamic stress reactivity in the middle-aged and elderlyPSYCHOPHYSIOLOGY, Issue 3 2005Douglas Carroll Abstract Recent versions of the reactivity hypothesis, which consider it to be the product of stress exposure and exaggerated hemodynamic reactions to stress that confers cardiovascular disease risk, assume that reactivity is independent of the experience of stressful life events. This assumption was tested in two substantial cohorts, one middle-aged and one elderly. Participants had to indicate from a list of major stressful life events up to six they had experienced in the previous 2 years. They were also asked to rate how disruptive and stressful they were, at the time of occurrence and now. Blood pressure and pulse rate were measured at rest and in response to acute mental stress. Those who rated the events as highly disruptive at the time of exposure and now exhibited blunted systolic blood pressure reactions to acute stress. The present results suggest that acute stress reactivity may not be independent of stressful life events experience. [source] | |||||||||||||||||||||||||||||||