Validated biological and psychological markers of acute stress in humans are an important tool in translational research. The Trier Social Stress Test (TSST), involving public interview and mental arithmetic performance, is among the most popular methods of inducing acute stress in experimental settings, and reliably increases hypothalamic-pituitary-adrenal axis activation. However, although much research has focused on HPA axis activity, the TSST also affects the sympathetic-adrenal-medullary system, the immune system, cardiovascular outputs, gastric function and cognition. We critically assess the utility of different biological and psychological markers, with guidance for future research, and discuss factors which can moderate TSST effects. We outline the effects of the TSST in stress-related disorders, and if these responses can be abrogated by pharmacological and psychological treatments. Modified TSST protocols are discussed, and the TSST is compared to alternative methods of inducing acute stress. Our analysis suggests that multiple readouts are necessary to derive maximum information; this strategy will enhance our understanding of the psychobiology of stress and provide the means to assess novel therapeutic agents.

Stress stimulates several adaptive hormonal responses. Prominent among these responses are the secretion of catecholamines from the adrenal medulla, corticosteroids from the adrenal cortex, and adrenocorticotropin from the anterior pituitary. A number of complex interactions are involved in the regulation of these hormones. Glucocorticoids regulate catecholamine biosynthesis in the adrenal medulla and catecholamines stimulate adrenocorticotropin release from the anterior pituitary. In addition, other hormones, including corticotropin-releasing factor, vasoactive intestinal peptide, and arginine vasopressin stimulate while the corticosteroids and somatostatin inhibit adrenocorticotropin secretion. Together these agents appear to determine the complex physiologic responses to a variety of stressors.

Abstract Sex differences in stress responses can be found at all stages of life and are related to both the organizational and activational effects of gonadal hormones and to genes on the sex chromosomes. As stress dysregulation is the most common feature across neuropsychiatric diseases, sex differences in how these pathways develop and mature may predict sex-specific periods of vulnerability to disruption and increased disease risk or resilience across the lifespan. The aging brain is also at risk to the effects of stress, where the rapid decline of gonadal hormones in women combined with cellular aging processes promote sex biases in stress dysregulation. In this Review, we discuss potential underlying mechanisms driving sex differences in stress responses and their relevance to disease. Although stress is involved in a much broader range of diseases than neuropsychiatric ones, we highlight here this area and its examples across the lifespan.

78 Vulnerability factors for PTSD may exist prior to experiencing trauma. 78 Biological factors include genetics and physiological stress reactivity. 78 Cognitive factors include neuropsychological ability and cognitive biases. 78 Prospective research will further elucidate pre-trauma vulnerability factors.

Lymphocyte beta adrenergic receptor binding using [ 125 I]CNP was determined in patients with panic disorder ( N =4) or agoraphobia with panic attacks ( N =17) and age- and sex-matched healthy subjects ( N =22). The patients showed a significantly lower number of -adrenergic receptor binding sites and a significantly higher affinity of binding than healthy subjects. A past or present history of major depression in the patients did not alter these findings. These results are consistent with a growing body of knowledge implicating noradrenergic dysfunction in the pathophysiology of panic anxiety.

Physiological resonance between individuals is considered fundamental to the biological capacity for empathy. Observers of pain and distress commonly exhibit increases in reported distress, autonomic arousal, facial mimicry, and overlapping neural activity. An important, unstudied question is whether physiological stress can also resonate. Physiological stress is operationalized as activation of the hypothalamic pituitary adrenocortical (HPA) and sympatho-adrenomedullary (SAM) axes. People often report an aversive state resulting from the stress of another, but this could be conveyed through resonating arousal or distress, without activating the physiological stress response. Physiological stress is particularly important to examine since it commonly occurs chronically, with known negative effects on health. Salivary cortisol and salivary alpha-amylase (sAA) were measured in both speakers and observers during a modified Trier Social Stress Test (TSST) to assess activation of the HPA and SAM axes (respectively). Cortisol (but not sAA) responses resonated between speakers and observers. The cortisol response of observers increased with trait empathy and was not related to the speaker's subjective fear or distress. This study provides a novel method for examining physiological resonance, and indicates that we can indeed catch another's physiological stress, suggesting a specific health risk for those in the social network of stressed individuals.

国外研究者认为高自尊个体的内控性高,因此其在心理性应激情境中的反应不那么强烈,而国内研究者从集体文化(中国)考虑,则认为高自尊个体的社会认可需求较高,因此在心理性应激情境中的反应更强烈。本研究采用特里尔社会应激测试作为应激情境,采集41名中国大学生被试在这一情境下的客观参数(心率)作为心理性应激反应的指标,通过问卷测量被试的自尊水平、内控性水平和社会认可需求水平,考察自尊影响心理性应激反应的机制。结果发现被试的自尊水平与应激情境下的心率呈正相关,并且社会认可需求在自尊与心理性应激的关系中起着显著的中介作用。本文从文化差异角度提出自尊预测心理性应激反应的模型可能需要在不同文化背景下来分别探讨。

ABSTRACT090000 This study examined whether individual differences in error-related self-regulation predict emotion regulation in daily life, as suggested by a common-systems view of cognitive and emotional self-regulation. Participants ( N = 47) completed a Stroop task, from which error-related brain potentials and behavioral measures of error correction were computed. Participants subsequently reported on daily stressors and anxiety over a 2-week period. As predicted by the common-systems view, a physiological marker of error monitoring and a behavioral measure of error correction predicted emotion regulation in daily life. Specifically, participants higher in cognitive control, as assessed neurally and behaviorally, were less reactive to stress in daily life. The results support the notion that cognitive control and emotion regulation depend on common or interacting systems.

Abstract In response to stress, the brain activates several neuropeptide-secreting systems. This eventually leads to the release of adrenal corticosteroid hormones, which subsequently feed back on the brain and bind to two types of nuclear receptor that act as transcriptional regulators. By targeting many genes, corticosteroids function in a binary fashion, and serve as a master switch in the control of neuronal and network responses that underlie behavioural adaptation. In genetically predisposed individuals, an imbalance in this binary control mechanism can introduce a bias towards stress-related brain disease after adverse experiences. New candidate susceptibility genes that serve as markers for the prediction of vulnerable phenotypes are now being identified.

This study examined the role of chronic (homelessness), coping style, and on beta-adrenergic receptors in a sample of homeless men. Sixteen healthy normotensive subjects and nine untreated hypertensive subjects were studied. was measured with the Brown and Harris categorization; coping style was measured with the Ways of Coping Scale. Lymphocyte beta-adrenergic receptors were characterized in terms of receptor density (Bmax). Individuals with high had lower Bmax (p <.005). In multiple regression analyses, 50% of the variance in Bmax was accounted for by and coping style (p =.01). Receptor measures may be useful for characterizing the physiological response to continuing life adversity.

The present study assessed the modulating effect of education level on cortisol reactivity to the Trier Social Stress Test (TSST) in a sample of 101 middle-aged adults (22 males, 79 females) between the ages of 50 and 65. The TSST involves a public speech and mental arithmetic task in front of an audience. No previous studies have assessed whether education level can have an impact on cortisol reactivity to this psychosocial stressor. It is plausible that greater exposure to academia may impact how one perceives and responds to the demands of the speech and arithmetic task. Should education have an impact on cortisol reactivity to the TSST, future studies will be required to control for this factor in order to reduce both statistical error and false interpretations. In addition to completing the TSST, participants were administered a battery of neurocognitive tests and personality questionnaires, including a report on education level (i.e. number of years total and degree: High School, Junior College, Technical, University). Results showed that adults with post-secondary education above Junior College tended to secrete higher cortisol levels overall, as measured by total area under the curve. However, it was the group with lower educational attainment who showed a greater stress response specific to the TSST, as measured by percentage increase in cortisol from pre- to post-TSST. Analyses also found that higher educated adults performed better than their less educated peers on verbal fluency. Considering that the TSST is an oral task, it is suggested that middle-aged individuals with a lower level of education may find the TSST more stressful due to lower verbal capacity, which may lead to an increased cortisol response to the TSST when compared to individuals with a higher level of education.

The multifunctional Ca/calmodulin-dependent protein kinase II (CaMKII) targets a number of Ca homeostatic proteins and regulates gene transcription. Many of the substrates phosphorylated by CaMKII are also substrates for protein kinase A (PKA), the best known downstream effector of β-adrenergic receptor (β-AR) signaling. While PKA and CaMKII are conventionally considered to transduce signals through separate pathways, there is a body of evidence suggesting that CaMKII is activated in response to β-AR stimulation and that some of the downstream effects of β-AR stimulation are actually mediated by CaMKII. The signaling pathway through which β-AR stimulation activates CaMKII, in parallel with or downstream of PKA, is not well-defined. This review considers the evidence for and mechanisms by which CaMKII is activated in response to β-AR stimulation. In addition the potential role of CaMKII in β-AR regulation of cardiac function is considered. Notably, although many CaMKII targets (e.g., phospholamban or the ryanodine receptor) are central to the regulation of Ca handling, and effects of CaMKII on Ca handling are detectable, inhibition or gene deletion of CaMKII has relatively little effect on the acute physiological contractile response to β-AR. On the other hand CaMKII expression and activity are increased in heart failure, a pathophysiological condition characterized by chronic stimulation of cardiac β-ARs. Blockade of β-ARs is an accepted therapy for treatment of chronic heart failure although the rationale for its beneficial effects in cardiomyocytes is uncertain. There is growing evidence that inhibition or gene deletion of CaMKII also has a significant beneficial impact on the development of heart failure. The possibility that excessive β-AR stimulation is detrimental because of its effects on CaMKII mediated Ca handling disturbances (e.g., ryanodine receptor phosphorylation and diastolic SR Ca leak) is an intriguing hypothesis that merits future consideration.

Generalized anxiety disorder (GAD) is characterized by “pathological” worry, suggesting that GAD worriers differ qualitatively from non-GAD worriers. However, results from taxometric studies of worry in undergraduate and community samples have been mixed and to date, no studies have utilized clinical samples. The current study examined the latent structure of worry and GAD symptoms in a diagnostically heterogeneous clinical sample. Indicators were selected from the Penn State Worry Questionnaire-Abbreviated (n=1175) and the GAD-7 (n=638) and submitted to three taxometric procedures: MAXCOV, MAMBAC, and L-Mode. Results from all three procedures suggested that both worry and generalized anxiety are best conceptualized as dimensional constructs. Findings also indicated that ongoing conceptualization, assessment, and treatment of worry and GAD may be hampered by the application of a categorical framework.

目的探讨老年自尊的发展趋势,并考察性别和教育水平对老年自尊的影响。方法使用罗森伯格自尊量表(SES)对202名60岁老年人和381名40~59岁的中年人进行调查。结果 (1)老年早期(60~69岁)、老年晚期(≥70岁)与40~49岁组、50~59岁组中年人的自尊水平没有显著差异;(2)老年人的自尊水平受到性别和受教育程度的影响。老年早期组男性的自尊水平比女性更高,老年晚期组女性自尊水平高于男性、老年早期组女性;受教育程度对老年早期组自尊水平影响不显著,但老年晚期组高学历(专科及以上)老年人自尊水平显著高于较低文化程度的老年人。结论从整体上看,老年人自尊水平与中年人相当,但老年人的自尊水平存在性别和受教育程度的差异,且这种差异会随着年龄而改变。老年早期、男性自尊水平较高、老年晚期、女性和受教育程度高的老年人自尊水平更高。

61Effect of age in the stress response.61Effect of sex in the stress response.61Effect of genotype in the stress response.

Cardiac vagal tone is proposed as a novel index of stress and stress vulnerability in . A model is described that emphasizes the role of the parasympathetic nervous system and particularly the vagus nerve in defining stress. The model details the importance of a branch of the vagus originating in the ambiguus. In the ambiguus not only coordinates sucking, swallowing, and breathing, but it also regulates heart rate and vocalizations in response to stressors. In it is possible, by quantifying the amplitude of respiratory sinus arrhythmia, to assess the tonic and phasic regulation of the vagal pathways originating in the ambiguus. Measurement of this component of vagal tone is proposed as a method to assess, on an individual basis, both stress and the vulnerability to stress.

A proportion of patients with panic disorder (PD) fail to show a remission after psychotherapy. Biological correlates of psychotherapy non-response have rarely been described in the literature. The aim of the present study was to research the relationship between the cortisol stress response and the psychotherapy outcome in PD patients. Twenty-eight PD patients (20 females, mean age卤SD: 35.71卤13.18) seeking psychological treatment for PD andn=32 age- and sex-matched healthy control participants (21 females, aged 34.66 12.07) participated in this study. The patients underwent five weeks of cognitive behavioural therapy (CBT). Within the first two weeks of the CBT, both study groups were confronted with the Trier Social Stress Test (TSST). Blood sampling for cortisol and adrenocorticotropic hormone (ACTH) evaluation as well as fear-rating (Visual Analogue Scale; Primary Appraisal and Secondary Appraisal Questionnaire, PASA) accompanied the TSST. The global severity of PD (Panic & Agoraphobia Scale; PAS), agoraphobic cognitions (Agoraphobic Cognitions Questionnaire; ACQ), fear of bodily sensations (Bodily Sensations Questionnaire; BSQ), agoraphobic avoidance (Mobility Inventory; MI), and depressiveness (Beck Depression Inventory; BDI) were assessed before and after the CBT (except the BDI). The statistical analysis revealed significant main effects of time for cortisol and the ACTH concentration in response to the TSST, independently of the study group. 42.9% of the PD patients and 65.6% of the healthy control participants showed a cortisol stress response to the TSST 55.2nmol/l (descriptive finding). The data showed a significant inverse association of the TSST cortisol stress response with the MI total score when accompanied. Further, a significant association of the PASA subjective level of fear and the BSQ as well as a trend for an association of the PASA with the ACQ were observed. Consistent with prior research, we could replicate findings of decreased cortisol concentrations in the PD patients in comparison to the healthy control participants. Furthermore, our findings agree with previous data showing an association of the attenuated cortisol stress response with the psychotherapy non-response. In the present sample, those patients with the lowest cortisol concentrations showed the least improvement in agoraphobic avoidance after psychotherapy. The patients with the highest level of fear showed the most improvement in fear of bodily sensations. Study limitations as well as implications for future studies will be discussed.

Abstract OBJECTIVE: To test the hypothesis that perfectionism is an important moderator of the neuroendocrine stress response, with higher perfectionism predicting increased neuroendocrine activation. METHODS: A total of 50 middle-aged men underwent an acute standardized psychosocial stress task (Trier Social Stress Test). Perfectionism, cognitive appraisal of the stressful situation, trait anxiety, and various personality characteristics were assessed with questionnaires. Salivary cortisol, plasma epinephrine and norepinephrine, blood pressure, and heart rate were analyzed before and after stress. Circadian profiles of cortisol secretion during the day and in response to awakening were analyzed to assess basal activity of the hypothalamus-pituitary-adrenal (HPA) axis. Multiple regression analyses were conducted to identify predictors of the neuroendocrine stress response. RESULTS: Perfectionism was significantly associated with area under the total response curve with respect to increase (AUCi) of cortisol (r = 0.322, p = .046), but not with AUCi of norepinephrine (r = -0.217, p = .152) or AUCi of epinephrine (r = 0.116, p = .477). Hence, AUCi of cortisol was the main criterion. As possible predictors, trait anxiety, neuroticism, vital exhaustion, secondary appraisal, depression, and openness were considered. Regression analyses demonstrated that only perfectionism (beta = 0.45, p = .002) and secondary appraisal (beta = 0.50, p = .001) were independent predictors of AUCi of cortisol, the final model explaining 45% of the total variance in cortisol response (R2 = 0.45, "shrunken" R2 [sR2] = 0.38); perfectionism alone accounted for 18% of this variance (deltaR2 = 0.18, sR2 = 0.19). CONCLUSION: The typical cognitions, and presumably the associated emotions, of perfectionists seem to contribute independently to stress-induced bodily responses, including HPA axis activation, in response to psychosocial stress.

Abstract There are substantial individual differences in the response towards acute stressor. The aim of the current study was to examine how the neural activity after an error response during a non-stressful state, prospectively predicts the magnitude of physiological stress response (e.g., cortisol response and heart rate) and negative affect elicited by a laboratory stress induction procedure in nonclinical participants. Thirty-seven healthy young male adults came to the laboratory for the baseline neurocognitive measurement on the first day during which they performed a Go/Nogo task with their electroencephalogram recorded. On the second day, they came again to be tested on their stress response using an acute psychosocial stress procedure (i.e., the Trier Social Stress Test, the TSST). Results showed that the amplitude of error positivity (Pe) significantly predicted both the heart rate and cortisol response towards the TSST. Our results suggested that baseline cognitive neural activity reflecting error consciousness could be used as a biological predictor of physiological response to an acute psychological stressor in men. Copyright 2017 Elsevier Ltd. All rights reserved.

Trier Social Stress Test(TSST) is a widely used psychosocial stress paradigm conducted in a laboratory setting which has been shown to reliably elicit a physiological stress response in various study samples.However,no study to date has investigated the responses to the TSST in Chinese sample.Therefore,in the present study,healthy male and female volunteers(N=30) performed the standardized TSST protocol,during which several subjective measures(Profile of Mood State and the visual rating scale) and objective measures(heart rate and salivary cortisol) were assessed.The results showed that participants exhibited a significant increase in heart rate and salivary cortisol,and reported more anxiety immediately following the TSST compared to baseline.Furthermore,while men and women did not differ with respect to physiological response to TSST,women did report higher levels of anxiety compared to men.The findings demonstrated that TSST is a protocol with good applicability in Chinese participants and could be used to conduct psychosocial stress research in China.Sex differences failed to reliably discriminate between male and female in objective measures to stressors which were achievement-oriented.

？特里尔社会应激测试(triersocialstresstest:tsst)是国外应用广泛的社会心理应激测试手段,然而还没有研究对其在中国的适用性进行报告。本研究以健康大学生为被试,分别采用主观应激报告(简明心境量表和5点量表)和客观应激参数(心率和唾液皮质醇)为指标,探讨tsst在中国的适用情况以及性别因素对个体在tsst应激情境中的影响。结果发现,tsst诱发了中国被试显著的应激反应,在经历了tsst情境后,被试主观报告紧张水平增加,同时心跳加速,唾液皮质醇水平增加。即使女性被试主观报告紧张与不安的程度显著高于男性,但是男性和女性在tsst应激情境下的心跳和唾液皮质醇指标没有差异。研究结果提示,tsst在中国被试中具有良好的适用性,可以利用其开展与社会心理应激相关的研究。男女被试在与成就动机相关的应激源(例如,tsst)中的客观应激参数差异不明显。

Objective: Increased cardiovascular reactivity has been proposed to be a critical mediator in the de

There is a complex interplay between psychological states and biochemical factors. β-Adrenergic receptor responsiveness is altered in some patients with depression and anxiety disorders, but the relation between various psychological states and receptor function in a normal population is unknown. We measured lymphocyte β-adrenergic receptor density (B max ), sensitivity (cAMP ratio), the Profile of Mood States (POMS), and Spielberger State–Trait Anxiety Inventory (STAI) in 39 hypertensives and 81 normotensives. We examined correlations between log normalized receptor variables and psychological states. Log B max showed negative correlations with age and with POMS tension-anxiety, depression-dejection, and anger-hostility. Log cAMP ratio did not show significant correlations with POMS and STAI ratings. In step-wise multiple regression analyses, 36% of the variance in B max was accounted for by POMS tension-anxiety, and age. Our study suggests that increased POMS tension-anxiety was highly associated with down-regulation of β-adrenergic receptors, even in subjects who do not have psychiatric illness. Numerous psychological states could be associated with changes of β-adrenergic receptor responsiveness in a normal population.