Onset Of Stressor Research Articles

Late acute stress effects on decision-making: The magnified attraction to immediate gains in the iowa gambling task

Previous literature indicates that the later phases of the acute stress response may promote poor decision-making, characterized by riskier choices and a likely inclination towards immediate reward-seeking. However, all studies addressing the effect of this phase have treated decisional capacity as a singular dimension, without analyzing the underlying processes under decision-making. Employing the Value-Plus-Perseveration (VPP) RL model, based on Bayesian logic, this study aims to gain specific insights into how late phase of acute stress impacts the cognitive processes underpinning decision-making in the Iowa Gambling Task (IGT), deciphering whether, as expected, gains are processed in a magnified manner. Seventy-three participants were randomly assigned to two groups, stress (N = 35) and control (N = 38). A virtual version of The Trier Social Stress Test (TSST-VR) was employed as a laboratory stressor. Decision-making was evaluated 35 minutes after the stressor onset, by means of the IGT. Results showed that stressed participants, in comparison to control group, displayed more perseverant and consistent decision-making, enhanced memory, and reinforcement learning capabilities, yet were guided by a greater attraction to decks offering immediate high gains. These results are analyzed with the understanding that in the IGT, short-term decisions focused on instant rewards are seen as counterproductive. This suggests that stress could limit the ability to switch to strategies that are more cautious and offer greater long-term benefits.

Stress and memory encoding: What are the roles of the stress-encoding delay and stress relevance?

The effects of acute stress on memory encoding are complex. Recent work has suggested that both the delay between stress and encoding and the relevance of the information learned to the stressor may modulate the effects of stress on memory encoding, but the relative contribution of each of these two factors is unclear. Therefore, in the present study, we manipulated (1) acute stress, (2) the delay between stress and encoding, and (3) the relevance of the information learned to the stressor. The results indicated that stress during encoding led to better memory for study materials that were related to the stressor relative to memory for study materials that were unrelated to the stressor. This effect was numerically reduced for materials that were encoded 40 min after stressor onset (23 min after the stressor had ended) compared with items encoded at the time of the stressor, but this difference was not significant. These results suggest that the relevance of the information learned to the stressor may play a particularly important role in the effects of stress on memory encoding, which has important implications for theories of stress and memory.

Posttraumatic growth after earthquake: A systematic review and meta-analysis.

Posttraumatic growth (PTG) represents a positive personal change after adverse events, such as natural disasters, including earthquake. However, the association between exposure to earthquake and level of PTG is still unknown. Thus, the aim of this systematic review and meta-analyses (MA) is to assess the level of PTG in people exposed to earthquake. Studies were identified via Scopus, PsycInfo, Web of Science, PubMed, EMBASE, ProQuest, Cochran Library, Ovid, Google Scholar, OpenGrey, congress, and conferences research papers. The level of PTG was presented as mean and standard deviation. Subgroup analyses were conducted to control for the amount of time that had passed since stressor onset and age of the study population. The meta-regression was used to explore the sources of between-study heterogeneity, including sample size and age. The MA of all 21 studies using no restrictions related to age and time of the PTG measurement since traumatic event showed low level of PTG (41.71; 95%CI = 34.26; 49.16, I2: 62.44%, p: .000). Subgroup analyses controlled for the age demonstrated that level of PTG was higher in adults (49.47; 95% CI = 42.35; 56.58, I2: 0%, p = .466) when compared to children and adolescents (35.38; 95% CI = 23.65; 47.11, I2: 69.09%, p < .00). Moreover, the pooled weight mean of PTG measured 1 year and less than 1 year since the earthquake varied between medium (46.04; 95%CI = 34.45; 57.63, I2:51.2%, p: .037) and high (59.03; 95%CI = 41.46; 76.41, I2: 0%, p: .990) levels, respectively. The results of our MA showed low level of PTG in earthquake survivors. However, the mean value of PTG in adults was higher when compared to children and adolescents. In addition, the mean PTG was found to decrease over time since traumatic events.

Effects of stress on 6- and 7-year-old children’s emotional memory differs by gender

Understanding effects of emotional valence and stress on children’s memory is important for educational and legal contexts. This study disentangled the effects of emotional content of to-be-remembered information (i.e., items differing in emotional valence and arousal), stress exposure, and associated cortisol secretion on children’s memory. We also examined whether girls’ memory is more affected by stress induction. A total of 143 6- and 7-year-old children were randomly allocated to the Trier Social Stress Test for Children (n = 103) or a control condition (n = 40). At 25 min after stressor onset, children incidentally encoded 75 objects varying in emotional valence (crossed with arousal) together with neutral scene backgrounds. We found that response bias corrected memory was worse for low-arousing negative items than for neutral and positive items, with the latter two categories not being different from each other. Whereas boys’ memory was largely unaffected by stress, girls in the stress condition showed worse memory for negative items, especially the low-arousing ones, than girls in the control condition. Girls, compared with boys, reported higher subjective stress increases following stress exposure and had higher cortisol stress responses. Whereas a higher cortisol stress response was associated with better emotional memory in girls in the stress condition, boys’ memory was not associated with their cortisol secretion. Taken together, our study suggests that 6- and 7-year-old children, more so girls, show memory suppression for negative information. Girls’ memory for negative information, compared with that of boys, is also more strongly modulated by stress experience and the associated cortisol response.

Effects of acute psychosocial stress on the hypothalamic-pituitary-thyroid (HPT) axis in healthy women

ObjectiveThe individual set point of the hypothalamic-pituitary-thyroid (HPT) axis is largely genetically determined. Apart from this genetic predisposition, the HPT axis may also be malleable to environmental demands such as psychosocial stress. Indeed, previous research has indicated that critical life events often precede the onset of autoimmune thyroid diseases, and subtle abnormalities in HPT functioning are present in some patients with stress-related disorders such as depression. However, no studies have investigated whether exposure to psychosocial stress leads to an immediate activation of the HPT axis. MethodsA total of N = 30 healthy women attended two laboratory appointments in a randomized order. An intravenous catheter was inserted at the beginning of each appointment. In the stress session, this was followed by the Trier Social Stress Test (TSST). Plasma samples to determine thyroid-stimulating hormone (TSH), triiodothyronine (T3), and thyroxine (T4) were taken at baseline and 20, 50, and 110 min after the TSST started. In the control session, participants rested and were instructed to read magazines, while the sampling schedule was maintained. ResultsThere was a significant rise in TSH concentrations in response to the TSST, with a peak observed 20 min after stressor onset, and a steady decline thereafter. No such response was observed in the control session. The TSST did not increase T3 or T4. ConclusionThe finding that acute psychosocial stress is able to elicit a significant increase in TSH is relevant to our understanding of a number of stress-related illnesses presenting with abnormalities of the HPT axis.

Effects of developmental stress on animal phenotype and performance: a quantitative review.

Developmental stressors are increasingly recognised for their pervasive influence on the ecology and evolution of animals. In particular, many studies have focused on how developmental stress can give rise to variation in adult behaviour, physiology, and performance. However, there remains a poor understanding of whether general patterns exist in the effects and magnitude of phenotypic responses across taxonomic groups. Furthermore, given the extensive phenotypic variation that arises from developmental stressors, it remains important to ascertain how multiple processes may explain these responses. We compiled data from 111 studies to examine and quantify the effect of developmental stress on animal phenotype and performance from juveniles to adulthood, including studies from birds, reptiles, fish, mammals, insects, arachnids, and amphibians. Using meta-analytic approaches, we show that across all studies there is, on average, a moderate to large negative effect of developmental stress exposure (posterior mean effect: |d| = -0.51) on animal phenotype or performance. Additionally, we demonstrate that interactive effects of timing of stressor onset and the duration of exposure to stressors best explained variation in developmental stress responses. Animals exposed to stressors earlier in development had more-positive responses than those with later onset, whereas longer duration of exposure to a stressor caused responses to be stronger in magnitude. However, the high amount of heterogeneity in our results, and the low degree of variance explained by fixed effects in both the meta-analysis (R2 = 0.034) and top-ranked meta-regression model (R2 = 0.02), indicate that phenotypic responses to developmental stressors are likely highly idiosyncratic in nature and difficult to predict. Despite this, our analyses address a critical knowledge gap in understanding what effect developmental stress has on phenotypic variation in animals. Additionally, our results highlight important environmental and proximate factors that may influence phenotypic responses to developmental stressors.

Targeting Kruppel-like Factor 9 in Excitatory Neurons Protects against Chronic Stress-Induced Impairments in Dendritic Spines and Fear Responses

SUMMARYStress exposure is associated with the pathogenesis of psychiatric disorders, including post-traumatic stress disorder (PTSD) and major depressive disorder (MDD). Here, we show in rodents that chronic stress exposure rapidly and transiently elevates hippocampal expression of Kruppel-like factor 9 (Klf9). Inducible genetic silencing of Klf9 expression in excitatory forebrain neurons in adulthood prior to, but not after, onset of stressor prevented chronic restraint stress (CRS)-induced potentiation of contextual fear acquisition in female mice and chronic corticosterone (CORT) exposure-induced fear generalization in male mice. Klf9 silencing prevented chronic CORT and CRS induced enlargement of dendritic spines in the ventral hippocampus of male and female mice, respectively. KLF9 mRNA density was increased in the anterior dentate gyrus of women, but not men, with more severe recent stressful life events and increased mortality. Thus, Klf9 functions as a stress-responsive transcription factor that mediates circuit and behavioral resilience in a sex-specific manner.

Chronic stress, hair cortisol and depression: A prospective and longitudinal study of medical internship

BackgroundStress plays a causal role in depression onset, perhaps via alteration of hypothalamic-pituitary-adrenal (HPA) axis functioning. HPA axis hyperactivity has been reported in depression, though inconsistently, and the nature of this relationship remains unclear, partly because cortisol measurement over time has been challenging. Development of hair cortisol assessment, a method that captures cortisol over prolonged periods of time, creates new possibilities. In this study, hair cortisol was incorporated into a prospective and longitudinal study of medical internship, stress and symptoms of depression. This provided a rare opportunity to 1) prospectively assess hair cortisol responses to stress, and 2) examine whether stress-induced changes in hair cortisol predict depressive symptom development. MethodsHair cortisol, depressive symptoms, and stress-relevant variables (work hours, sleep, perceived stress, mastery/control) were assessed in interns (n = 74; age 25–33) before and repeatedly throughout medical internship. ResultsHair cortisol sharply increased with stressor onset, decreased as internship continued, and rose again at year’s end. Depressive symptoms rose significantly during internship, but were not predicted by cortisol levels. Hair cortisol also did not correlate with increased stressor demands (work hours, sleep) or stress perceptions (perceived stress, mastery/control); but these variables did predict depressive symptoms. DiscussionHair cortisol and depressive responses increased with stress, but they were decoupled, following distinct trajectories that likely reflected different aspects of stress reactivity. While depressive symptoms correlated with stressor demands and stress perceptions, the longitudinal pattern of hair cortisol suggested that it responded to contextual features related to anticipation, novelty/familiarity, and social evaluative threat.

Stigma Consciousness Modulates Cortisol Reactivity to Social Stress in Women.

The aim of the current study was to examine whether stigma consciousness shapes cortisol responses to social stress among women in the lab. Undergraduate women (N = 45) completed background measures and then participated in a public speaking task, with assessments of cortisol prior to the stressor as well as 20- and 40-minutes post stressor onset. Results from multilevel models revealed that women higher in stigma consciousness evidenced blunted cortisol reactivity following social stress across the study session compared to women lower in stigma consciousness. This interaction was robust to adjustment for a number of covariates, including demographic (e.g., age), physiological (e.g., menstrual cycle) and psychological (e.g., depressive symptomatology) factors. Potential explanations for observed cortisol patterns are discussed, including hypo-reactivity of the hypothalamic-pituitary-adrenal (HPA) axis and elevated anticipatory stress. To conclude, implications for health disparities research are considered.

Stress in the zoo: Tracking the impact of stress on memory formation over time

Although stress is well known to modulate human memory, precisely how memory formation is altered by a stressful encounter remains unclear. Stress effects on cognition are mainly mediated by the rapidly acting sympathetic nervous system, resulting in the release of catecholamines, and the slower acting hypothalamus-pituitary-adrenal axis secreting cortisol, which induces its effects on cognition through fast, non-genomic actions and delayed, genomic actions. Importantly, these different waves of the physiological stress response are thought to dynamically alter neural processing in brain regions important for memory such as the amygdala and the hippocampus. However, the precise time course of stress effects on memory formation is still unclear. To track the development of stress effects on memory over time, we tested individuals who underwent a stressful experience or a control procedure before a 2-h walk through a zoo, while an automatic camera continuously photographed the events they encoded. In a recognition memory test one week later, participants were presented with target photographs of their own zoo tour and lure photographs from an alternate tour. Stressed participants showed better memory for the experimental treatment than control participants, and this memory enhancement for the stressful encounter itself was directly linked to the sympathetic stress response. Moreover, stress enhanced memory for events encoded 41–65min after stressor onset, which was associated with the cortisol stress response, most likely arising from non-genomic cortisol actions. However, memory for events encoded long after the stressor, when genomic cortisol actions had most likely developed, remained unchanged. Our findings provide novel insights into how stress effects on memory formation develop over time, depending on the activity of major physiological stress response systems.

The impact of positive reappraisal on positive (and negative) emotion among older adults.

Positive reappraisal is an important cognitive strategy for older adults associated with wide-ranging improvements in psychological well-being. However, little is known about the relationship between positive reappraisal and positive and negative emotion, anxiety and depression, and whether positive reappraisal is associated with continued increases in positive emotion over time. In the first study, 61 participants aged 62 to 88 years (M = 72, SD = 5.8) completed current measures of cognitive emotion regulation, positive emotion, negative emotion, anxiety and depression regarding their most distressing aging-related adverse life event, and rated (retrospectively) positive reappraisal use at the time of the stressor. Utilizing a longitudinal design, in a second study 60 participants aged 62 to 88 years (M = 71.2, SD = 5.7) completed the same measures for a recent adverse life event and repeated the measures 3 and 6 months later. In the first study, positive reappraisal reported for both time periods was significantly correlated with current positive emotion, but not negative emotion with mixed findings for anxiety and depression, and positive reappraisal use increased with time since stressor onset. In the second study, positive reappraisal was significantly correlated with positive emotion and significantly predicted positive emotion from 3-month to 6-month follow-up, and was related to anxiety and depression but not general negative emotion. These findings indicate that positive reappraisal is related to positive emotion but not consistently with negative emotion, and continues to be beneficial over time in older adults who have experienced a stressor.

A friend in need: Time-dependent effects of stress on social discounting in men

Stress is often associated with a tend-and-befriend response, a putative coping mechanism where people behave generously towards others in order to invest in social relationships to seek comfort and mutual protection. However, this increase in generosity is expected to be directed only towards a delimited number of socially close, but not distant individuals, because it would be maladaptive to befriend everyone alike. In addition, the endocrinological stress response follows a distinct temporal pattern, and it is believed that tend-and-befriend tendencies can be observed mainly under acute stress. By contrast, the aftermath (>1h after) of stress is associated with endocrinological regulatory processes that are proposed to cause increased executive control and reduced emotional reactivity, possibly eliminating the need to tend-and-befriend. In the present experiment, we set out to investigate how these changes immediately and >1h after a stressful experience affect social-distance-dependent generosity levels, a phenomenon called social discounting. We hypothesized that stress has a time-dependent effect on social discounting, with decisions made shortly after (20min), but not 90min after stress showing increased generosity particularly to close others. We found that men tested 20min after stressor onset indeed showed increased generosity towards close but not distant others compared to non-stressed men or men tested 90min after stressor onset. These findings contribute to our understanding on how stress affects prosocial behavior by highlighting the importance of social closeness and the timing of stress relative to the decision as modulating factors in this type of decision making in men.

Poor sleep quality potentiates stress-induced cytokine reactivity in postmenopausal women with high visceral abdominal adiposity

Sleep disturbance is a key behavioral risk factor for chronic medical conditions observed at high rates among overweight and obese individuals. Systemic inflammation, including that induced by stress, may serve as a common biological mechanism linking sleep, adiposity, and disease risk. To investigate these relationships, 48 postmenopausal women (mean age=61.8) completed a standardized laboratory stress task during which time blood was collected at baseline and 30, 50 and 90+ min after stressor onset to assess circulating levels of interleukin (IL)-6, IL-10, and IL-6/IL-10 ratio. Self-reported global sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI) while adiposity was estimated by body mass index. Sagittal diameter was obtained in clinic to estimate visceral abdominal adiposity. Multi-level growth curve models revealed that poorer self-reported sleep quality was associated with greater stress-induced increases in IL-6/IL-10 ratio. In terms of adiposity, higher sagittal diameter, but not BMI, was associated with greater IL-6 reactivity (p's<0.05). Further, associations between sleep quality and cytokine reactivity varied as a function of sagittal diameter. Among poor sleepers (1 SD above mean of PSQI score), stress-induced increases in IL-6 and IL-6/IL-10 ratio were significantly steeper in those with high visceral adiposity (1 SD above the mean of sagittal diameter) compared to those with low visceral adiposity (1 SD below the mean of sagittal diameter). In sum, poorer sleep quality and greater visceral adiposity, separately and especially in combination, are associated with greater stress-related increases in systemic inflammation. This research may help elucidate the complex link between sleep, obesity and inflammatory disease risk.

Amygdala functional connectivity is reduced after the cold pressor task

The amygdala forms a crucial link between central pain and stress systems. Previous research indicates that psychological stress affects amygdala activity, but it is less clear how painful stressors influence subsequent amygdala functional connectivity. In the present study, we used pulsed arterial spin labeling (PASL) to investigate differences in healthy male adults' resting-state amygdala functional connectivity following a cold pressor versus a control task, with the stressor and control conditions being conducted on different days. During the period of peak cortisol response to acute stress (approximately 15-30 min after stressor onset), participants were asked to rest for 6 min with their eyes closed during a PASL scanning sequence. The cold pressor task led to reduced resting-state functional connectivity between the amygdalae and orbitofrontal cortex (OFC) and ventromedial prefrontal cortex, and this occurred irrespective of cortisol release. The stressor also induced greater inverse connectivity between the left amygdala and dorsal anterior cingulate cortex (ACC), a brain region implicated in the down-regulation of amygdala responsivity. Furthermore, the degree of poststressor left amygdala decoupling with the lateral OFC varied according to self-reported pain intensity during the cold pressor task. These findings indicate that the cold pressor task alters amygdala interactions with prefrontal and ACC regions 15-30 min after the stressor, and that these altered functional connectivity patterns are related to pain perception rather than cortisol feedback.

Dietary oils mediate cortisol kinetics and the hepatic mRNA expression profile of stress-responsive genes in gilthead sea bream (Sparus aurata) exposed to crowding stress. Implications on energy homeostasis and stress susceptibility

Juveniles of gilthead sea bream were fed with plant protein-based diets with fish oil (FO diet) or vegetable oils (66VO diet) as dietary lipid sources. No differences in growth performance were found between both groups, and fish with an average body mass of 65–70g were crowded (90–100kg/m3) to assess the stress response within the 72h after the onset of stressor. The rise in plasma cortisol and glucose levels was higher in stressed fish of group 66VO (66VO-S) than in FO group (FO-S), but the former stressed group regained more quickly the cortisol resting values of the corresponding non-stressed diet group. The cell–tissue repair response represented by derlin-1, 75kDa glucose-regulated protein and 170kDa glucose-regulated protein was triggered at a lower level in 66VO-S than in FO-S fish. This occurred in concert with a long-lasting up-regulation of glucocorticoid receptors, antioxidant enzymes, enzyme subunits of the mitochondrial respiratory chain, and enzymes involved in tissue fatty acid uptake and β-oxidation. This gene expression pattern allows a metabolic phenotype that is prone to “high power” mitochondria, which would support the replacement of fish oil with vegetable oils when theoretical requirements in essential fatty acids for normal growth are met by diet.

Depressive Symptoms and Diurnal Salivary Cortisol Patterns Among Female Caregivers of Stroke Survivors

Informal caregivers of stroke survivors experience elevated chronic stress and are at risk of developing depressive symptoms. The cumulative effects of chronic stress can increase allostatic load and dysregulate biological processes, thus increasing risk of stress-related disease. Stress-induced alterations in the pattern of cortisol secretion vary with respect to stressor onset, intensity, and chronicity. Little is known about the psychoendocrine response to stress in female caregivers of stroke survivors. The purpose of this study was to examine perceived stress, caregiver burden, and the association between caregiver depressive symptoms and diurnal cortisol in 45 females caring for a significant other who experienced a stroke within the past year. Women completed the Center for Epidemiologic Studies Depression Scale (CES-D) and collected saliva for cortisol upon awakening, 30 min postawakening, noon, and bedtime for 2 consecutive days. Results revealed that women had high levels of perceived stress and caregiver burden. In women with CES-D scores ≥ 16, salivary cortisol levels were significantly lower across the day relative to women with CES-D scores < 16. This difference persisted after adjusting for age, number of caregiving hours per week, perceived social support, and quality of sleep. Younger age was associated with more depressive symptoms as well as lower levels of cortisol at awakening and 30 min postawakening. Results demonstrate that the burden of caregiving increases risk of depressive symptoms and hypocortisolism across the day. Hypocortisolism may contribute to increased risk of depressive symptoms as a result of the loss of glucocorticoid attenuation of stress-induced inflammation.

Effects of acute psychosocial stress exposure on endocrine and affective reactivity in college students differing in the 5-HTTLPR genotype and trait neuroticism

Enhanced stress vulnerability has been implicated in the pathogenesis of affective disorders. Although both genetic (5-HTTLPR) and cognitive (neuroticism) factors are known to increase stress vulnerability, no experimental study has investigated the interaction between these two factors on psychobiological reactivity following acute stress exposure. This study used a balanced experimental design to examine the interaction between the 5-HTTLPR genotype and trait neuroticism in neuroendocrine and affective stress responses. From a large group of 771 students, 48 carriers of the short/short (S/S) allele and 48 carriers of the long/long (L/L) allele with the lowest and the highest neuroticism scores (77 females, 19 males; mean age ± SD: 20.6 ± 2 years) were selected and exposed to an acute psychosocial stressor. Mood was assessed before and after the stressor, and salivary cortisol concentrations were measured before and at 20, 30, and 60 min after stressor onset. Acute stress increased salivary cortisol concentration regardless of either 5-HTTLPR genotype or neuroticism, but it caused a less profound negative mood change in L/L compared to S/S-allele carriers with the lowest neuroticism scores. The 5-HTTLPR genotype influences affective reactivity to acute stress conditional upon neuroticism, improving resilience to acute stress in L/L-allele carriers if they do not already possess high cognitive–affective (neuroticism) vulnerability.

The Serotonin Transporter Promoter Polymorphism Is Associated with Cortisol Response to Psychosocial Stress

Across multiple mental health-related measures, a polymorphism (5-HTTLPR) within the promoter of the serotonin transporter gene has been associated with differential psychological sensitivity to stressful experiences. Yet, the specific mechanisms by which this polymorphism contributes to risk for psychological dysfunction is unclear. Therefore, we investigated cortisol reactivity to psychosocial stress as a potential intermediate phenotype that might predispose to such risk. A psychologically healthy sample of 182 young adults were genotyped for the 5-HTTLPR. Each participant delivered a speech and performed mental arithmetic in one of three audience conditions: a critical evaluative audience, a supportive evaluative audience, or no audience. Salivary cortisol was sampled at baseline and at 20, 40, and 75 min after stressor onset. The two evaluative audience conditions elicited similar, significant increases in cortisol that were significantly greater than in the no audience control. Together, the evaluative audience conditions revealed a significant relationship between cortisol reactivity and the 5-HTTLPR, with the short/short genotype showing the greatest reactivity. Internal analyses revealed that the 5-HTTLPR was significantly associated with cortisol reactivity in the negative audience condition only, suggesting that short/short individuals might be especially vulnerable to social threat. The short/short genotype of the 5-HTTLPR is associated with greater cortisol reactivity to social threat. When short/short individuals experience stressful life events, they might be at greater risk for the adverse psychological and physical health consequences associated with heightened cortisol exposure.

Corticotropin‐releasing Hormone Receptor Subtypes in the Rat Anterior Pituitary after Two Types of Restraint Stress

The stress response in anterior pituitary (AP) is mediated by corticotropin-releasing hormone (CRH) acting through CRH-R1 and -R2, however, the function of CRH-R2 in AP is still not fully elucidated. We used 1-h long restraint (IMO) as well as restraint combined with water immersion (IMO+C). Using real-time PCR we quantified mRNA expression of CRH-R1, CRH-R2alpha-soluble and -insoluble, and cAMP response element binding (CREB), with reference gene GAPDH. In control AP, CRH-R1 mRNA was up to 20-fold higher than levels of CRH-R2alpha-soluble or CRH-R2alpha-insoluble mRNA. IMO reduced CRH-R1 mRNA to 47% and 63% of control levels 1 and 2 h after the onset of stressor, respectively, while IMO+C did not produce significant changes. Our data demonstrated that these stressors did not change CRH-R2alpha mRNA, unlike the very significant response of CRH-R1 to IMO.

Peripheral biomarker composite associated with smaller hippocampal volume

Animal and human studies demonstrate an association between smaller hippocampal volume and stress. A composite index of peripheral biomarkers used to objectively quantify human psychosocial stress has demonstrated utility, but has not yet been linked to hippocampal volume in putative 'high stress' groups. Structural magnetic resonance imaging exams and a composite of biomarkers representing cardiovascular, atherosclerosis, hypothylamic-pituitary-adrenal axis, glucose metabolism, and sympathetic nervous system activity were assessed in 30 healthy women with histories of stress precipitated by their child's diagnosis of a life-threatening illness. Hippocampal volume was significantly predicted by age, time since stressor onset, and the composite. An objective biomarker index may improve temporal tracking of brain changes in relation to stress-related psychological symptoms, with implications for basic and clinical research.