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The aim of the study was to determine the influence of immediate and 1-hr-delayed carbohydrate (CHO) and protein (PRO) feeding after prolonged exercise on leukocyte trafficking, bacterially stimulated neutrophil degranulation, saliva secretory IgA (S-IgA) responses, and circulating stress hormones. In randomized order, separated by 1 wk, 9 male runners completed 3 feeding interventions after 2 hr of running at 75% VO2max. During control (CON), participants received water (12 ml/kg body mass [BM]) immediately and 1 hr postexercise. During immediate feeding (IF), participants received a CHO-PRO solution equal to 1.2 g CHO/kg BM and 0.4 g PRO/kg BM immediately postexercise and water 1 hr postexercise. During delayed feeding (DF), participants received water immediately postexercise and CHO-PRO solution 1 hr postexercise. Unstimulated saliva and venous blood samples were collected preexercise, immediately postexercise, and every 20 min until 140 min postexercise. No significant interactions were observed for circulating leukocytes and T-lymphocyte subset counts, S-IgA secretion rate, or plasma cortisol, epinephrine, or norepinephrine concentration. Bacterially stimulated neutrophil degranulation decreased during recovery on CON and DF (24% and 31%, respectively, at 140 min; p < .01) but not on IF. Compared with CON, neutrophil degranulation was higher on IF at 100 min postexercise and higher on IF than DF at 80 min and 100 min onward postexercise (p < .05). Ingestion of a CHO-PRO solution immediately after, but not 1 hr after, prolonged strenuous exercise prevented the decrease in neutrophil degranulation but did not alter circulating stress hormone, leukocyte trafficking, or S-IgA responses. Further research should identify the independent effect of different quantities of CHO and PRO ingestion during recovery on neutrophil responses and other aspects of immune function. [ABSTRACT FROM AUTHOR]

Multiple neuropeptides are known to regulate water and ion balance in Drosophila melanogaster. Several of these peptides also have other functions in physiology and behavior. Examples are corticotropin-releasing factor-like diuretic hormone (diuretic hormone 44; DH44) and leucokinin (LK), both of which induce fluid secretion by Malpighian tubules (MTs), but also regulate stress responses, feeding, circadian activity and other behaviors. Here, we investigated the functional relations between the LK and DH44 signaling systems. DH44 and LK peptides are only colocalized in a set of abdominal neurosecretory cells (ABLKs). Targeted knockdown of each of these peptides in ABLKs leads to increased resistance to desiccation, starvation and ionic stress. Food ingestion is diminished by knockdown of DH44, but not LK, and water retention is increased by LK knockdown only. Thus, the two colocalized peptides display similar systemic actions, but differ with respect to regulation of feeding and body water retention. We also demonstrated that DH44 and LK have additive effects on fluid secretion by MTs. It is likely that the colocalized peptides are coreleased from ABLKs into the circulation and act on the tubules where they target different cell types and signaling systems to regulate diuresis and stress tolerance. Additional targets seem to be specific for each of the two peptides and subserve regulation of feeding and water retention. Our data suggest that the ABLKs and hormonal actions are sufficient for many of the known DH44 and LK functions, and that the remaining neurons in the CNS play other functional roles. [ABSTRACT FROM AUTHOR]

Background Itch is one of the most prevalent and familiar nociceptions in humans and can result in impaired quality of life. The central processing of itch is known to be important in perceptions of itch and strategies for coping with it, and various triggers have been reported to be associated with patterns of brain activation in pruritus. Stress is known to be an important aggravating factor in itch, but the precise mechanism by which brain activation results in stress-induced pruritus remains elusive. Methods Using functional magnetic resonance imaging (f MRI), we attempted to evaluate if stress-induced pruritus is associated with the activation of certain areas of the brain. Furthermore, we investigated whether sedating antihistamines are more effective than non-sedating antihistamines in decreasing stress-induced pruritus. Memories of stressful events followed by visual stimuli using a series of pictures depicting fearful and stressful conditions, mixed with neutralizing pictures, were used to evoke pruritus. Results The hippocampus and subcortical structures were found to be involved in stress-associated pruritus. Interestingly, sedating antihistamines were involved in the deactivation of brain regions associated with the relief of itch by active scratching, which suggests that sedating antihistamines may mitigate pruritus by instigating patterns of brain activity similar to those induced by scratching behavior. Conclusions Itch scratching reflects a complicated pattern of brain activity. Activation of the hippocampus appears to be involved in stress-associated pruritus, and sedating antihistamines may work in a manner similar to that of scratching behavior. To our knowledge, this is the first study to evaluate brain functioning in relation to stress-induced pruritus. [ABSTRACT FROM AUTHOR]

Study Design: Experimental animal study of treatment of SCI.Objective: To explore whether HBO treatment protects against secondary SCI by inhibiting the ER stress response.Summary Of Background Data: SCI is a neurological disorder that can severely limit the execution of the simplest day-to-day functions. ER stress plays an important role in the induction of neuronal apoptosis after SCI. HBO treatment can alleviate secondary injury and benefit neurological recovery after SCI, but the effect of HBO on ER stress response after SCI is yet to be characterized.Methods: The spinal cord of rats was injured via T10 laminectomy. Experimental animals were randomly assigned to 1 of 3 groups: sham-operated, SCI, and SCI+HBO. Each group was analyzed 1, 2, 3, 7, and 14 days after injury. Neurological recovery was evaluated using the Basso-Beattie-Bresnahan (BBB) scoring system and the TdT-mediated dUTP nick-end labeling reaction was carried out to visualize apoptotic cells. The expression of ER stress-related factors was evaluated by immunohistochemical, western blot, and real-time reverse transcription-polymerase chain reaction analyses.Results: SCI-induced apoptosis and an increase in the levels of CCAAT-enhancer-binding protein homologous protein (CHOP), and caspase-12 and caspase-3 compared with the sham-operated group. HBO treatment decreased CHOP and caspase-12 and caspase-3 expression as well as apoptosis compared with the SCI group. In addition, BBB scores were improved in the SCI+HBO relative to the SCI group at 7 and 14 days.Conclusion: These results suggest that HBO treatment alleviates secondary injury to the spinal cord by inhibiting ER stress induced apoptosis, thereby promoting the recovery of neurological function.Level Of Evidence: N/A. [ABSTRACT FROM AUTHOR]

There is increasing interest in measuring endocrine and immune parameters in free-ranging seals and sea lions, but there is a lack of understanding in how an acute stress response, often associated with capture and handling, influences these parameters of interest. The main objective of this study was to assess the impact of a simulated stressor on both endocrine and immune parameters. During two seasons, exogenous adrenocorticotrophic hormone (ACTH) was administered to seven female juvenile harbor seals and the response of several hormones (cortisol, aldosterone, total and free thyroxine and total triiodothyronine) and immunological parameters (total and differential leukocyte counts and peripheral blood mononuclear cells (PBMC) proliferation) were assessed. Cortisol peaked at 165 min (winter 203.1 ± 84.7 ng/ml; summer 205.3 ± 65.7 ng/ml) and remained significantly elevated 240 min after ACTH infusion in both seasons. Aldosterone peaked at 90 min (winter 359.3 ± 249.3 pg/ml; summer 294.1 ± 83.7 pg/ml) and remained elevated 240 min after administration of ACTH in both seasons. An increase in circulating total white blood cells was driven primarily by the increase in neutrophils which occurred simultaneously with a decrease in lymphocytes leading to an overall increase in neutrophil to lymphocyte ratio. These findings demonstrate that a simulated stress response in juvenile harbor seals results in a predictable increase in both cortisol and aldosterone concentrations, and were associated with altered immunological parameters. [ABSTRACT FROM AUTHOR]

Stress necessitates an immediate engagement of multiple neural and endocrine systems. However, exposure to a single stressor causes adaptive changes that modify responses to subsequent stressors. Recent studies examining synapses onto neuroendocrine cells in the paraventricular nucleus of the hypothalamus demonstrate that stressful experiences leave indelible marks that alter the ability of these synapses to undergo plasticity. These adaptations include a unique form of metaplasticity at glutamatergic synapses, bidirectional changes in endocannabinoid signalling and bidirectional changes in strength at GABAergic synapses that rely on distinct temporal windows following stress. This rich repertoire of plasticity is likely to represent an important building block for dynamic, experience-dependent modulation of neuroendocrine stress adaptation. [ABSTRACT FROM AUTHOR]

Organisms have to cope with an unpredictable and dynamic environment. It is crucial for any living being to respond to these changes by buffering the effects on cellular homeostasis. Failure to appropriately respond to stress can have severe consequences for health and survival. Eukaryotic cells possess several organelle-specific stress responses to cope with this challenge. Besides their central role in stress resistance, these pathways have also been shown to be important in the regulation of proteome maintenance, development and longevity. Intriguingly, many of these effects seem to be controlled by only a subset of cells implying a systemic regulation in a cell non-autonomous manner. The understanding of the nature of this stress communication across tissues, its mechanisms and impact, will be paramount in understanding disease etiology and the development of therapeutic strategies. [ABSTRACT FROM AUTHOR]

In recent years, studies have suggested a novel pathway for cell survival, which faces scientific skepticism and interest in its concept of cell 'resurrection' - that is, the anastasis of cells at late-stage apoptosis. While biomarkers have been discovered, many of these are related to the endoplasmic reticulum (ER) stress response - acting also to promote cell survival in the presence of perturbation. The promises of anastasis, if accepted, will greatly impact translational medicine especially in the treatment of cancer, since apoptosis is generally irreversible in the late stages, and chemotherapy is performed to maximize tumor death and minimize off-target effects. As with all new concepts, there is a need to demarcate anastasis from a well-studied survival mechanism - the ER stress response - if the concept is to progress any further. In this article, it is proposed that anastasis and the ER stress response are one and the same mechanism, demarcated only by the presence of persistent stress. Further, anastasis solves the paradox of the unfolded protein response (UPR) in cancer by providing rationale in C/EBP homologous protein (CHOP)-induced tumor survival, such that CHOP-mediated apoptosis initiates genetic alterations in favor of its survival. After which, the cell regenerates through an enhanced ER stress response. Hence, anastatic cell recovery is the ER stress response post-apoptosis. [ABSTRACT FROM AUTHOR]

Stressors are imminent or perceived challenges to homeostasis. The stress response is an innate, stereotypic, adaptive response to stressors that has evolved in the service of restoring the nonstressed homeostatic set point. It is encoded in specific neuroanatomical sites that activate a specific repertoire of cognitive, behavioral and physiologic phenomena. Adaptive responses, though essential for survival, can become dysregulated and result in disease. A clear example is autoimmune disease. I postulate that depression, like autoimmunity, represents a dysregulated adaptive response: a stress response that has gone awry. The cardinal manifestation of the normal stress response is anxiety. Cognitive programs shift from complex associative operations to rapid retrieval of unconscious emotional memories acquired during prior threatening situations. These emerge automatically to promote survival. To prevent distraction during stressful situations, the capacity to seek and experience pleasure is reduced, food intake is diminished and sexual activity and sleep are held in abeyance. Monoamines, cytokines, glutamate, GABA and other central mediators have key roles in the normal stress response. Many central loci are involved. The subgenual prefrontal cortex restrains the amygdala, the corticotropin-releasing hormone/hypothalamic-pituitary-adrenal (CRH/HPA) axis and the sympathomedullary system. The function of the subgenual prefrontal cortex is moderately diminished during normal stress to disinhibit these loci. This disinhibition promotes anxiety and physiological hyperarousal, while diminishing appetite and sleep. The dorsolateral prefrontal cortex is downregulated, diminishing cognitive regulation of anxiety. The nucleus accumbens is also downregulated, to reduce the propensity for distraction by pleasurable stimuli or the capacity to experience pleasure. Insulin resistance, inflammation and a prothrombotic state acutely emerge. These provide increased glucose for the brain and establish premonitory, proinflammatory and prothrombotic states in anticipation of either injury or hemorrhage during a threatening situation. Essential adaptive intracellular changes include increased neurogenesis, enhancement of neuroplasticity and deployment of a successful endoplasmic reticulum stress response. In melancholic depression, the activities of the central glutamate, norepinephrine and central cytokine systems are significantly and persistently increased. The subgenual prefrontal cortex is functionally impaired, and its size is reduced by as much as 40%. This leads to sustained anxiety and activations of the amygdala, CRH/HPA axis, the sympathomedullary system and their sequella, including early morning awakening and loss of appetite. The sustained activation of the amygdala, in turn, further activates stress system neuroendocrine and autonomic functions. The activity of the nucleus accumbens is further decreased and anhedonia emerges. Concomitantly, neurogenesis and neuroplasticity fall significantly. Antidepressants ameliorate many of these processes. The processes that lead to the behavioral and physiological manifestations of depressive illness produce a significant decrease in lifespan, and a doubling of the incidence of premature coronary artery disease. The incidences of premature diabetes and osteoporosis are also substantially increased. Six physiological processes that occur during stress and that are markedly increased in melancholia set into motion six different mechanisms to produce inflammation, as well as sustained insulin resistance and a prothrombotic state. Clinically, melancholic and atypical depression seem to be antithesis of one another. In melancholia, depressive systems are at their worst in the morning when arousal systems, such as the CRH/HPA axis and the noradrenergic systems, are at their maxima. In atypical depression, depressive symptoms are at their worst in the evening, when these arousal systems are at their minima. Melancholic patients experience anorexia and insomnia, whereas atypical patients experience hyperphagia and hypersomnia. Melancholia seems like an activation and persistence of the normal stress response, whereas atypical depression resembles a stress response that has been excessively inhibited. It is important that we stratify clinical studies of depressed patients to compare melancholic and atypical subtypes and establish their differential pathophysiology. Overall, it is important to note that many of the major mediators of the stress response and melancholic depression, such as the subgenual prefrontal cortex, the amygdala, the noradrenergic system and the CRH/HPA axis participate in multiple reinforcing positive feedback loops. This organization permits the establishment of the markedly exaggerated, persistent elevation of the stress response seen in melancholia. Given their pronounced interrelatedness, it may not matter where in this cascade the first abnormality arises. It will spread to the other loci and initiate each of their activations in a pernicious vicious cycle. [ABSTRACT FROM AUTHOR]

Despite widespread recognition that the physiological systems underlying stress reactivity are well coordinated at a neurobiological level, surprisingly little empirical attention has been given to delineating precisely how the systems actually interact with one another when confronted with stress. We examined cross-system response proclivities in anticipation of and following standardized laboratory challenges in 664 4- to 14-year-olds from four independent studies. In each study, measures of stress reactivity within both the locus coeruleus-norepinephrine system (i.e., the sympathetic and parasympathetic branches of the autonomic nervous system) and the corticotrophin releasing hormone system (i.e., the hypothalamic–pituitary–adrenal axis) were collected. Latent profile analyses revealed six distinctive patterns that recurred across the samples: moderate reactivity (average cross-system activation; 52%–80% of children across samples), parasympathetic-specific reactivity (2%–36%), anticipatory arousal (4%–9%), multisystem reactivity (7%–14%), hypothalamic–pituitary–adrenal axis specific reactivity (6%–7%), and underarousal (0%–2%). Groups meaningfully differed in socioeconomic status, family adversity, and age. Results highlight the sample-level reliability of children's neuroendocrine responses to stress and suggest important cross-system regularities that are linked to development and prior experiences and may have implications for subsequent physical and mental morbidity. [ABSTRACT FROM PUBLISHER]

This article presents a narrative review of the relationship between the biological processes that mediate the stress response - in this case, limiting ourselves to the hypothalamic - pituitary - adrenal cortex - and internal working models derived from early attachment relationships in with respect to infants. It explains the successive phases of the biological response against a stressful event and emphasizes the importance of understanding how these internal models can be correlated with symptoms of chronic stress, states of dysregulation of the HPA axis and hyper-or hypocortisolism situations functional. In this sense, contradictory data are evident when trying to relate dysfunctions of said shaft and specific attachment styles. It does seem to be evidence of the relationship between the nature of the stressor and different patterns of response and subsequent sensitization. More research is needed in order to design more psychotherapeutic interventions tailored to different attachment styles. [ABSTRACT FROM AUTHOR]

Background: It is known that epinephrine/norepinephrine inhibit acute pain transmission. However, the role of β-adrenoceptors is not clear. Thus, we analyzed if β-1 and/or β-2 adrenoceptors can modulate acute pain transmission by performing in vivo single unit recordings during painful and non-painful peripheral stimulation in rats. Methods: Longitudinal study in which we analyzed seven groups of male rats Wistar: control group (n = 11): saline (0.9 %); EPI group (n = 8): epinephrine 100 mcg; AGOβ1 group (n = 8): dobutamine 125 mcg; ANTβ1 group (n = 9): metoprolol 100 mcg; AGOβ2 group (n = 7): clenbuterol 100 mcg; ANTβ2 group (n = 8): butoxamine 100 mcg; ANTβ1 + EPI group (n = 10): metoprolol 100 mcg + epinephrine 100 mcg. For the statistical analysis we used ANOVA. Results: Epinephrine significantly reduced the basal firing rate (BFR) in 34.1 % (p < 0.05) and also the evoked response by painful stimulation in 56 % (p < 0.05). No change was observed in the evoked response by non-painful stimulation. ANTβ1 was the only β-adrenoceptor acting drug that significantly reduced the evoked response by painful stimulation in 41 % (p < 0.05). None of the other drugs alone affected either the BFR or the evoked response to non-painful or painful stimulation. Conclusion: It is the first time that a β1-adrenoceptor antagonist (metoprolol) probes to be effective in reducing the response to painful stimulation in WDR neurons. [ABSTRACT FROM AUTHOR]

Although past research has suggested a link between chronic stress and both physical and mental well-being in older adults, less is known about the degree to which neuroendocrine markers of stress are associated with higher-order cognitive processes such as decision-making. In a sample of healthy older adults (55-85 years), we tested the degree to which variation in the diurnal cortisol rhythm, an index of hypothalamic-adrenal-pituitary axis dynamics, was related to differences in risky decision-making. We found that diurnal cortisol fall predicted performance on the Cups Task, a risky decision-making task that independently tests risk-taking to achieve gains and risk-taking to avoid losses. For potential gains, we found that greater risk-taking was associated with lower diurnal cortisol fall, independent of age or sex of the participant. For risks to avoid potential losses, we found that lower diurnal fall was associated with suboptimal decision-making for men only. Compared with males with more typical diurnal fall, those who displayed lower diurnal fall made more risky choices and demonstrated lower sensitivity to the expected value of the risky choice. We integrate these results with the extant literature on the effects of stress on decision-making and cognitive aging. [ABSTRACT FROM AUTHOR]

Abstract: There is growing evidence that positive social interactions can attenuate the effects of stressful life experiences. However, little is known about the benefits of social partners on stress responses in farm animals. Therefore, in this study we examined the effects of social support on the endocrine and immune stress responses to a single 4h social deprivation in domestic piglets at 7, 21 or 35days of age. The piglets were socially deprived of their mother and littermates. They were left alone (DA) or in the presence of a familiar (DF) or unfamiliar (DU) age-matched piglet. Non-socially deprived piglets served as a control. DA piglets displayed elevated plasma cortisol levels, higher lipopolysaccharide (LPS)-stimulated proliferation of splenocytes and increased TNF-α and IL-6 production in splenocyte cultures than the control piglets. There were no significant buffering effects of social partners on stress-induced plasma cortisol levels and splenocyte proliferation in response to LPS. However, the presence of an age-matched conspecific diminished the IL-6 production by splenocytes in younger, socially deprived piglets, and it reduced the TNF-α release in the older piglets. Compared to the controls, LPS-stimulated splenocytes from DA piglets were more resistant to the inhibitory effects of cortisol, which was demonstrated by a higher proliferative response and increased production of pro-inflammatory cytokines. The dose-dependent cortisol resistance was attenuated by the presence of a familiar or an unfamiliar conspecific at each of the three age categories. Indeed, in the present study, the familiarity level of the social partners did not seem to play a role in the alleviation of social stress-induced inflammatory activity and splenocyte cortisol resistance. In addition, the buffering effect of social support provided by an age-matched conspecific was more pronounced in older piglets. Conclusively, these findings suggest that social support is an important factor for enhancing piglets' abilities to cope with stressful challenges, and it may be a key approach needed to improve the health and welfare of farm animals. [Copyright &y& Elsevier]

Highlights: [•] The glucocorticoid stress response (GCSR) promotes homeostasis. [•] Global change is associated with changes in the regime of stressors. [•] Global change may disrupt the efficiency of the GCSR to maintain homeostasis. [•] The GCSR might be adjusted to new stressors through different mechanisms. [•] Studying the GCSR helps understanding how global change affects different species. [Copyright &y& Elsevier]

This study aimed to investigate psychological stress and endocrine responses during 5 days of head-down tilt bed rest (HDTBR) with or without the impact of artificial gravity (AG). Participants were assigned to one of three bed-rest-protocols either with (i) no centrifugation, (ii) continuous 30 min (AG1) or (iii) discontinuous 6 × 5 min (AG2) centrifugation periods at 1G in the center of mass periods. Centrifugations were performed daily in one session. Questionnaires for assessing psychological stress and the corresponding biological sample collection were performed before, during and after HDTBR or centrifugation. Overall, questionnaires showed no significant changes of anxiety or emotional stress during HDTBR. In the AG1-group, salivary cortisol levels were significantly higher after centrifugation irrespective of the progress of the HDTBR and day of intervention. The AG2-group showed higher cortisol concentrations after centrifugation only on the first days of head-down tilt but no more on day 5 of HDTBR. During bed rest, urine epinephrine excretion increased in all groups, but showed the highest day concentrations in the AG1-group, which were also significantly higher when compared with AG2. These results indicate that 5 days of HDT alone is not a major stressor and accordingly resulted only in moderate changes of neuroendocrine responses over time. However, daily centrifugation for a continuous duration of 30 min induced a significant neuroendocrine response, which was not subject to a habituation as compared with daily but intermittent centrifugation for 6 × 5 min. Discontinuous centrifugation is better tolerated and associated with lower adrenocortical stress responses during HDTBR. [ABSTRACT FROM AUTHOR]

Endocrine-disrupting chemicals can affect reproduction and development in humans and wildlife. We developed a computational model of the hypothalamic-pituitary-gonadal (HPG) axis in female fathead minnows to predict dose-response and time-course (DRTC) behaviors for endocrine effects of the aromatase inhibitor, fadrozole (FAD). The model describes adaptive responses to endocrine stress involving regulated secretion of a generic gonadotropin (LH/FSH) from the hypothalamic-pituitary complex. For model development, we used plasma 17β-estradiol (E2) concentrations and ovarian cytochrome P450 (CYP) 19A aromatase mRNA data from two time-course experiments, each of which included both an exposure and a depuration phase, and plasma E2 data from a third 4-day study. Model parameters were estimated using E2 concentrations for 0, 0.5, and 3 µg/l FAD exposure concentrations, and good fits to these data were obtained. The model accurately predicted CYP19A mRNA fold changes for controls and three FAD doses (0, 0.5, and 3 µg/l) and plasma E2 dose response from the 4-day study. Comparing the model-predicted DRTC with experimental data provided insight into how the feedback control mechanisms in the HPG axis mediate these changes: specifically, adaptive changes in plasma E2 levels occurring during exposure and “overshoot” occurring postexposure. This study demonstrates the value of mechanistic modeling to examine and predict dynamic behaviors in perturbed systems. As this work progresses, we will obtain a refined understanding of how adaptive responses within the vertebrate HPG axis affect DRTC behaviors for aromatase inhibitors and other types of endocrine-active chemicals and apply that knowledge in support of risk assessments. [ABSTRACT FROM AUTHOR]

Abstract: 2,4-Dichlorophenoxyacetic acid (2,4-D) was evaluated in both the Amphibian Metamorphosis Assay (AMA) and the Fish Short Term Reproduction Assay (FSTRA). In the AMA, tadpoles were exposed to mean measured 2,4-D concentrations of 0 (water control), 0.273, 3.24, 38.0 and 113mg acid equivalents (ae)/L for either seven or 21 days. In the FSTRA, fathead minnows were exposed to mean measured 2,4-D concentrations of 0 (water control), 0.245, 3.14, 34.0, and 96.5mg ae/L for 21 days. The respective concentrations of 2,4-D were not overtly toxic to either Xenopus laevis tadpoles or fathead minnows (Pimephales promelas). In the AMA, there were no signs of either advanced or delayed development, asynchronous development, or significant histopathological effects of the thyroid gland among 2,4-D exposed tadpoles evaluated on either day seven or day 21 of the exposure. Therefore, following the AMA decision logic, 2,4-D is considered “likely thyroid inactive” in the AMA with a No Observable Effect Concentration (NOEC) of 113mg ae 2,4-D/L. In the FSTRA, there were no significant differences between control and 2,4-D exposed fish in regard to fertility, wet weight, length, gonado-somatic indices, tubercle scores, or blood plasma concentrations of vitellogenin. Furthermore, there were no treatment-related histopathologic changes in the testes or ovaries in any 2,4-D exposed group. The only significant effect was a decrease in fecundity among fish exposed to 96.5mg ae 2,4-D/L. The cause of the reduced fecundity at the highest concentration of 2,4-D tested in the assay was most likely due to a generalized stress response in the fish, and not due to a specific endocrine mode of action of 2,4-D. Based on fish reproduction, the NOEC in the FSTRA was 34.0mg ae 2,4-D/L. [Copyright &y& Elsevier]

Recent theories have suggested that chronic pain could be partly maintained by maladaptive physiological responses of the organism facing a recurrent stressor. The present study examined the associations between basal levels of cortisol collected over seven consecutive days, the hippocampal volumes and brain activation to thermal stimulations administered in 16 patients with chronic back pain and 18 healthy control subjects. Results showed that patients with chronic back pain have higher levels of cortisol than control subjects. In these patients, higher cortisol was associated with smaller hippocampal volume and stronger pain-evoked activity in the anterior parahippocampal gyrus, a region involved in anticipatory anxiety and associative learning. Importantly, path modelling—a statistical approach used to examine the empirical validity of propositions grounded on previous literature—revealed that the cortisol levels and phasic pain responses in the parahippocampal gyrus mediated a negative association between the hippocampal volume and the chronic pain intensity. These findings support a stress model of chronic pain suggesting that the sustained endocrine stress response observed in individuals with a smaller hippocampii induces changes in the function of the hippocampal complex that may contribute to the persistent pain states. [ABSTRACT FROM AUTHOR]

Abstract: Hypothalamic abnormalities in schizophrenia have been associated with endocrine dysfunctions and stress response. The hypothalamus is involved in several pathways found disrupted in schizophrenia (e.g. hypothalamic–pituitary–adrenal axis, HPA axis); however the available results on potential structural hypothalamic alterations are still controversial. The aim of the study was to investigate the volumes of the hypothalamus and the mammillary bodies in patients with schizophrenia and healthy controls. Twenty-six patients with schizophrenia and 26 healthy controls underwent a 3 Tesla magnetic resonance imaging (MRI) scan. Hypothalamus and mammillary bodies were manually traced by a rater who was blind to subjects'' identity. The General Linear Model was used in group comparisons of the volumes of the hypothalamus and the mammillary bodies. The hypothalamus and mammillary body volumes were significantly larger in patients with schizophrenia than controls, with significant enlargement of the left hypothalamus and trends for significantly increased right hypothalamus and right mammillary body. The size of the mammillary bodies was inversely correlated with negative symptoms and directly correlated with anxiety. This study showed abnormally increased sizes of the hypothalamus and the mammillary bodies in schizophrenia. Mammillary bodies volumes were associated to negative symptoms and anxiety. Future longitudinal studies on the volumes of the hypothalamus and the mammillary bodies with respect to the levels of related hormones will clarify their role in modulating HPA axis in schizophrenia. [Copyright &y& Elsevier]

Abstract: Over the past decade, an increasing awareness has arisen of the role of neuroendocrine hormones in the susceptibility of mammalian hosts to a bacterial infection. During a stress response, glucocorticoids, catecholamines and neuroendocrine factors are released into the circulation of the host. For a long time the effects of stress on the course of an infection have been exclusively ascribed to the direct effect of stress-related hormones on the immune system and the intestinal barrier function. Chronic stress is known to cause a shift from T helper 1-mediated cellular immunity toward T helper 2-mediated humoral immunity, which can influence the course of an infection and/or the susceptibility to a microorganism. Bacteria can however also respond directly to stress-related host signals. Catecholamines can alter growth, motility, biofilm formation and/or virulence of pathogens and commensal bacteria, and as a consequence influence the outcome of infections by these bacteria in many hosts. For some bacteria, such as Salmonella, Escherichia coli and Pseudomonas aeruginosa it was shown that this influence is regulated by quorum sensing mechanisms. In this manuscript an overview of how and when stress influences the outcome of bacterial infections in animals is provided. [Copyright &y& Elsevier]

Abstract: Prenatal stress can alter hypothalamic–pituitary–adrenal axis function with potential consequences for later life. The aim of our study was to examine in guinea pigs (Cavia aperea f. porcellus) the effects of stress experienced during F0 pregnancy on glucocorticoid levels in plasma and feces, as well as challenge performance, in F1 offspring (n =44) and fecal glucocorticoid levels in F2 offspring (n =67). F1 animals were either born to F0 dams that had been stressed with strobe light during early to mid pregnancy, resulting in a short term increase but long-term down-regulation of maternal glucocorticoid levels, or to undisturbed F0 dams. The same stressor was used as a challenge for F1 offspring at age 26days and around 100days. Basal plasma cortisol concentrations during early F1 development, as well as overall glucocorticoid levels at challenge tests, were lower in F1 animals that were prenatally stressed than in control animals. Fecal cortisol metabolites were initially at lower levels in prenatally stressed F1 animals, relative to control animals, but shifted to higher levels around day 68, with an additional sex difference. Effects were also seen in the F2 generation, as male but not female offspring of prenatally stressed F1 animals had significantly higher levels of cortisol metabolites in feces after weaning. We conclude that stress exposure of F0 dams resulted in lower basal glucocorticoid levels in F1 offspring during the pre-pubertal phase and during stress exposure, but higher glucocorticoid levels in post-adolescent F1 animals. Also in males of F2 generation effects of stress exposure of F0 dams were detected. [Copyright &y& Elsevier]

Abstract: Cortisol, the primary circulating corticosteroid in teleosts, is elevated during stress following activation of the hypothalamus–pituitary–interrenal (HPI) axis. Cortisol exerts genomic effects on target tissues in part by activating glucocorticoid receptors (GR). Despite a well-established negative feedback loop involved in plasma cortisol regulation, the role of GR in the functioning of the HPI axis during stress in fish is still unclear. We used mifepristone (a GR antagonist) to suppress GR signaling in rainbow trout (Oncorhynchus mykiss) and assessed the resultant changes to HPI axis activity. We show for the first time that mifepristone caused a functional knockdown of GR by depleting protein expression 40–75%. The lower GR protein expression corresponded with a compensatory up-regulation of GR mRNA levels across tissues. Mifepristone treatment completely abolished the stressor-induced elevation in plasma cortisol and glucose levels seen in the control fish. A reduction in corticotropin-releasing factor (CRF) mRNA abundance in the hypothalamic preoptic area was also observed, suggesting that GR signaling is involved in maintaining basal CRF levels. We further characterized the effect of mifepristone treatment on the steroidogenic capacity of interrenal tissue in vitro. A marked reduction in cortisol production following adrenocorticotropic hormone stimulation of head kidney pieces was observed from mifepristone treated fish. This coincided with the suppression of steroidogenic acute regulatory protein, but not P450 side chain cleavage mRNA abundances. Overall, our results underscore a critical role for central and peripheral GR signaling in the regulation of plasma cortisol levels during stress in fish. [Copyright &y& Elsevier]

Background. Effective intrapartum analgesia attenuates pain, stress, and anxiety which cause release of stress hormones as well as beta-endorphins. Aim. The purpose of this study was to determine the effect of adding dexmedetomidine to hyperbaric bupivacaine for neuraxial analgesia for labor. Methods. Ninety laboring multiparous women were allocated to have single shot intrathecal bupivacaine alone (B), bupivacaine with fentanyl (BF), or bupivacaine with dexmedetomidine (BD). Sensory and motor block characteristics; time from injection to two dermatome sensory regression, sensory regression to S1 dermatome, and motor block regression to Bromage 1 were recorded. Labor pain was assessed with a 10 cm verbal pain scale. Results. Peak sensory block levels in the three groups were essentially the same (P = 0.56). The time for sensory and motor blocks to reach T10 dermatome and Bromage 1, respectively, was faster in group BD than in the other groups (P = 0.0001). The time for sensory regression to S1 was significantly prolonged in the group BD (P = 0.0001). Motor block regression time to Bromage 1 was also prolonged in the group BD (P = 0.0001). Neonatal outcome was normal in all groups. Conclusion. Single shot intrathecal bupivacaine/dexmedetomidine significantly prolonged sensory block in laboring women. [ABSTRACT FROM AUTHOR]

The effect of acute L-alanyl-L-glutamine (AG) ingestion on selected hormonal and electrolyte measures was examined during repetitive, short duration, high intensity exercise with mild hypohydration. Subjects (20.3±1.1 yrs; 180.3±10.4 cm; 83.1±14.0 kg; 11.6±3.6% body fat) reported to the Human Performance Laboratory on four occasions. During each trial subjects were hypohydrated to -2.5% of their baseline body mass. During one trial (DHY) subjects rested in a recumbent position for 45 minutes before commencing the exercise session. During the other three trials subjects were rehydrated to 1.5% of their baseline body mass, before exercise, by drinking water only (W), or with two different doses of AG - a low dose (LDAG: 0.05 g-kg-1) and a high dose (HDAG: 0.2 g-kg-1). The exercise protocol consisted of ten 10-second sprints on a cycle ergometer with a 1-min rest between each sprint. Blood draws were collected once the subject achieved the desired level of hypohydration, immediately pre-exercise, immediately post-exercise, and 24 hrs postexercise. Blood samples were analyzed for glutamine, potassium, sodium, aldosterone, arginine vasopressin, C-reactive protein, interleukin-6, malondialdehyde, testosterone, cortisol, ACTH, and growth hormone. The area under the curve (AUC) analysis demonstrated significantly greater sodium concentrations for DHY compared to all other trials. The AUC analysis for aldosterone showed significantly lower concentrations at LDAG compared to DHY. No other differences between trials were observed in any other hormonal or biochemical responses. AG ingestion during a short duration, anaerobic exercise and mild hypohydration stress had a limited effect on selected hormonal and biochemical measures. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the effects of three different duration (1, 3 or 5 min) rest intervals on hormonal response in 10x10 hurdle jumping series. Eleven adolescent male sprinters and jumpers (16.2±0.9 years, height 170.5±7.9 cm, body mass 70.9±11.1 kg, body mass index 22.0±3.4 kg/m2) participated in the study. An exercise session consisted of 10 two-legged jumps with arm swing over ten 76 cm high hurdles in 10 series which were separated by either 1-, 3- or 5-minute rest intervals. Venous blood samples were obtained before and after the session and cortisol (CORT), testosterone (TEST) and the growth hormone (GH) concentrations were analyzed. Mean jumping times over 10 hurdles using one (7.67±0.92 sec), three (7.44±0.66 sec) or five (7.14±0.54 sec) minutes of recovery were not significantly different from each other (p>.05). No significant changes were noted in CORT and TEST concentrations as a result of different exercise sessions. Compared with the initial value, GH increased rapidly (p<.001) after the jumping test with a 1-min rest interval. A negative correlation (r=-.791) was found between mean jumping time using 5-min rest intervals and changes in the TEST concentration. This study indicates that short jumping series with different length rest intervals do not significantly change TEST or CORT concentrations. However, the shortest rest interval (one minute) causes significant changes in GH concentration in adolescent sprinters and jumpers. [ABSTRACT FROM AUTHOR]

Abstract: Stress is thought to be a potent suppressor of reproduction. However, the vast majority of studies focus on the relationship between chronic stress and reproductive suppression, despite the fact that chronic stress is rare in the wild. We investigated the role of fasting in altering acute stress physiology, reproductive physiology, and reproductive behavior of male zebra finches (Taeniopygia guttata) with several goals in mind. First, we wanted to determine if acute fasting could stimulate an increase in plasma corticosterone and a decrease in corticosteroid binding globulin (CBG) and testosterone. We then investigated whether fasting could alter expression of undirected song and courtship behavior. After subjecting males to fasting periods ranging from 1 to 10h, we collected plasma to measure corticosterone, CBG, and testosterone. We found that plasma corticosterone was elevated, and testosterone was decreased after 4, 6, and 10h of fasting periods compared with samples collected from the same males during nonfasted (control) periods. CBG was lower than control levels only after 10h of fasting. We also found that, coincident with these endocrine changes, males sang less and courted females less vigorously following short-term fasting relative to control conditions. Our data demonstrate that acute fasting resulted in rapid changes in endocrine physiology consistent with hypothalamo–pituitary–adrenal axis activation and hypothalamo–pituitary–gonadal axis deactivation. Fasting also inhibited reproductive behavior. We suggest that zebra finches exhibit physiological and behavioral flexibility that makes them an excellent model system for studying interactions of acute stress and reproduction. [Copyright &y& Elsevier]

Stress and corticosteroid hormones are known to affect learning and memory processes. In this study, we examined whether stress and corticosteroids are capable of facilitating the switch between multiple memory systems in mice. For this purpose, we designed a task that allowed measurement of nucleus caudate-based stimulus-response and hippocampus-based spatial learning strategies. Naive mice used spatial strategies to locate an exit hole on a circular hole board at a fixed location flagged by a proximal stimulus. When the mice were either stressed or administered corticosterone before the task, 30-50% of the mice switched to a stimulus-response strategy. This switch between learning strategies was accompanied by a rescue of performance, whereas performance declined in the stressed mice that kept using the spatial strategy. Pretreatment with a mineralocorticoid receptor antagonist prevented the switch toward the stimulus-response strategy but led to deterioration of hippocampus-dependent performance. These findings (i) show that corticosteroids promote the transition from spatial to stimulus-response memory systems, (ii) provide evidence that the mineralocorticoid receptor underlies this corticosteroid-mediated switch, and (iii) suggest that a stress-induced switch from hippocampus-based to nucleus caudate-based memory systems can rescue performance. [ABSTRACT FROM AUTHOR]

Stress hormones in Rocky Mountain bighorn sheep (Ovis canadensis canadensis), produced in response to environmental changes, road development, or high population density, may impact their immune systems to a threshold level that predisposes them to periodic, large-scale mortality. We compared the stress response to a novel environmental situation and repeated handling between bighorn sheep born and raised in captivity (CR) and bighorn sheep born in the wild (WC) and brought into captivity. We measured plasma epinephrine, norepinephrine, cortisol, and fecal glucocorticoid metabolites (FGM). Three weeks after each group's arrival we used a one-time drop-net event to elicit an acute stress response, and we collected blood samples from each sheep over 35 minutes, as well as one fecal sample. We collected blood and fecal samples from both groups on 7 other occasions over the subsequent 6 months. We also collected fecal samples from the pen at approximately 24-hour intervals for 3 days following every handling event to monitor the stress response to handling. We found that CR sheep had a stronger autonomic nervous system response than WC sheep, as measured by epinephrine and norepinephrine levels, but we found a very similar hypothalamic-pituitary-adrenal axis (HPA) response, measured by cortisol levels, to the acute stress event of a drop-net restraint. We also found that once the WC sheep had acclimated, as indicated by the return to the initial baseline FGM levels within 12 weeks, the CR and WC groups' HPA responses to sampling events were not significantly different from one another. Fecal samples can provide a noninvasive mechanism for managers to monitor baseline FGM for a given herd. Using long-term monitoring of FGM rather than values from a single point in time may allow managers to correlate these levels to outside influences on the herd and better understand the impacts of management changes, population density, or increased human developments on the health of the sheep population. [ABSTRACT FROM AUTHOR]

Abstract: Within the comparative literature, corticosteroid-binding globulin (CBG) has recently emerged as a potential modulator of the glucocorticoids-driven stress response. Many avian field studies include the measurement of CBG with the goal of making behavioral and ecological inferences. However, the field of stress physiology is divided on how to interpret the biological importance of the different states of circulating hormones. Here we review evidence for the biological relevance of each fraction of glucocorticoid hormone; the CBG–glucocorticoid complex (the bound fraction) and the remainder which is either unbound or loosely attached to albumin (the free fraction). We suggest that the biological importance of free vs. bound hormone depends on the location of interest (plasma or tissues), and the time frame of interest (current or future need). While a large body of evidence suggests that free hormones are the biologically active fraction, evidence also suggests that the bound fraction is a biologically relevant reservoir of glucocorticoids. We review two salient topics from the avian stress literature; stress-induced decreases in CBG capacity and glucocorticoid influences in life history strategies. These topics are discussed with an emphasis on free vs. bound hormone concentration and how that compares to current vs. future glucocorticoid needs. [Copyright &y& Elsevier]

The consequences of prenatal maternal stress for development were examined in 125 full-term infants at 3, 6, and 12 months of age. Maternal cortisol and psychological state were evaluated 5 times during pregnancy. Exposure to elevated concentrations of cortisol early in gestation was associated with a slower rate of development over the 1st year and lower mental development scores at 12 months. Elevated levels of maternal cortisol late in gestation, however, were associated with accelerated cognitive development and higher scores at 12 months. Elevated levels of maternal pregnancy-specific anxiety early in pregnancy were independently associated with lower 12-month mental development scores. These data suggest that maternal cortisol and pregnancy-specific anxiety have programming influences on the developing fetus. [ABSTRACT FROM AUTHOR]

Child obesity is a public health priority with numerous and complex causes. This study focuses on factors within the family, namely stressful experiences, which may be associated with child obesity. We examine data from the Child Development Supplement of the Panel Study of Income Dynamics for children in two age groups: 5–11 and 12–17 years old. Results from an ordered probit regression model of child weight categorizations (healthy weight, overweight, obese) indicate positive associations between a range of family stressors (lack of cognitive stimulation and emotional support in the household among younger children, and mental and physical health problems and financial strain in the household among older children) and child overweight and obesity. We discuss how public policies that reduce family stressors may, in turn, help reduce child obesity. [Copyright &y& Elsevier]

This article shows age and gender differences in the magnitude and day-to-day variability of the cortisol awakening response (CAR) using a national sample of 1.143 adults who completed the second wave of the National Study of Daily Experiences, a part of the Midlife Development in the United States survey. Participants between the ages of 33 and 84 years completed 8 consecutive nightly interviews and provided 4 saliva samples (upon waking, 30 min after waking, before lunch, and before bed) on 4 consecutive interview days. Results revealed substantial day-to-day variability in the CAR as well as significant Age x Gender interactions, indicating that although no systematic age-related differences emerged for women, the magnitude and day-to-day variability of the CAR increased with age among men. [ABSTRACT FROM AUTHOR]

Abstract: Protein tyrosine phosphatase 1B (PTP1B) was considered as a potential therapeutic target of type 2 diabetes (T2DM) because of its negative regulation of insulin signaling. It located on the cytosolic surface of endoplasmic reticulum (ER) and played an essential role in the ER stress signaling. Activating transcription factor 6 (ATF6) was an ER stress regulated transmembrane transcription factor that activated the transcription of ER molecular chaperones. We hypothesized that the expression of PTP1B may be regulated by ATF6 when ER stress happened. Our previous studies showed that Astragalus polysaccharide (APS) increased the insulin sensitivity through decreasing the overexpression of PTP1B in T2DM animal models. In this study, we intended to investigate the possible mechanisms involved in this effect. A rat model of T2DM was established using high fat diet associated with intraperitoneal injection of 25mg/kg streptozocin; 25mmol/l d-glucose and 5×10−7 mol/l insulin were used as in vitro investigations to mimic T2DM-like environment. 4-(2-Aminoethyl) benzenesulfonyl fluoride hydrochloride (AEBSF) and pCI-Flag-ATF6(N)(2-366) plasmid were treated separately on human hepatocyte line HL-7702 to observe the effect of ATF6 on the expression of PTP1B. The results suggested that APS not only restored the glucose homeostasis but also reduced the ER stress in this rat model of T2DM; ATF6 was involved in mediating the expression of PTP1B when ER stress happened; APS decreased the expression of PTP1B at least partly through inhibiting the activation of ATF6. [Copyright &y& Elsevier]

Summary: The development and exacerbation of many psychiatric and neurologic conditions are associated with dysregulation of the hypothalamic pituitary adrenal (HPA) axis as measured by aberrant levels of cortisol secretion. Here we report on the relationship between the amplitude of diurnal cortisol secretion, measured across 3 typical days in 18 healthy individuals, and blood oxygen level dependant (BOLD) response in limbic fear/stress circuits, elicited by in-scanner presentation of emotionally negative stimuli, specifically, images of the World Trade Center (WTC) attack. Results indicate that subjects who secrete a greater amplitude of cortisol diurnally demonstrate less brain activation in limbic regions, including the amygdala and hippocampus/parahippocampus, and hypothalamus during exposure to traumatic WTC-related images. Such initial findings can begin to link our understanding, in humans, of the relationship between the diurnal amplitude of a hormone integral to the stress response, and those neuroanatomical regions that are implicated as both modulating and being modulated by that response. [Copyright &y& Elsevier]

The importance of restraining stress-induced activation of the hypothalamic-pituitary-adrenocortical (HPA) system within tolerable limits requires efficient mechanisms for feedback inhibition. Recently, central corticotrophin-releasing hormone (CRH) receptor type 1 (CRHR1) has been shown to mediate HPA system feeback inhibition. To date, most of the data regarding stress-associated expression changes of CRHR1 and CRHR2 mRNA and their ligand CRH have been generated in rats. Taken considerable species differences into consideration, and with the growing importance of transgenic mice, a systematic analysis of the time course of expression changes of CRH and its two receptors in the mouse brain is needed to provide more insight into the regulation of the HPA system, both under physiological and pathophysiological conditions in this species. We analysed in detail the time course of expression changes of CRH, CRHR1 and CRHR2 mRNA after of restraint stress in mice in stress-relevant brain regions (paraventricular nucleus, hippocampus, neocortex). We could show a rapid, strong and long-lasting decrease in cortical and hippocampal CRHR1 mRNA expression after stress, whereas CRHR2 mRNA increased in the same neuroanatomical areas. In situ hybridisation analyses could be further confirmed at the protein level by CRH receptor autoradiography with changes in CRH binding that persisted even 7 days after a single episode of restraint stress. Our observation that stress has opposing effects on CRHR1 and CRHR2 neuronal systems supports the idea that regulation of the relative contribution of the two CRH receptors to brain CRH pathways may be essential in coordinating physiological responses to stress. We further hypothesise that the sustained alteration of CRH receptor expression and binding after a single episode of stress could mediate the long-term effects of stress on neuroendocrine function and emotional regulation. [ABSTRACT FROM AUTHOR]

Self-report measures assess mental processes or representations that are consciously accessible. In contrast, implicit measures assess automatic processes that often operate outside awareness. Whereas self-report measures have often failed to show expected relationships with endocrine stress responses, little effort has been made to relate implicit measures to endocrine processes. The present work examines whether implicit affectivity as assessed by the Implicit Positive and Negative Affect Test (IPANAT) predicts cortisol regulation. In Study 1 , implicit low positive affectivity, but not negative affectivity, significantly predicted circadian cortisol release. In Study 2 , implicit negative affectivity, but not positive affectivity, significantly predicted the cortisol response to acute stress. By contrast, cortisol regulation was not predicted by self-reported affectivity. The findings support the use of implicit affectivity measures in studying individual differences in endocrine stress responses and point to a differential role of positive and negative affectivity in baseline versus stress-contingent cortisol release, respectively. [ABSTRACT FROM AUTHOR]

Objective:Cortisol is elevated in individuals with both increased emotional stress and higher percentages of body fat. Cortisol is also known to affect cognitive performance, particularly spatial processing and working memory. We hypothesized that increased body fat might therefore be associated with decreased performance on a spatial processing task, in response to an acute real-world stressor.Design:We tested two separate samples of participants undergoing their first (tandem) skydive. In the first sample (N=78), participants were tested for salivary cortisol and state anxiety (Spielberger State Anxiety Scale) during the plane's 15-min ascent to altitude in immediate anticipation of the jump. In a second sample (N=20), participants were tested for salivary cortisol, as well as cardiac variables (heart rate, autonomic regulation through heart rate variability) and performance on a cognitive task of spatial processing, selective attention and working memory.Results:In response to the skydive, individuals with greater body fat percentages showed significantly increased reactivity for both cortisol (on both samples) and cognition, including decreased accuracy of our task of spatial processing, selective attention and working memory. These cognitive effects were restricted to the stress response and were not found under baseline conditions. There were no body fat interactions with cardiac changes in response to the stressor, suggesting that the cognitive effects were specifically hormone mediated rather than secondary to general activation of the autonomic nervous system.Conclusions:Our results indicate that, under real-world stress, increased body fat may be associated with endocrine stress vulnerability, with consequences for deleterious cognitive performance.International Journal of Obesity (2009) 33, 157–165; doi:10.1038/ijo.2008.218; published online 18 November 2008 [ABSTRACT FROM AUTHOR]

Psychosocial resources have been tied to lower psychological and biological responses to stress. The present research replicated this relationship and extended it by examining how differences in dispositional reactivity of certain neural structures may underlie this relationship. Two hypotheses were examined: (a) psychosocial resources are tied to decreased sensitivity to threat and/or (b) psychosocial resources are associated with enhanced prefrontal inhibition of threat responses during threat regulation. Results indicated that participants with greater psychosocial resources exhibited significantly less cortisol reactivity following a stress task, as predicted. Analyses using functional magnetic resonance imaging revealed that psychosocial resources were associated with greater right ventrolateral prefrontal cortex and less amygdala activity during a threat regulation task but were not associated with less amygdala activity during a threat sensitivity task. Mediational analyses suggest that the relation of psychosocial resources to low cortisol reactivity was mediated by lower amygdala activity during threat regulation. Results suggest that psychosocial resources are associated with lower cortisol responses to stress by means of enhanced inhibition of threat responses during threat regulation, rather than by decreased sensitivity to threat. [ABSTRACT FROM AUTHOR]

The anti-diuretic hormone arginine vasopressin (AVP) is synthesised in the magnocellular neurosecretory cells (MNCs) in the paraventricular nucleus (PVN) and the supraoptic nucleus (SON) of the hypothalamus. AVP-containing MNCs that project their axon terminals to the posterior pituitary can be identified using immunohistochemical techniques with specific antibodies recognising AVP and neurophysin II, and by virtue of their electrophysiological properties. Recently, we generated transgenic rats expressing an AVP-enhanced green fluorescent protein (eGFP) fusion gene in AVP-containing MNCs. In this transgenic rat, eGFP mRNA was observed in the PVN and the SON, and eGFP fluorescence was seen in the PVN and the SON, and also in the posterior pituitary, indicating transport of transgene protein down MNC axons to storage in nerve terminals. The expression of the AVP-eGFP transgene and eGFP fluorescence in the PVN and the SON was markedly increased after dehydration and chronic salt-loading. On the other hand, AVP-containing parvocellular neurosecretory cells in the PVN that are involved in the activation of the hypothalamic-pituitary adrenal axis exhibit robust AVP-eGFP fluorescence after bilateral adrenalectomy and intraperitoneal administration of lipopolysaccharide. In the median eminence, the internal and external layer showed strong fluorescence for eGFP after osmotic stimuli and stressful conditions, respectively, again indicating appropriate transport of transgene traslation products. Brain slices and acutely-dissociated MNCs and axon terminals also exhibited strong fluorescence, as observed under fluorescence microscopy. The AVP-eGFP transgenic animals are thus unique and provide a useful tool to study AVP-secreting cells in vivo for electrophysiology, imaging analysis such as intracellular Ca2+ imaging, organ culture and in vivo monitoring of dynamic change in AVP secretion. [ABSTRACT FROM AUTHOR]

Neuroendocrinology links experience and behaviour to the action of hormones. This review focusses on the corticosteroids, released in hourly pulses and after stress, to illustrate the integration of body, brain and mind achieved by these hormones. Corticosteroids coordinate cell and organ function in concert with other mediators of the stress response over time spans from seconds to hours, days, weeks, or even permanently. The actions exerted by these stress hormones are mediated by two receptor types that control initial stress reactions and manage the later adaptive phases. How the balance between the stress and adaptive responses contributes to resilience and health is a conundrum to be resolved during the next two decades of the existence of the Journal of Neuroendocrinology. [ABSTRACT FROM AUTHOR]

Evolutionary success depends on our ability to adapt to changing circumstances. The neuroendocrine response to stress is an excellent example of a plastic system that responds to threats to homeostasis and alters its output to meet current and expected future demands. At the level of the hypothalamus, the corticotroph secretagogues corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) respond rapidly to an acute stressor but, following chronic stress, they adapt with a reduction of CRH but a major increase in AVP. The release of CRH and AVP activates pro-opiomelanocortin in anterior pituitary corticotroph cells and the release of adrenocorticotrophic hormone into peripheral blood from where it targets receptors in the adrenal cortex to release glucocorticoid hormones. These hormones (i.e. corticosterone in the rat and cortisol in man) are released in a pulsatile ultradian pattern which defines the normal circadian rhythm. The frequency of the pulses is increased under states of chronic stress, and in rats with genetically determined hyper-responsiveness of the hypothalamic-pituitary-adrenal axis. Interestingly, neonatal influences can also programme alterations in ultradian rhythmicity, implicating epigenetic factors in its regulation. At the level of tissue receptors, the alteration in pattern of glucocorticoid ultradian rhythm has differential effects on mineralocorticoid receptor and glucocorticoid receptor (GR) binding to DNA and offers a mechanism for tissue specific responses to altered glucocorticoid dynamics. The effects of neonatal experience are not only seen at the level of CRH and GR regulation, but also are evident in behavioural responses to stress and in the responsiveness of brain stem serotonergic pathways, as measured by tryptophan hydroxylase mRNA in the brain stem. [ABSTRACT FROM AUTHOR]

This short review goes back to early discoveries concerning the neuroendocrinology of aging, discussing the Brown-Sequard experiment on rejuvenation at the end of the 19th century and Steinach’s subsequent experiments in the early 20th century. It also considers the seminal experiments of Pierre Ascheim, Ming Tsung Peng and Joseph Meites in the 1960s on the aging of the gonadotrophic axis. Major age-associated changes in neuroendocrine regulatory processes involved in the menopausal transition, andropause, somatopause and adrenopause are also reviewed. Finally, some views on future directions of research into the neuroendocrinology of aging are proposed, based on the pleiotropy of neuroendocrine messengers and functions. [ABSTRACT FROM AUTHOR]

In addition to various reproductive stimuli, the neuropeptide oxytocin (OXT) is released both from the neurohypophysial terminal into the blood stream and within distinct brain regions in response to stressful or social stimuli. Brain OXT receptor-mediated actions were shown to be significantly involved in the regulation of a variety of behaviours. Here, complementary methodological approaches are discussed which were utilised to reveal, for example, anxiolytic and anti-stress effects of OXT, both in females and in males, effects that were localised within the central amygdala and the hypothalamic paraventricular nucleus. Also, in male rats, activation of the brain OXT system is essential for the regulation of sexual behaviour, and increased OXT system activity during mating is directly linked to an attenuated anxiety-related behaviour. Moreover, in late pregnancy and during lactation, central OXT is involved in the establishment and fine-tuned maintenance of maternal care and maternal aggression. In monogamous prairie voles, brain OXT is important for mating-induced pair bonding, especially in females. Another example of behavioural actions of intracerebral OXT is the promotion of social memory processes and recognition of con-specifics, as revealed in rats, mice, sheep and voles. Experimental evidence suggests that, in humans, brain OXT exerts similar behavioural effects. Thus, the brain OXT system seems to be a potential target for the development of therapeutics to treat anxiety- and depression-related diseases or abnormal social behaviours including autism. [ABSTRACT FROM AUTHOR]

This paper utilizes complexity theory to analyze the implications of systemic changes that have occurred over the last 30 years in the automotive industry. We argue by dint of complexity analysis that the networked automotive production system characterized by just-in-time and lean production creates states far from equilibrium in individual parts manufacturers and assembly plants. Positive feedback creates system disturbances and adverse health and safety issues in the local plant environments. In addition, we examine four mechanisms that serve as negative feedback loops to absorb stresses in local plant environments and rectify health and safety related issues. This paper draws on thirty interviews with health and safety representatives at automotive manufacturing and assembly plants. [ABSTRACT FROM AUTHOR]

In this commentary, we discuss Gersten''s findings particularly in relation to the challenge of accurately measuring stress, neuroendocrine markers and allostatic load. Allostatic load is a timely, potentially useful tool to measure the degree in which the body''s physiological function is outside of optimal range. As with most biomarkers early on in development, there are sound opportunities to advance methods that will help understand the etiology of allostatic load and allow it to become more accurately measured. We present a biomarker development framework that should aid in furthering measurement of allostatic load, emphasizing the importance of biomarker measurement accuracy, standardization of methods, and relevance to clinically meaningful outcomes. [Copyright &y& Elsevier]

Allostatic load (AL) is thought to represent the physiological toll that builds up over the life course as a consequence of the body''s response to stress. An important aim of this paper is to test this widely held—but little investigated—understanding of what AL represents. More specifically, using the Social Environment and Biomarkers of Aging Study (SEBAS), a nationally representative survey of Taiwan conducted in year 2000, this paper scrutinizes the connection between stressful life histories and neuroendocrine allostatic load (NAL). Stressful life histories are operationalized through the use of two sets of indicators: one set makes use of respondents’ subjective interpretations of various life domains and the other makes use of non-subjective data about conditions that are expected to be stressful (e.g., widowhood, living alone, and low education). NAL is an index of four neuroendocrine biomarkers (cortisol, dehydroepiandrosterone sulfate (DHEAS), epinephrine, and norepinephrine) collected in blood and urine samples under resting, basal states. The major findings of this paper are twofold. First, there is little evidence to support the hypothesis that baseline levels of the neuroendocrine markers stem from stressful life histories. Second, report of current stress (among women only) is positively correlated with higher NAL levels. Taken together, these findings question whether the neuroendocrine markers of the AL construct reflect long-term processes over the life course. Indeed, evidence here suggests that the neuroendocrine markers may reflect the exact opposite—a transient state at the time of the study. [Copyright &y& Elsevier]

Background: Severe physical and environmental stress seems to have a suppressive effect on the hypothalamic—pituitary—gonadal (HPG) axis in men. Examining hormonal responses to an extreme 160-km competition across frozen Alaska provides a unique opportunity to study this intense stress. Objective: To examine hormonal responses to an ultra-endurance race. Methods: Blood samples were obtained from 16 men before and after racing and analyzed for testosterone, interleukin-6 (IL-6), growth hormone (GH) and cortisol. Six subjects (mean (SD) age 42 (7) years; body mass 78.9 (7.1) kg; height 1.78 (0.05) m raced by bicycle (cyclists) and 10 subjects (age 35 (9) years; body mass 77.9 (10.6) kg; height, 1.82 (0.05) m) raced by foot (runners). Mean (SD) finish times were 21.83 (6.27) and 33.98 (6.12) h, respectively. Results: In cyclists there were significant (p ≤ 0.05) mean (SD) pre-race to post-race increases in cortisol )254.83 (135.26) to 535.99 (232.22) nmol/l), GH (0.12 (0.23) to 3.21 (3.33) μg/ml) and IL-6 (2.36 (0.42) to 10.15 (3.28) pg/ml), and a significant decrease in testosterone (13.81 (3.19) to 5.59 (3.74) nmol/l). Similarly, in runners there were significant pre-race to post-race increases in cortisol (142.09 (50.74) to 452.21 (163.40) ng/ml), GH (0.12 (0.23) to 3.21 (3.33) ¼g/ml) and IL-6 (2.42 (0.68) to 12.25 (1.78) pg/ml), and a significant decrease in testosterone (12.32 (4.47) to 6.96 (3.19) nmol/l). There were no significant differences in the hormonal levels between cyclists and runners (p>0.05). Conclusions: These data suggest a suppression of the hypopituitary—gonadal axis potentially mediated by amplification of adrenal stress responses to such an ultra-endurance race in environmentally stressful conditions. [ABSTRACT FROM AUTHOR]