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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The anteroventral region of the bed nucleus of the stria terminalis (BST) stimulates hypothalamic-pituitary-adrenocortical (HPA) axis responses to acute stress. However, the role of the anterior BST nuclei in chronic drive of the HPA axis has yet to be established. Therefore, this study tests the role of the anteroventral BST in physiological responses to chronic drive, using a chronic variable stress (CVS) model. Male Sprague-Dawley rats received either bilateral ibotenate lesions, targeting the anteroventral BST, or vehicle injection into the same region. Half of the lesion and control rats were exposed to a 14-d CVS paradigm consisting of twice-daily exposure to unpredictable, alternating stressors. The remaining rats were nonhandled control animals that remained in home cages. On the morning after the end of CVS exposure, all rats were exposed to a novel restraint stress challenge. CVS induced attenuated body weight gain, adrenal hypertrophy, thymic involution, and enhanced CRH mRNA in hypophysiotrophic neurons of the hypothalamic paraventricular nucleus, none of which were affected by anteroventral BST lesions. In the absence of CVS, lesions attenuated the plasma corticosterone and paraventricular nucleus c-fos mRNA responses to the acute restraint stress. In contrast, lesions of the anteroventral BST elevated plasma ACTH and corticosterone responses to novel restraint in the rats previously exposed to CVS. These data suggest that the anterior BST plays very different roles in integrating acute stimulation and chronic drive of the HPA axis, perhaps mediated by chronic stress-induced recruitment of distinct BST cell groups or functional reorganization of stress-integrative circuits.
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PMID:The anteroventral bed nucleus of the stria terminalis differentially regulates hypothalamic-pituitary-adrenocortical axis responses to acute and chronic stress. 1803 88

The bed nucleus of the stria terminalis (BST) plays a prominent role in brain integration of acute responses to stressful stimuli. This study tests the hypothesis that the BST plays a complementary role in regulation of physiological changes associated with chronic stress exposure. Male Sprague-Dawley rats received bilateral ibotenate lesions or sham lesions of the posterior medial region of the BST (BSTpm), an area known to be involved in inhibition of HPA axis responses to acute stress. Chronic stress was induced by 14-day exposure to twice daily stressors in an unpredictable sequence (chronic variable stress, CVS). In the morning after the end of CVS, stressed and non-stressed controls were exposed to a novel restraint stress challenge. As previously documented, CVS caused adrenal hypertrophy, thymic involution, and attenuated body weight gain. None of these endpoints were affected by BSTpm lesions. Chronic stress exposure facilitated plasma corticosterone responses to the novel restraint stress and elevated CRH mRNA. Lesions of the BSTpm increased novel stressor-induced plasma ACTH and corticosterone secretion and enhanced c-fos mRNA induction in the paraventricular nucleus of the hypothalamus (PVN). In addition, lesion of the BSTpm resulted in an additive increase in CVS-induced facilitation of corticosterone responses and PVN CRH expression. Collectively these data confirm that the BSTpm markedly inhibits HPA responses to acute stress, but do not strongly support an additional role for this region in limiting HPA axis responses to chronic drive. The data further suggest that acute versus chronic stress integration are subserved by different brain circuitry.
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PMID:The role of the posterior medial bed nucleus of the stria terminalis in modulating hypothalamic-pituitary-adrenocortical axis responsiveness to acute and chronic stress. 1837 95

The hypothalamic-pituitary-adrenal (HPA) axis exhibits a circadian rhythm, activation by stress, and inhibition by corticosteroids. Activity in the HPA axis is very sensitive to inhibition by corticosteroids when they are administered exogenously. When stress-induced corticosteroid secretion occurs, however, normal activity in the HPA is not inhibited and may even be augmented. Experiments in rats have shown that stress also induces facilitation of subsequent activity in the HPA axis that appears to balance the inhibitory effects of corticosterone and thus maintains responsiveness to new, acute stresses in chronically stressed rats. Stress-induced facilitation of HPA axis activity may be mediated by a parallel stress-induced (CRH-dependent) increase in the capacity of brain noradrenergic cell groups to respond to acute stress. A continually responsive HPA axis, even under conditions of chronic stress, appears to be important for survival. Stress-induced increases in glucocorticoid secretion to levels sufficient to occupy glucocorticoid receptors enable appropriate thermoregulatory and cardiovascular responses to acute stress. There is, however, an overall metabolic cost to the animal of maintaining continued activity in the HPA axis during chronic stress.
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PMID:Stress update Adaptation of the hypothalamic-pituitary-adrenal axis to chronic stress. 1840 36

The manifestations of stress, defined as a biological response to an event that the individual perceives as a threat to its homeostasis, are commonly linked to enhanced activity of the hypothalamo-pituitary-adrenal (HPA) axis and the activation of the sympathetic adreno-medullary (SA) system. Activation of the HPA system results in the secretion of peptides from the hypothalamus, principally corticotropin releasing hormone (CRH), which stimulates the release of adrenocorticotropic hormone (ACTH) and beta-endorphin. ACTH induces the secretion of corticosteroids from the adrenal cortex, which can be seen in pigs exposed to acute physical and/or psychological stressors. The present paper is a review of studies on the influence of stressors on reproduction in pigs. The effects of stress on reproduction depend on the critical timing of stress, the genetic predisposition to stress, and the type of stress. The effect of stress on reproduction is also influenced by the duration of the responses induced by various stressors. Prolonged or chronic stress usually results in inhibition of reproduction, while the effects of transient or acute stress in certain cases is stimulatory (e.g. anoestrus), but in most cases is of impairment for reproduction. Most sensitive of the reproductive process are ovulation, expression of sexual behaviour and implantation of the embryo, since they are directly controlled by the neuroendocrine system.
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PMID:Stress and its influence on reproduction in pigs: a review. 1907 1

Physiological responses to acute stress proceed with the activation of the hypothalamus-pituitary-adrenal gland (HPA) system. Many brain regions are known to modulate the HPA axis activation in stress responses, but the detailed neural circuits and signaling system in the upstream of the HPA axis have to be explored further. Type 5 adenylyl cyclase (AC5) is highly concentrated in the dorsal striatum and nucleus accumbens, which are implicated in reward and stress-related behavior. AC5(-/-) mice exposed to daily 2-hr restraint stress for only 3-5 days showed poor stress-coping responses, including severe body weight loss, poor coat condition, respiratory difficulties, and freezing behavior. Plasma corticosterone levels during 2-hr stress sessions increased in AC5(-/-) mice compared with those of AC5(+/+) mice. However, neither the corticosterone receptor antagonist RU486 nor the CRH receptor antagonist NBI27914 blocked their poor stress coping, whereas the administration of the GABA(A) receptor allosteric modulator diazepam or the D1 dopamine receptor antagonist SCH23390 prior to restraint stress sessions changed their stress-coping response to the stressed AC5(+/+) mouse level. Stress-triggered c-Fos expression was completely blunted in the dorsal striatum of AC5(-/-). These results suggest that the AC5-associated signal system and neural network are involved in the regulation of anxiety and stress-coping response.
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PMID:Mice lacking adenylyl cyclase-5 cope badly with repeated restraint stress. 1940 50

Stressful life events increase the susceptibility for subsequent onset of psychiatric disorders in humans. Previous research has implicated neurotrophins in the onset of some stress-related diseases, such as major depression disorder, post-traumatic stress disorder or panic disorder. We have tested the hypothesis that the neurotrophin-3 (NT-3)/TrkC system is a genetic interface mediating the deleterious effects of stress on the initiation of panic disorder and other pathologies. To this aim, we have analyzed the functionality of HPA axis and the behavioral consequences of different types of stressful conditions in a mouse model of panic disorder, which overexpresses TrkC, the high affinity-receptor for NT-3 (TgNTRK3). Our results reveal that TgNTRK3 mice exhibit an altered circadian corticosterone rhythm that is reversed by clonidine treatment, but normal expression of genes involved in the control of the hypothalamus-pituitary-adrenal (HPA) axis (CRH, GR) and normal corticosterone response to acute and chronic stressors. In contrast, they exhibit an altered pattern of activation of stress-related brain areas and showed enhanced anxiety-related behavior and more passive strategies than wild types under some chronic stress conditions. We conclude that TgNTRK3 mice present differences in their response to stress characterized by subtle changes in the HPA axis, marked changes in acute stress-induced brain activation and altered coping strategies, suggesting a key role of TrkC receptor in the stress neural circuitry and in the behavioral consequences of chronic stress.
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PMID:Susceptibility to stress in transgenic mice overexpressing TrkC, a model of panic disorder. 1969 58

Depression is potentially life-threatening. The most important neuroendocrine abnormality in this disorder is hypothalamo-pituitary-adrenocortical (HPA) axis hyperactivity. Recent findings suggest that all depression treatments may boost the neurotrophin production especially brain-derived neurotrophic factor (BDNF). Moreover, BDNF is highly involved in the regulation of HPA axis activity. The aim of this study was to determine the impact of chronic stress (restraint 3h/day for 3 weeks) on animal behavior and HPA axis activity in parallel with hippocampus, hypothalamus and pituitary BDNF levels. Chronic stress induced changes in anxiety (light/dark box test) and anhedonic states (sucrose preference test) and in depressive-like behavior (forced swimming test); general locomotor activity and body temperature were modified and animal body weight gain was reduced by 17%. HPA axis activity was highly modified by chronic stress, since basal levels of mRNA and peptide hypothalamic contents in CRH and AVP and plasma concentrations in ACTH and corticosterone were significantly increased. The HPA axis response to novel acute stress was also modified in chronically stressed rats, suggesting adaptive mechanisms. Basal BDNF contents were increased in the hippocampus, hypothalamus and pituitary in chronically stressed rats and the BDNF response to novel acute stress was also modified. This multiparametric study showed that chronic restraint stress induced a depressive-like state that was sustained by mechanisms associated with BDNF regulation.
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PMID:Brain-derived neurotrophic factor and hypothalamic-pituitary-adrenal axis adaptation processes in a depressive-like state induced by chronic restraint stress. 2070 81

Chronic stress is associated with dysregulation of energy homeostasis, but the link between the two is largely unknown. For most rodents, periods of chronic stress reduce weight gain. We hypothesized that these reductions in weight are an additional homeostatic challenge, contributing to the chronic stress syndrome. Experiment #1 examined cardiovascular responsivity following exposure to prolonged intermittent stress. We used radio-telemetry to monitor mean arterial pressure and heart rate in freely moving, conscious rats. Three groups of animals were tested: chronic variable stress (CVS), weight-matched (WM), and controls. Using this design, we can distinguish between effects due to stress and effects due to the changing body weight. WM, but not CVS, markedly reduced basal heart rate. Although an acute stress challenge elicited similar peak heart rate, WM expedited the recovery to baseline heart rate. The data suggest that CVS prevents the weight-induced attenuation of cardiovascular stress reactivity. Experiment #2 investigated hypothalamic-pituitary-adrenal axis and metabolic hormone reactivity to novel psychogenic stress. WM increased corticosterone area under the curve. CVS blunted plasma glucose, leptin, and insulin levels in response to restraint. Experiment #3 tested the effects of WM and CVS on PVN oxytocin and corticotrophin-releasing hormone mRNA expression. CVS increased, while WM reduced PVN CRH mRNA expression, whereas both CVS and WM reduced dorsal parvocellular PVN oxytocin mRNA. Overall, the data suggest that weight loss is unlikely to account for the deleterious effects of chronic stress on the organism, but in fact produces beneficial effects that are effectively absent or indeed, reversed in the face of chronic stress exposure.
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PMID:Opposing effects of chronic stress and weight restriction on cardiovascular, neuroendocrine and metabolic function. 2139 86

Detailed dynamics of the hypothalamic-pituitary-adrenal (HPA) axis is complex, depending on the individual metabolic load of an organism, its current status (healthy/ill, circadian phase (day/night), ultradian phase) and environmental impact. Therefore, it is difficult to compare the HPA axis activity between different individuals or draw unequivocal conclusions about the overall status of the HPA axis in an individual using single time-point measurements of cortisol levels. The aim of this study is to identify parameters that enable us to compare different dynamic states of the HPA axis and use them to investigate self-regulation mechanisms in the HPA axis under acute and chronic stress. In this regard, a four-dimensional stoichiometric model of the HPA axis was used. Acute stress was modeled by inducing an abrupt change in cortisol level during the course of numerical integration, whereas chronic stress was modeled by changing the mean stationary state concentrations of CRH. Effects of acute stress intensity, duration and time of onset with respect to the ultradian amplitude, ultradian phase and the circadian phase of the perturbed oscillation were studied in detail. Bifurcation analysis was used to predict the response of the HPA axis to chronic stress. Model predictions were compared with experimental findings reported in the literature and relevance for pharmacotherapy with glucocorticoids was discussed.
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PMID:Predictive modeling of the hypothalamic-pituitary-adrenal (HPA) axis response to acute and chronic stress. 2185 42

Stress is generally a natural phenomenon that affects behaviour, physiological processes, and neuroendocrine, neurochemical, neurological and immune responses. Many somatic and mental disorders are thought to result from chronic stress. Stress-induced gonadal dysfunction is not restricted to humans, but is observed in all higher animals. Stress-induced gonadal dysfunction comprises disturbances of the hypothalamic-pituitary-gonadal axis and of spermatogenesis. Various stressors induce changes in the secretion of neurotransmitters and hormones, such as CRH, ADH, beta-endorphins, somatostatin, VIP, PRL, GH, TSH, dopamine, serotonin, neuropeptide Y, melatonin, ACTH, glucocorticosteroids, catecholamines and androgens. In acute stress, testicular function is principally modified by cytokines and fluctuating concentrations of gonadotropins, while in chronic stress, hypogonadotropic hypogonadism and disruption of spermatogenesis of varying severity, including spermatogenetic arrest, are observed. In spite of the decades-long interest in the relationships between psychological stress and the function of male gonads, many questions in this area remain unanswered.
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PMID:Psychological stress and the function of male gonads. 2237 97


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