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

The brain noradrenergic system is activated by stress, modulating the activity of forebrain regions involved in behavioral and neuroendocrine responses to stress. In this study, we characterized brain noradrenergic reactivity to acute immobilization stress in three rat strains that differ in their neuroendocrine stress response: the inbred Lewis (Lew) and Wistar-Kyoto (WKY) rats, and outbred Sprague-Dawley (SD) rats. Noradrenergic reactivity was assessed by measuring tyrosine hydroxylase mRNA expression in locus coeruleus, and norepinephrine release in the lateral bed nucleus of the stria terminalis. Behavioral measures of arousal and acute stress responsivity included locomotion in a novel environment, fear-potentiated startle, and stress-induced reductions in social interaction and open-arm exploration on the elevated-plus maze. Neuroendocrine responses were assessed by plasma adrenocorticotropic hormone. Compared to SD, adrenocorticotropic hormone responses of Lew rats were blunted, whereas those of WKY were enhanced. The behavioral effects of stress were similar in Lew and SD rats, despite baseline differences. Lew had similar elevations of tyrosine hydroxylase mRNA, and initially greater norepinephrine release in the lateral bed nucleus of the stria terminalis during stress, although both noradrenergic responses returned toward baseline more rapidly than in SD rats. WKY rats showed depressed baseline startle and lower baseline exploratory and social behavior than SD. However, unlike the Lew or SD rats, WKY exhibited a lack both of fear potentiation of the startle response and of stress-induced reductions in exploratory and social behavior, indicating attenuated stress responsivity. Acute noradrenergic reactivity to stress, measured by either tyrosine hydroxylase mRNA levels or norepinephrine release, was also attenuated in WKY rats. Thus, reduced arousal and behavioral responsivity in WKY rats may be related to deficient brain noradrenergic reactivity. This deficit may alter their ability to cope with stress, resulting in the exaggerated neuroendocrine responses and increased susceptibility to stress-related pathology exhibited by this strain.
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PMID:Stress reactivity of the brain noradrenergic system in three rat strains differing in their neuroendocrine and behavioral responses to stress: implications for susceptibility to stress-related neuropsychiatric disorders. 1240 36

Corticotropin-releasing factor (CRF) is involved in the regulation of stress responses. The actions of CRF in the brain are mediated through two distinct CRF receptor subtypes, CRF(1) and CRF(2) receptors. In the present study, we examined the effects in rat of chronic administration of a nonpeptidic CRF(1) receptor-selective antagonist, CRA1000, 2-[N-(2-methylthio-4-isopropylphenyl)-N-ethylamino]-4-[4-(3-fluorophenyl)-1,2,3,6-tetrahydropyridin-1-yl]-6-methylpyrimidine), on locomotor activity, feeding behavior and the hypothalamic-pituitary-adrenal axis. Chronic CRA1000 treatment significantly decreased locomotor activity in the dark phase of the diurnal cycle. However, chronic CRA1000 treatment showed no effect on food and water intake, or on body weight. After a 10-day period of CRA1000 treatment, plasma concentrations of adrenocorticotropic hormone (ACTH) and corticosterone in basal conditions and under immobilization stress were no different from those in rats treated with vehicle. However, CRA1000 administered 2 h before immobilization stress significantly reduced ACTH and corticosterone responses to stress with no effect on basal ACTH and corticosterone concentrations. These results suggest that CRF(1) receptors are involved in the regulation of locomotor activity during the dark period, but are not involved in the regulation of feeding behavior under non-stressful conditions. Furthermore, the results suggest that a 10-day treatment with CRA1000 does not affect hypothalamic-pituitary-adrenal axis activity either under basal conditions or after acute stress.
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PMID:Effect of chronic administration of a CRF(1) receptor antagonist, CRA1000, on locomotor activity and endocrine responses to stress. 1246 67

Many psychiatric disorders, including depression, post-traumatic stress disorder and other anxiety disorders, result from an interaction between genetic factors and exposure to a sufficiently sensitizing environmental stressor. The inbred Wistar Kyoto (WKY) rat strain has been proposed as a model of stress vulnerability, exhibiting an exaggerated hypothalamic-pituitary-adrenal (HPA) response to stress and susceptibility to gastric ulceration. Previously, we showed that stress-activation of the brain noradrenergic system was deficient in WKY rats, and they lacked noradrenergic facilitation of the HPA response in the lateral bed nucleus of the stria terminalis (BSTL), compared to outbred Sprague-Dawley (SD) controls. Deficient modulatory function of the noradrenergic system may contribute to the stress susceptibility of WKY rats. Thus, we investigated the influence of a sensitizing stimulus, chronic intermittent cold exposure, on neuroendocrine and noradrenergic stress reactivity, and on noradrenergic facilitation of the HPA response in these two strains. Chronic cold exposure (7 days, 4 h/day, 4 degrees C) potentiated activation of the HPA axis by acute immobilization stress, assessed by measuring plasma adrenocorticotropic hormone (ACTH), in both strains, although to a greater extent in WKY rats, and enhanced stress-induced norepinephrine (NE) release in BSTL of WKY but not SD rats. We then compared the influence of chronic cold exposure on noradrenergic modulation of the HPA stress response in BSTL, by measuring changes in acute stress-induced elevation of plasma ACTH after microinjecting the alpha(1)-adrenoreceptor antagonist benoxathian into the BSTL. As shown previously, benoxathian attenuated stress-induced ACTH secretion in control SD but not control WKY rats. After chronic cold, the ACTH response to acute stress was attenuated by benoxathian administration into BSTL of both strains, such that the WKY response was not different from that of SD rats. Thus, chronic cold not only sensitized the release of NE in BSTL of WKY rats, but also restored noradrenergic facilitation of their already-elevated HPA response. Such functional sensitization of a previously-deficient facilitatory system may be one mechanism whereby exposure to repeated or severe stress may induce pathologic dysregulation of the stress response in susceptible individuals, resulting in psychiatric illness.
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PMID:Chronic cold stress sensitizes brain noradrenergic reactivity and noradrenergic facilitation of the HPA stress response in Wistar Kyoto rats. 1269 37

In teleosts, the stress hormone cortisol and the calcium regulatory hormone stanniocalcin (STC) are both involved in the regulation of ion balance. Under stressful conditions, ion balance is easily disturbed as stressors via the stress signals they evoke disturb easily and primarily gill function. The gills are key in fish gas exchange and ion regulation. The present work evaluates the effect of the pivotal stress signal cortisol, the eventual output of the stress axis on STC secretion in freshwater rainbow trout (Oncorhynchus mykiss). Plasma cortisol levels were manipulated by intraperitoneal injections of porcine ACTH(1-39) or dexamethasone (Dex), and plasma cortisol, STC and mineral status were assessed. A perifusion assay of trout Stannius corpuscles was validated and used to study the direct effects of stress-related signals on STC release. In perifusion, cortisol, adrenocorticotropic hormone (ACTH), and dexamethasone did not affect STC release. ACTH injections increase plasma cortisol (corresponding to an acute stress) and STC concentrations, but did not affect mineral status. Dexamethasone injections resulted either in a classical hypocortisolinemia or, unexpectedly, in hypercortisolinemia. However, independently of the resulting cortisol status Dex induced a chronic stress effect, as indicated by decreased plasma Na, Cl, and Ca levels, and increased plasma STC concentrations. The increased STC secretion cannot be explained by the classical elevation of plasma calcium concentration. Thus, plasma parameters other than calcium could be involved and we propose that STC secretion might be stimulated also by a decrease of NaCl concentrations, implying a broader function than the classical hypocalcemic action of STC.
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PMID:The stress axis, stanniocalcin, and ion balance in rainbow trout. 1520 Oct 64

To characterize individual differences in neuroendocrine and neurochemical correlates of stress coping, two lines of wild house mice were studied. These mice are genetically selected for high and low aggression and show distinctly different behavioral strategies toward environmental stimuli. Long attack latency (LAL), low aggressive mice display a passive coping style, whereas short attack latency (SAL), high aggressive mice show an active coping style. It was hypothesized that this difference in behavioral coping style is associated with differences in stress system reactivity. This was tested by investigating the regulation of the hypothalamus-pituitary-adrenal (HPA) axis and the serotonin (5-HT) system and hippocampal cell proliferation rate in these mice under baseline and stress conditions. Baseline corticosterone output in LAL mice was found to be more sensitive to adrenocorticotropic hormone, but showed less day/night variation than in SAL mice. Furthermore, LAL mice showed lower hippocampal 5-HT(1A) receptor gene expression and function. Basal hippocampal cell proliferation rate was slightly lower in LAL than in SAL mice. Exposure to acute stress (forced swimming for 5 min) resulted in a hyper-reactive HPA response, a reduced increase in brain 5-HT metabolism, and an almost 50% reduction in hippocampal cell proliferation rate in LAL compared with SAL mice. Chronic psychosocial stress (sensory contact stress) induced long-lasting changes in the HPA axis in LAL, but not in SAL mice. In conclusion, these studies show that a genetic trait in behavioral coping style in wild house mice is associated with differences in HPA regulation, 5-HT neurotransmission, and hippocampal cell proliferation rate. The results further indicate that LAL mice have a higher stress responsivity than SAL mice. These results may have implications for a differential susceptibility for stress-related mood disorders.
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PMID:Basal and stress-induced differences in HPA axis, 5-HT responsiveness, and hippocampal cell proliferation in two mouse lines. 1524 Mar 76

Activation of the brain noradrenergic system during stress plays an important integrative function in coping and stress adaptation by facilitating transmission in many brain regions involved in regulating behavioural and physiological components of the stress response. The medial amygdala (MeA) has been implicated in modulation of stress-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis, and MeA is a target of innervation from brainstem noradrenergic neurones. However, it is not known whether, and to what extent, activation of the ascending noradrenergic innervation of MeA might modulate stress-induced adrenocorticotropic hormone (ACTH) secretion. In the first experiment in this study, we measured extracellular norepinephrine (NE) levels in MeA using in vivo microdialysis. The concentration of NE in dialysate samples collected in MeA was elevated by more than three-fold over baseline in response to acute immobilisation stress, providing evidence of a possible modulatory role for NE in the MeA during stress. This potential role was then assessed in the second experiment by measuring changes in the elevation of plasma ACTH concentration induced by acute immobilisation stress immediately following bilateral microinjections of alpha1- or beta-adrenergic receptor antagonists directly into MeA. Compared to vehicle-injected controls, the alpha1-receptor antagonist benoxathian dose-dependently and significantly attenuated the ACTH response to acute stress, whereas combined beta1/beta2-receptor blockade in MeA had only a modest effect. These results indicate that MeA does play a role in the stress response, and support the hypothesis that stress-induced activation of NE release in MeA, acting primarily through alpha1 receptors, facilitates activation of the HPA axis in response to acute stress.
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PMID:Norepinephrine release in medial amygdala facilitates activation of the hypothalamic-pituitary-adrenal axis in response to acute immobilisation stress. 1572 Apr 72

Social relationships protect against the development of stress-related psychiatric disorders, yet little is known about the neurobiology that regulates this phenomenon. Recent evidence suggests that oxytocin (OT), a neuropeptide involved in social bond formation, may play a role. This experiment investigated the effects of chronic intranasal OT administration on acute stress-induced hypothalamic-pituitary-adrenal (HPA) axis activation in adult female squirrel monkeys. Subjects were randomized to one of two experimental conditions. Monkeys were intranasally administered either 50 microg oxytocin (N = 6 monkeys) or 0 microg oxytocin (N = 6 monkeys)/300 microl saline once a day for eight consecutive days. Immediately after drug administration on the eighth day, all monkeys were exposed to acute social isolation. Blood samples for determinations of adrenocorticotropic hormone (ACTH) and cortisol concentrations were collected after 30 and 90 min of stress exposure. Consistent with an anti-stress effect, OT-treated monkeys exhibited lower ACTH concentrations compared to saline-treated monkeys after 90 min of social isolation (F(1,7) = 6.891; P = 0.034). No drug-related differences in cortisol levels were observed, indicating that OT does not directly attenuate the adrenal stress response. Intranasal peptide administration has been shown to penetrate the central nervous system, and research must determine whether intranasally delivered OT exerts its effect(s) at a pituitary and/or brain level. This primate model offers critical opportunities to improve our understanding of the anti-stress effects of OT and may lead to novel pharmacological treatments for stress-related psychiatric disorders.
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PMID:Intranasal oxytocin administration attenuates the ACTH stress response in monkeys. 1594 3

In order to assess the biological significance of weaning and water deprivation on the control of plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol, growth hormone (GH) and metabolites in response to stimulation with arginine-vasopressin (AVP) and corticotropin-releasing hormone (CRH), we carried out three experiments in which male goats before and after weaning were intravenously injected with AVP or CRH alone, or in combination with each other. In experiment 1, 17-week-old (post-weaning) goats were intravenously injected with AVP or CRH alone at the doses of 0.1, 0.3 and 1.0 nmol/kg body weight (BW). The AVP injection significantly and dose dependently increased plasma levels of ACTH, cortisol, GH and metabolites, whereas the injection with CRH did not cause significant increases in the levels of these parameters. In experiment 2, 4-week-old (pre-weaning) and 13-week-old (post-weaning) goats were injected with either AVP or CRH alone, followed by a combined injection of both secretagogues at a dose of 0.3 nmol/kg BW. Although the basal levels of the hormones and metabolites, with the exception of glucose, were greater in the 4-week-old goats, the hormone responses induced by stimulation with AVP were weaker than those induced in 13-week-old goats. Additionally, there were no responses in any hormone patterns to CRH stimulation in 4-week-old goats. In experiment 3, 13-week-old goats were injected with CRH alone followed by injection with AVP for two consecutive days of water deprivation. The animals were subjected to withdrawal of up to 20% of the total blood volume and water deprivation for up to 28 h. However, no significant differences in plasma ACTH, cortisol or GH levels were observed between days 1 and 2. Based on these results, we concluded that: (1) AVP is a more potent stimulant than CRH in terms of its ability to induce increases in plasma levels of ACTH, cortisol and GH; (2) the role of AVP as a secretagogue of hypothalamus-pituitary-adrenal hormones is strengthened, whereas the ineffective role of CRH remains unaltered, by weaning; (3) acute stress such as massive withdrawal of blood volume and subjection to water deprivation may not be sufficient burdens to alter stress-related hormone levels in young goats.
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PMID:Responses induced by arginine-vasopressin injection in the plasma concentrations of adrenocorticotropic hormone, cortisol, growth hormone and metabolites around weaning time in goats. 1629 72

The endocrine stress response is pivotal in vertebrate physiology. The stress hormone cortisol-the end product of the endocrine stress axis-(re-)directs energy flows for optimal performance under conditions where homeostasis may be or become at risk. Key players in the continuous adaptation process are corticotropin-releasing factor (CRF) from the hypothalamic nucleus preopticus (NPO), pituitary adrenocorticotropic hormone (ACTH) and cortisol produced by the interrenal cells in the headkidney (adrenal equivalent of fish). CRF is a member of a large family of related peptides that signals through CRF-receptor subtypes specific for central and peripheral actions of the peptide. CRF is "chaperoned" by a unique and phylogenetically very well-conserved binding protein (CRFBP); the functions of the CRFBP can only be speculated on so far, but its mRNA and protein abundance are important indicators of the central CRF-system activity, and indeed its mRNA levels are altered by restraint stress. Moreover, the unique structure and size of the CRFBP provide good tools in phylogenetic studies, that date the CRF-system to at least one billion years old. Pro-opiomelanocortin is produced and processed to ACTH and endorphin in the hypothalamic NPO and pituitary pars distalis ACTH-cells, to MSH and acetylated endorphins in the pituitary pars intermedia MSH-cells. ACTH is the prime corticotrope in acute stress conditions. In carp, MSH, considered a mild corticotrope in chronic stress responses in other fish, lacks corticotropic effects (in line with the absence of the melanocortin-5 receptor in headkidney); yet, an unknown corticotropic signal substance in the pars intermedia of carp awaits elucidation. Interesting observations were made on the CRF control of pituitary cells. CRF stimulates ACTH-cells, but only when these cells experience a mild dopaminergic block. Endorphin, produced in the NPO and transported via axons to the pituitary gland in vivo, reverses the stimulatory CRF action on MSH-cells to a differential inhibition of N-acetyl beta-endorphin release in vitro (MSH release is not affected). We speculate that the consistently observed elevation of plasma MSH during chronic stress may exert central actions related to feeding and leptin regulated processes. A BOLD-fMRI study revealed the functional anatomy of the stress response at work in a paradigm, where carp were exposed to a sudden water temperature drop. In carp (and other fish), the endocrine stress axis is already operational in very early life stages, viz., around hatching and comprises hypothalamic, pituitary, and interrenal signaling to adjust the physiology of the hatchling to its dynamically changing environment. Understanding of stress during early life stages is critical as the consequent rises in cortisol may have long lasting effects on survival and fish quality.
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PMID:CRF and stress in fish. 1640 2

The aim of the study was to evaluate the effect of adrenal stimulation by adrenocorticotropic hormone (ACTH) on blood cortisol concentration and on circulating total and differential leukocyte counts during and in the 16 days after ACTH administration. Swedish Landrace boars aged approximately 6-7 months were used. ACTH-treated animals (n = 7) were given ACTH intravenously at 10 microg/kg body mass for 3 days. A control group of animals (n = 7) received 1 ml of sterile 0.9% saline intramuscularly. ACTH induced a highly significant increase (p>0.0001) in serum cortisol in treated boars. On the day after the last ACTH dose, the cortisol concentration was significantly higher, but the level of significance was lower than during ACTH administration (p>0.05). During ACTH treatment, a significant increase was recorded in total leukocyte count and neutrophil percentage (p>0.05 to p>0.0001), along with the increase in blood cortisol concentration, whereas percentage lymphocyte count showed a significant decrease. Lymphopenia disappeared upon cessation of treatment, but neutropenia developed in the week after treatment. On all three days of ACTH challenge, the neutrophil-to-lymphocyte ratio was significantly increased. An increase in eosinophil percentage was recorded on treatment days 1 and 2, whereas ACTH treatment had no effect on basophil percentage. In conclusion, three-day administration of ACTH to young boars during restraint caused effects similar to acute stress situations, as suggested by disappearance of the effects on immune function after the last drug dosage.
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PMID:Cortisol and immune measures in boars exposed to three-day administration of exogenous adrenocorticotropic hormone. 1650 11


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