Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of chronic stress on basal and stress-induced alterations of TSH and GH was studied in adult male rats. Chronically stressed rats were subjected 6 days per week for 4 weeks to several acute stressors including saline injections, noise, ether and forced swimming. Each day, one stressor was chosen randomly. Twenty hr after the last stress session, basal levels of TSH were normal or increased, with no altered pituitary response to TRH. In contrast, the TSH rise induced by acute stress was blunted in chronically stressed rats. Chronic stress resulted in lower basal and acute stress levels of GH. These modifications were probably due to changes in the release of hypothalamic regulatory hormones, because no evidence for altered TSH response to TRH, and GH response either to GHRH or to somatostatin, was found. Some abnormal responses of GH to TRH and of TSH to GHRH were observed in chronically stressed rats. These data indicate that this type of chronic stress induced significant changes in basal and acute stress levels of GH and TSH in the rat.
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PMID:The effects of chronic intermittent stress on basal and acute stress levels of TSH and GH, and their response to hypothalamic regulatory factors in the rat. 289 9

Somatostatin (SRIF) and vasopressin (AVP) were measured in hypothalamic and extrahypothalamic areas in normotensive Wistar-Kyoto (WK) and in spontaneously hypertensive, adult rats (SRH) under control conditions and after acute immobilization stress. Hypothalamic areas included the median eminence (ME) and the periventricular, suprachiasmatic, paraventricular, supraoptic, ventromedial and dorsomedial nuclei. Extra-hypothalamic areas included the striae medullaris, striae terminalis (N. Interst.), locus coeruleus, central gray, Areas 1 and 2 (NTS), and circumventricular organs. Under basal conditions, SHR and WK rats did not differ in their content of SRIF and AVP for most areas examined. After acute stress, however, striking differences were found in peptide content. Somatostatin content was not changed in SHR, but was significantly decreased in most areas in WK rats. On the contrary, generalized increases in AVP content were found in SHR after stress, with no changes in WK animals. An exception was the ME, which showed a decrease in peptide levels in both groups of rats. These results suggest that both hypothalamic and extra-hypothalamic AVP and SRIF are involved in the central stress response. The different changes in peptide levels observed for SHR and normotensive rats after acute stress further support the hypothesis of a role of both AVP and SRIF in central regulation of cardiovascular function.
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PMID:Changes in brain somatostatin and vasopressin levels after stress in spontaneously hypertensive and Wistar-Kyoto rats. 610 6

The effect of specific stressful stimuli on neuropeptide levels was studied in rat brain regions known to be involved in the mediation of stress responses and anxiety. Rats were sequentially removed, one by one with 20-min intervals from group cages and immediately decapitated. A selective increase of the somatostatin level was observed in the amygdala in the rats taken for sacrifice second last and last, compared to the rats taken earlier from the respective group cage (increases by 40 to 69%, p < 0.05 or p < 0.01). Isolation of rats in single cages for 24 h or 1 week before sacrifice, increased the substance P level in the dorsal periaqueductal grey by 26 and 27% (p < 0.05 in both cases), respectively, compared to group housed rats. In group housed rats treated with diazepam (5 mg/kg, s.c.) 140 min before sacrifice, the level of substance P in the rostral hippocampus and dorsal periaqueductal grey was reduced by 40% (p < 0.001) and 28% (p < 0.05), respectively, compared to saline treated controls. In conclusion, handling, as well as a single dose of the anxiolytic drug diazepam, appears to induce rapid, selective and region-specific changes of regional brain peptide levels in the rat. The effects of handling are likely to be related to the acute stress response and are probably not secondary to increased plasma glucocorticoid levels.
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PMID:Effects of sequential removal of rats from a group cage, and of individual housing of rats, on substance P, cholecystokinin and somatostatin levels in the periaqueductal grey and limbic regions. 751 54

The effects of acute stress on growth hormone (GH) secretion and the mechanisms involved in its changes have been investigated in sheep. An acute isolation-restraint stress induced a rapid and significant increase in jugular GH levels in 12 out of 14 rams. GH-releasing hormone (GHRH) and somatostatin secretion during the same stress were studied in 5 animals prepared for hypophysial portal blood collection. A 3.5-fold increase in portal GHRH levels was observed concomitantly with a slight elevation in portal somatostatin. Portal corticotropin-releasing hormone (CRH) and jugular cortisol plasma levels increased during the same stress. Our data suggest that an isolation-restraint stress stimulates GH secretion in the sheep and that GHRH may be responsible for GH response.
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PMID:Acute stress stimulates secretion of GHRH and somatostatin into hypophysial portal blood of conscious sheep. 781 15

In the present work we have investigated to what extent somatostatin (SRIF) release from median eminence (ME) is affected by stress immobilization (IMO) in unanesthetized rats stereotaxically implanted with a push-pull cannula (PPC). One week after implantation, the ME was perfused with artificial cerebrospinal fluid for 1 hour in basal, stress and recovery conditions respectively. Samples were collected every 15 min and SRIF was measured by RIA. In another group of animals, a jugular cannula was inserted the day before and plasma samples were taken off simultaneously with the ME perfusate for GH and SRIF analysis respectively. SRIF release from the ME is rapidly (15 min) and significantly increased (58 +/- 11 vs 28 +/- 5 pg/15 min; n = 7; P < 0.01) in rats bearing only PPC. Intriguingly, animals bearing a jugular catheter plus a PPC showed no increase in SRIF release during the first 15 min of IMO in spite of a striking decrease of plasma GH (27.2 +/- 3.8 vs 3.6 +/- 1.3 ng/ml; n = 6; P < 0.001) observed at this time. However, in spite that the animals responded with a significant increase in SRIF, the response was later and more reduced than in animals without jugular cannula. Since our two rat groups--as result of jugular cannula surgery 24 hours before--showed differences such as a food intake, body weight gain, plasma GH levels and basal SRIF release, we think that these differences could explain the modifications in the regulatory mechanisms involved in GH control under acute stress.
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PMID:Role of somatostatin in the acute immobilization stress-induced GH decrease in rat. 809 30

We have previously reported the rapid response of hypothalamic somatostatin (SS) neurons to acute stress. Since it is well known that glucocorticoids (GC) are involved in neuroendocrinal stress regulation, we investigate in this study the effects of acute administration of dexamethasone (Dex) on both in vivo and in vitro SS release. Freely moving animals received stereotaxic implant of a push-pull cannula into the median eminence for 10 days, and then they were perfused with artificial cerebrospinal fluid for 120-150 min. An i.p. injection of Dex (200 or 300 micrograms/100 g) induced, 15-30 min later, a mean increase in SS hypothalamic output of 62.6 +/- 6.2% of basal secretion. By contrast, after 15 min incubation of hypothalamic fragments with either 10(-7) or 10(-6) M Dex, SS release decreased abruptly to 57.3 +/- 3.3% (n = 16; P < 0.001 compared with basal release) and 78.0 +/- 9.5% (n = 13; P < 0.05 compared with basal release) of basal release, respectively. Other Dex concentrations induced no variations, giving the dose-effect curve an abrupt "on-off" effect. The inhibitory effect was blocked by picrotoxin (10(-4) M) and was immediately reversed when Dex was removed from the medium. Specificity was tested by using another steroid, estradiol, and another tissue, cortex. The rapid action of GC whatever the model used and in particular the blocking in vitro effect of picrotoxin could suggest that GCs act at the level of the membrane and could operate physiologically in response to stress. In addition, the opposite in vivo and in vitro effects on SS release would indicate that GCs exert two different controls on SS neurons.
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PMID:Rapid and opposite effects of dexamethasone on in vivo and in vitro hypothalamic somatostatin release. 906 19

We have demonstrated that the activation of 5-hydroxytryptamine (5-HT) receptor 3 in the submucosal plexus suppresses 5-HT-induced colonic ion secretion by increasing submucosal somatostatin release. A number of psychological and physical stresses have impacts on the intestinal mucosal functions, including secretion and the epithelial barrier. Whether the 5-HT(3) receptor-mediated somatostatin-dependent secretoinhibitory pathway in the rat distal colon is involved in the stress process is still unknown. The present study aims to investigate the effect of the water-immersion restraint stress on this inhibitory pathway and its underlying mechanisms. Mucosa/submucosa preparations from the rat distal colon were mounted in the Ussing chambers for the measurement of short-circuit current (I(SC)). Real-time PCR and western blot were performed to study the expression of the 5-HT(3) receptor, 5-HT(4) receptor, and somatostatin receptor 2. Radioimmunoassay was used to measure somatostatin release. After 2h of water-immersion restraint stress, the membrane resistance (Rte) of rat mucosa/submucosa preparations was significantly decreased, but the baseline I(SC) and 5-HT-induced I(SC) responses were significantly increased. The protein expression of the submucosal 5-HT(3) receptors and mucosal somatostatin receptor 2 were down-regulated, and the 5-HT-induced somatostatin release from the mucosa/submucosa preparations was significantly reduced in the stress group. Taken together, these results suggest that the 5-HT(3) receptor-mediated somatostatin-dependent secretoinhibitory pathway is suppressed in the water-immersion restraint stressed rats, which may contribute to the acute stress-induced increase in colonic secretion.
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PMID:Colonic submucosal 5-HT(3) receptor-mediated somatostatin-dependent secretoinhibitory pathway is suppressed in water-immersion restraint stressed rats. 2129 81

Thyroid hormones are essential regulators of growth, development and normal bodily function and their release is coordinated by the hypothalamic-pituitary-thyroid (HPT) axis. While the HPT axis has been established as an acutely stress-responsive neuroendocrine system, relatively little is known about the mechanisms of its stress regulation. The present study examined acute stress-induced changes in peripheral hormone levels [triiodothyronine (T3); thyroxine (T4), thyroid-stimulating hormone (TSH), reverse triiodothyronine (rT3)] and central mRNA levels of regulators of the HPT axis [thyrotropin-releasing hormone (TRH), somatostatin (SST), type II deiodinase (D2)] in response to an inescapable tail-shock, a rodent model of stress. Additionally, we examined whether individual differences in spontaneous exploratory behavior in an open field test predicted basal levels of TH or differential susceptibility to the effects of stress. The stress condition was associated with decreases in peripheral T3, T4 and TSH, but not rT3, when compared with controls. No changes were observed in TRH or SST mRNA levels, but there was a trend suggesting stress-related increases in D2 mRNA. We also found that an animal's exploratory behavior in an unfamiliar open field arena was positively related to peripheral thyroid hormone levels and predicted the magnitude of stress-induced changes. In conclusion, we found suggestive evidence for stress-induced decrease in central drive HPT axis, but the central mechanisms of its stress regulation remain to be elucidated. Additionally, we found that individual differences in animals' exploratory behavior were correlated with peripheral TH levels.
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PMID:Thyroid hormone regulation by stress and behavioral differences in adult male rats. 2168 56

Chronic stress, understood as a disturbance of the body homeostasis, is partially driven by many hormonal pathways. Prolactine, TSH (Thyrotropin), vasopresin, FSH (Follicle-Stimulating Hormone), LH (Luteinizing Hormone), and GH (Growth Hormone) have been involved in many stress reactions. In acute stress, there are many evidences for the increased both cathecolaminergic and hypothalamic-pituitary-adrenal axis. In chronic conditions, these hyperactivations are controversial and some cases may present a true hypoadrenalism. There is no evidence that treating such androgen/glucocorticoids deficiency may relief chronic pain processes such as fibromyalgia. However, treating somatotroph axis dysfunctions (somatostatin, GH/IGF1 [growth hormone/ insulin-like growth factor-1]) with recombinant GH in carefully seleccioned subgroups of fibromyalgic syndrome, offers us an in-vivo model of the capacity of some hormones to modulate pain.
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PMID:[Stress and chronic pain: An endocrine perspective]. 2179 52

Exposure to acute stress by forced swim impairs spatial learning and memory in rats. The retrosplenial cortex plays an important role in spatial learning and memory. A cell population that expresses immature neuronal markers, including doublecortin (DCX), plays a key role in plasticity of the adult brain through formation of new neurons. Here, we aimed to determine whether rats exposed to acute stress showed changes in DCX expression in retrosplenial cortex cells. Twelve male Sprague-Dawley rats were used. Six were subjected to acute stress by forced swim (group S), and the remaining six served as controls (group C). Immunohistochemical staining was performed for DCX, neuron-specific nuclear protein, parvalbumin, calbindin, calretinin, and somatostatin. Newly generated cells were immunohistochemically detected by daily administration of 5-bromo-2'-deoxyuridine for 1 week. Fluoro-Jade B staining was performed to detect cell death. Group S showed lower number of DCX-expressing cells than group C (P<0.001). The proportion of DCX-expressing cells showing neuron-specific nuclear protein co-localization (24% in group S; 27% in group C) or parvalbumin co-localization (65% in group S; 61% in group C) remained unchanged after acute stress exposure. Neither 5-bromo-2'-deoxyuridine-positive nor Fluoro-Jade B-positive cells were found in the retrosplenial cortex of groups S and C. DCX-expressing cells in the retrosplenial cortex decreases markedly without cell death after acute stress exposure. Neuronal differentiation of these cells toward gamma aminobutyric acidergic interneurons appears to be unaltered. The decrease in DCX expression may reduce plasticity potential within the retrosplenial cortex and attenuate spatial learning and memory function.
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PMID:Decrease in doublecortin expression without neuronal cell death in rat retrosplenial cortex after stress exposure. 2219 88


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