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

Two paradigms of acute stress in the rat were used to produce changes in the stomach. The first involved restraint stress combined with water immersion and the second utilized acute intragastric exposure to absolute ethanol. The mRNA expression of immediate early genes (IEG) such as c-fos, c-jun and NGFI-A, cyclooxygenase (COX)-2 and heat shock proteins (HSP) 70 in the stomach were studied using in situ hybridization histochemistry. Upregulation of IEG and HSP70 mRNAs were observed in the smooth muscle cells of muscularis mucosae, muscularis externa and blood vessels in response to water immersion-restraint stress or intragastric application of absolute ethanol. In the restraint stress model, IEG (c-fos and NGFI-A) mRNAs were induced in the pit and isthmus of the mucosa, while in the ethanol exposure model, IEG (c-fos, c-jun and NGFI-A) and HSP70 mRNAs were upregulated in the damaged epithelium, especially surrounding the deep erosions. COX-2 mRNA was detected in surface mucous cells under desquamation. These distinct gene expressions in the mucosa indicate that the two stress paradigms produce different cellular responses. These data provide new insights into cellular mechanisms that occur during the pathogenesis of acute gastric mucosal lesions.
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PMID:Distinct gene expression in the stomach following stress and alcohol exposure. 1172 71

Clinical and epidemiological studies have found an association between aversive experiences early in life and an increased risk for depression, anxiety and substance abuse. In order to elucidate the mechanisms by which adverse life events are translated into behavioral and psychological abnormalities, we used a rat model to study the impact of chronic injection and 24 h maternal deprivation on the developing rat brain. Specifically, we investigated the regulation of molecules related to the 5-HT (5-HT) system and studied the effect of desipramine administration on animals that were maternally deprived (DEP) on day 13 of life compared with non-deprived animals. We found that maternal deprivation caused an enhanced corticosterone response to an acute stress. Maternally deprived animals also showed a decrease in corticosteroid receptors and an increase in 5-HT 1A and 1B receptors restricted to the CA1 region of the hippocampus. Desipramine prevented the maternal deprivation induced up-regulation of the 5-HT 1B receptor and the enhanced adrenocortical response observed in these animals. Interestingly, non-deprived animals receiving chronic injections showed a decrease in hippocampal 5-HT1B receptor mRNA. At 80 days of age, a group of animals that were treated as infants were given the option of drinking from two identical water bottles, one bottle contained tap water, while the second contained ethanol at increasing concentrations. Animals that received chronic injections during the newborn period consumed more alcohol than those that were not injected. On the other hand, maternal deprivation did not have an impact on alcohol consumption. Alcohol preference has implications to the organism since studies of drug self-administration in laboratory animals have shown that ethanol ingestion is positively related to the use of other drugs, principally opioids and psychostimulants. Our findings suggest that the quality and/or chronicity of early life stressors can influence the neurobiological substrates that may trigger and/or predispose individuals to substance abuse in adulthood.
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PMID:Brain 5-HT receptor system in the stressed infant rat: implications for vulnerability to substance abuse. 1175 Jul 82

Systemic administration of ethanol elevates plasma and cerebral cortical GABAergic neuroactive steroids. The increase in neurosteroids is responsible for specific behavioural and electrophysiological actions of ethanol in rodents. This article recapitulates the current knowledge of the novel interaction between ethanol and neurosteroids and addresses the potential mechanism for ethanol-induced increase in brain neurosteroid levels. Ethanol-induced increase in the cortical neurosteroid content is modified by neurosteroid biosynthesis inhibitors and completely prevented by adrenalectomy in male rats. In line with this, adrenalectomy prevented the anticonvulsant and hypnotic effects of acute ethanol administration. It is speculated that acute ethanol administration might resemble acute stress and increase neuroactive steroids due to activation of hypothalamic-pituitary adrenal axis. Ethanol-induced increases in neuroactive steroids might be responsible for the antidepressant, anxiolytic, spatial learning deficits and drug discriminatory actions in rodents. Thus ethanol-induced increases in neuroactive steroids represent a novel mechanism of ethanol's action, responsible for several pharmacological and behavioural actions of ethanol. The development of new therapeutic strategies for alcoholism may arise based on the novel interaction between ethanol and neurosteroids in the brain.
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PMID:GABAergic neurosteroid modulation of ethanol actions. 1247 81

Systemic ethanol administration elevates plasma and brain levels of GABAergic neuroactive steroids, including 3alpha-hydroxy-5alpha-pregnan-20-one (3alpha,5alpha-THP) that contribute to specific behavioral actions of ethanol. The present study determined the effect of adrenalectomy and 5alpha-reductase type-1/type-2 enzyme inhibition, known to reduce neuroactive steroids, on ethanol-induced increases in cerebral cortical levels of 3alpha,5alpha-THP and hypnotic effects in male rats. Systemic ethanol administration to male rats increases plasma levels of progesterone and corticosterone similar to acute stress, indicating release of these steroids from adrenal glands. Adrenalectomy markedly reduced the elevation of cerebral cortical 3alpha,5alpha-THP and plasma progesterone levels and reduced the duration of ethanol-induced loss of righting reflex. Prior systemic administration of 5alpha-dihydroprogesterone (10 or 15 mg/kg, i.p.), an immediate precursor of 3alpha,5alpha-THP, to adrenalectomized rats not only restored the ethanol-induced increases in cerebral cortical 3alpha,5alpha-THP levels but also reversed the effect of adrenalectomy on ethanol-induced loss of righting reflex. Prior administration of the 5alpha-reductase inhibitor finasteride (2 x 25, 2 x 75 or 2 x 150 mg/kg, s.c.) and the 5alpha-reductase type-1 inhibitor SKF-105,111 (50 mg/kg, i.p.) did not reduce ethanol-induced increases in the cerebral cortical levels of 3alpha,5alpha-THP at hypnotic doses of ethanol. Furthermore, these drugs did not alter the duration of loss of righting reflex. However, significant correlations between cerebral cortical 3alpha,5alpha-THP levels and the duration of loss of righting reflex were obtained regardless of finasteride administration. These results demonstrate the contributory role of neuroactive steroids in the ethanol-induced loss of righting reflex and the source of ethanol-induced elevation of GABAergic neuroactive steroids. Ethanol-induced increases in neurosteroids could be pertinent to the etiology of sleep-related disorders associated with alcoholism.
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PMID:Neuroactive steroid 3 alpha-hydroxy-5 alpha-pregnan-20-one modulates ethanol-induced loss of righting reflex in rats. 1286 66

Male albino rats of Wistar strain were exposed to overcrowding stress in two different groups for a period of seven days. One group of rats was kept under stress for six hours per day (acute stressed group) and the other group rats was kept under stress continuously (chronic stressed group). The effect of these acute and chronic stresses on voluntary alcohol (2% w/v) intake was monitored during the 7 days of stress exposure, and ethanol preference and total ethanol intake in terms of g/kg body weight were also studied. A significant increase in ethanol preference and ethanol intake was observed in one-day and 7 days chronic stressed group. No significant increase in ethanol intake was observed in acute stress. Thus a short lasting stressor may not increase ethanol-drinking behavior, whereas when animals were exposed to more intense stressor continuously for 7 days, an increase in voluntary drinking behavior may be seen.
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PMID:Effect of acute and chronic conditions of over-crowding on free choice ethanol intake in rats. 1472 19

Social stress is a common occurrence in our society that can negatively impact health. Therefore, we wanted to study the effects of a mild stressor designed to model social stress on seizure susceptibility and GABAA receptors in male and female rats. The mild chronic stress of individual housing consistently decreased bicuculline (but not pentylenetetrazol, PTZ) seizure thresholds by 10-15% in both sexes. Housing conditions did not alter the anticonvulsant activity of diazepam or ethanol, although the anticonvulsant effect of ethanol was significantly greater against PTZ-induced seizures. Experiments testing the addition of an acute restraint stress unmasked sex differences in seizure induction. The acute stress also selectively decreased the potency of GABA to modulate GABAA receptor-mediated chloride uptake in group-housed females. There were additional sex differences by housing condition for GABAA receptor-gated chloride uptake but no differences in [3H]flunitrazepam binding. We also found significant effects of sex and housing on ethanol-induced increases in corticosterone (CORT) levels. In summary, there were complex and sex-selective effects of mild chronic stress on seizure induction and GABAA receptors. Gaining a better understanding of mechanisms underlying interactions between sex and stress has important implications for addressing health concerns about stress in men and women.
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PMID:Sex differences in effects of mild chronic stress on seizure risk and GABAA receptors in rats. 1525 Dec 58

Stress increases plasma and brain concentrations of corticosteroids and neuroactive steroids. Cortisol is the most important stress hormone in the hypothalamic pituitary adrenocortical system. However, significant amounts of the mineralocorticoid deoxycorticosterone are also released during stress. Deoxycorticosterone undergoes biotransformation to allotetrahydrodeoxycorticosterone, a neuroactive steroid with anxiolytic and anticonvulsant properties. Our studies indicate that the anticonvulsant activity of deoxycorticosterone is mediated by its conversion to allotetrahydrodeoxycorticosterone, which is a potent positive allosteric modulator of GABA(A) receptors. Although the role of allotetrahydrodeoxycorticosterone within the brain is undefined, recent studies indicate that stress induces increases in allotetrahydrodeoxycorticosterone to levels that can activate GABA(A) receptors. These results might have significant implications for human stress-sensitive conditions such as epilepsy, panic disorder, post-traumatic stress disorder, and major depression. In epilepsy, a role for adrenal allotetrahydrodeoxycorticosterone in seizure susceptibility has been suggested. Recent preclinical studies indicate a role of neuroactive steroids in ethanol actions. Although these studies provide a better understanding of the role of allotetrahydrodeoxycorticosterone and related neuroactive steroids in acute stress, further studies are clearly warranted to ascertain the specific role of neuroactive steroids in the pathophysiology of chronic stress and related brain conditions.
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PMID:Physiological role of adrenal deoxycorticosterone-derived neuroactive steroids in stress-sensitive conditions. 1632 48

Social isolation of rats both reduces the cerebrocortical and plasma concentrations of 3a-hydroxy-5a-pregnan-20-one (3a,5a-TH PROG) and 3a,5a-tetrahydrodeoxycorticosterone and potentiates the positive effects of acute stress and ethanol on the concentrations of these neuroactive steroids. We now show that social isolation decreased the plasma level of adrenocorticotropin (ACTH), moreover, intracerebroventricular administration of corticotropin releasing factor (CRF) induced a marked increase in the plasma corticosterone level in both isolated and group-housed rats, but this effect was significantly greater in the isolated rats (+121%) than in the group-housed rats (+86%). In addition, in isolated rats, a low dose of dexamethasone had no effect on the plasma corticosterone concentration, whereas, a high dose significantly reduced it; both doses of dexamethasone reduced plasma corticosterone in group-housed rats. Furthermore, the corticosterone level after injection of dexamethasone at the high dose was significantly greater in the isolated animals than in the group-housed rats. These results suggest that social isolation increased sensitivity of the pituitary to CRF and impaired negative feedback regulation of the hypothalamic-pituitary-adrenal (HPA) axis.
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PMID:Social isolation-induced changes in the hypothalamic-pituitary-adrenal axis in the rat. 1642 14

Numerous reports document altered drinking behavior following acute stressors but few describe physiological responses to acute stress of chronic ethanol consuming subjects. We tested rats' responses to 120-min foot restraint immobilization (Immo) after 1 week of liquid diet containing 5% wt/vol ethanol (ethanol-fed). Controls consumed isocaloric liquid diet ad libitum (adlib-fed) or in amounts equal to that of ethanol-fed subjects on the previous day (pair-fed). Each rat was implanted with a tail artery cannula on day 7 to allow remote blood collection before and during Immo on day 8. Plasma epinephrine (Epi); norepinephrine (NE); corticosterone (Cort); prolactin (PRL); adrenomedullary gene expression of catecholamine biosynthetic enzymes tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DBH), and phenylethanolamine-N-methyl transferase (PNMT); and TH protein levels were measured. Ethanol-fed rats had two to threefold higher basal plasma Epi and NE and tended to have increased Cort compared to adlib-fed or pair-fed rats. Immo increased Epi and NE in ethanol-fed rats more than twofold above those observed in controls, and also increased Cort more in ethanol-fed than in control rats. PRL was marginally affected. Ethanol potentiated the normal immobilization-induced increase in adrenomedullary TH, DBH, and PNMT messenger RNA (mRNA). TH protein increased only in ethanol-fed rats. Increased plasma catecholamine levels, adrenomedullary gene expression, and TH protein concentration in nonimmobilized ethanol-fed rats strongly suggest that ethanol consumption was itself a stressor, which potentiated the subsequent response to acute Immo. Moreover, the observed interaction of ethanol and stress on plasma catecholamine levels illustrates the importance of minimizing additional stressful stimuli when investigating ethanol's physiological effects.
Alcohol 2005 Nov
PMID:Ethanol consumption increases rat stress hormones and adrenomedullary gene expression. 1671 4

Pregnenolone (PREG) is an endogenous neuroactive steroid that is increased in rodent brain and plasma after hypothalamic-pituitary-adrenal (HPA) activation by acute stress or ethanol administration. Plasma levels of PREG metabolites are altered by pharmacological challenges of the HPA axis, however little is known about HPA regulation of PREG levels in monkeys. PREG concentrations were determined by radioimmunoassay in plasma samples from cynomolgus monkeys, following challenge with naloxone (125 and 375 microg/kg), corticotropin-releasing factor (CRF; 1 microg/kg), dexamethasone (130 microg/kg), adrenocorticotropic hormone (ACTH; 10 ng/kg; 4-6 h after 0.5 mg/kg dexamethasone) and ethanol (1.0 and 1.5 g/kg). Naloxone increased PREG levels, while CRF appeared to increase metabolism of PREG to deoxycorticosterone (DOC). ACTH, administered after dexamethasone, reduced PREG levels, despite an increase in plasma cortisol. Ethanol did not alter PREG levels. Changes in PREG levels were correlated with changes in DOC levels after naloxone 125 microg/kg, CRF, ethanol 1.5 g/kg, and dexamethasone challenges. Furthermore, dexamethasone-induced changes in PREG levels were correlated with subsequent alcohol intake. These data suggest that PREG responses to dexamethasone challenge may represent a trait marker of alcohol drinking. The lack of effect of ethanol on PREG levels suggests differential regulation in non-human primates vs. rodents.
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PMID:Plasma pregnenolone levels in cynomolgus monkeys following pharmacological challenges of the hypothalamic-pituitary-adrenal axis. 1679 Feb 66


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