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)

Male Sprague-Dawley rats maintained under controlled lighting and temperature conditions were used in this experiment. Animals were exposed to acute cold (4 degrees C) and immobilization stress for one hour, exposed to cold stress for 7 days (chronic stress) or treated with corticosterone (2 mg/kg) 1 hr prior to sacrificing. Animals with their proper controls were sacrificed and the stomach, duodenum, ileum and colon were separated and assayed for choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities. The data obtained indicated that exposure to acute stress resulted in significant decline in ChAT activity in all tissues studied. The administration of corticosterone resulted in significant decline in ChAT activity in all tissues studied except for the duodenum. Meanwhile, the exposure to chronic stress did not have any significant effect on ChAT activity. On the other hand, acute stress caused significant increase in AChE activity in all tissues studied except for the ileum and stomach. The duodenal AChE activity of stressed animals increased thirty-fold when compared to control. The administration of glucocorticoids significantly reduced AChE in all tissues studied, except for the duodenum and stomach where there was thirty-two-fold increase as compared to the control levels. The exposure to chronic stress also caused significant increase in AChE of all tissues studied, except for the colon. The results of this experiments indicate that the duodenal AChE is extremely sensitive to stress or glucocorticoids and that stress induced changes in the cholinergic enzymes of the gastrointestinal tract may be mediated by adrenal steroids.
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PMID:Effect of stress and glucocorticoids on the gastrointestinal cholinergic enzymes. 371 75

Acetylcholinesterase (AchE, EC 3.1.1.7) activity was determined in cerebral cortex, hypothalamus, adenohypophysis and adrenal gland in response to acute and chronic stress. Chronic exposure of animals to cold stress (at 4 degrees C for 7 days) resulted in significant decline of AchE activity in all tissues studied. Similar results were obtained when animals were exposed to acute immobilization and cold stress (at 4 degrees C) simultaneously. In another experiment, animals were treated with 2 mg/kg of corticosterone prior to AchE determination. Corticosterone administration resulted in a significant decline in AchE activity of the cortex, the hypothalamus and the adrenal but failed to affect the adenohypophysis AchE level. Exposing adrenalectomized animals to acute stress resulted in no significant changes in the cortex and the hypothalamus but caused a significant decline in AchE of the adenohypophysis. It was concluded from this study that corticosterone might mediate the stress effect on AchE activity.
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PMID:Effect of stress on the acetylcholinesterase activity of the hypothalamus-pituitary-adrenal axis in the rat. 684 Jun 71

We have previously reported that acute stress alters intestinal transport physiology in Wistar-Kyoto rats, a stress-susceptible strain. In this study, we tested the hypothesis that the abnormalities in these rats are due to cholinergic mechanisms. Atropine- or saline-treated rats were exposed to acute restraint stress, and, subsequently, electrophysiological parameters of excised jejunal segments were assessed in Ussing chambers. Compared with the parent Wistar rat strain, Wistar-Kyoto rats demonstrated significantly greater stress-induced changes in ion secretion and permeability. The activity of cholinesterase in intestinal mucosal homogenates was significantly less in Wistar-Kyoto than in Wistar rats. Atropine pretreatment of rats before stress corrected the epithelial pathophysiology. Our results suggest that stress stimulated the release of acetylcholine, resulting in altered epithelial function in these genetically predisposed rats.
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PMID:Cholinergic nerves mediate stress-induced intestinal transport abnormalities in Wistar-Kyoto rats. 927 29

Acute traumatic stress may lead to post-traumatic stress disorder (PTSD), which is characterized by delayed neuropsychiatric symptoms including depression, irritability, and impaired cognitive performance. Curiously, inhibitors of the acetylcholine-hydrolysing enzyme acetylcholinesterase may induce psychopathologies that are reminiscent of PTSD. It is unknown how a single stressful event mediates long-term neuronal plasticity. Moreover, no mechanism has been proposed to explain the convergent neuropsychological outcomes of stress and of acetylcholinesterase inhibition. However, acute stress elicits a transient increase in the amounts released of the neurotransmitter acetylcholine and a phase of enhanced neuronal excitability. Inhibitors of acetylcholinesterase also promote enhanced electrical brain activity, presumably by increasing the survival of acetylcholine at the synapse. Here we report that there is similar bidirectional modulation of genes that regulate acetylcholine availability after stress and blockade of acetylcholinesterase. These calcium-dependent changes in gene expression coincide with phases of rapid enhancement and delayed depression of neuronal excitability. Both of these phases are mediated by muscarinic acetylcholine receptors. Our results suggest a model in which robust cholinergic stimulation triggers rapid induction of the gene encoding the transcription factor c-Fos. This protein then mediates selective regulatory effects on the long-lasting activities of genes involved in acetylcholine metabolism.
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PMID:Acute stress facilitates long-lasting changes in cholinergic gene expression. 2660 28

The peripherally acting cholinesterase inhibitor pyridostigmine was widely used during the Gulf War as a pretreatment against possible chemical warfare attack. Following consistent reports on long-term illness among Gulf War veterans, pyridostigmine was examined for its possible long-term effects. These effects were suggested to be induced by the combination of pyridostigmine administration and stress exposure that allowed this quaternary compound to enter the brain through stress induced changes in blood-brain barrier (BBB) permeability. Recently, pyridostigmine administration was demonstrated to inhibit brain cholinesterase following acute stress in mice. However, the effect was not replicated under similar conditions in guinea pigs. Because of the significant implication of these findings, we tested brain cholinesterase (ChE) inhibition following the administration of pyridostigmine, or the tertiary carbamate physostigmine, with or without stress in mice. Different experiments were performed to examine the contribution of gender, age (young and adults), stress (type and intensity), or strain (CD-1 and FVB/n) parameters. No inhibition of brain ChE was detected in any of these experiments. At the same time, physostigmine induced the expected decrease in brain ChE in all the experiments. Thus, we could not replicate the findings that suggest pyridostigmine can affect brain cholinesterase following stress.
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PMID:Stress does not enable pyridostigmine to inhibit brain cholinesterase after parenteral administration. 1079 40

Acute stress increases the risk for neurodegeneration, but the molecular signals regulating the shift from transient stress responses to progressive disease are not yet known. The "read-through" variant of acetylcholinesterase (AChE-R) accumulates in the mammalian brain under acute stress. Therefore, markers of neurodeterioration were examined in transgenic mice overexpressing either AChE-R or the "synaptic" AChE variant, AChE-S. Several observations demonstrate that excess AChE-R attenuates, whereas AChE-S intensifies, neurodeterioration. In the somatosensory cortex, AChE-S transgenics, but not AChE-R or control FVB/N mice, displayed a high density of curled neuronal processes indicative of hyperexcitation. In the hippocampus, AChE-S and control mice, but not AChE-R transgenics, presented progressive accumulation of clustered, heat shock protein 70-immunopositive neuronal fragments and displayed a high incidence of reactive astrocytes. Our findings suggest that AChE-R serves as a modulator that may play a role in preventing the shift from transient, acute stress to progressive neurological disease.
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PMID:Excess "read-through" acetylcholinesterase attenuates but the "synaptic" variant intensifies neurodeterioration correlates. 1089 Aug 84

In the present study, the effect of acute and chronic immobilization stress on brain acetylcholinesterase (AChE) enzyme activity and cognitive function in mice was investigated. Mice were immobilized by strapping for 150 min. One group of mice were only immobilized once (acute stress) while in another group mice were immobilized (150 min) daily for 5 consecutive days (chronic stress). Specific AChE enzyme activity (micromol min(-1)mg(-1)) was estimated by a spectrophotometric method in the whole brain of mice subjected to acute and chronic stress. In the acute stress group, AChE activity (0.24922 +/- 0.011) in the detergent-soluble fraction was found to be significantly decreased in comparison to the control group (0.33561 +/- 0.022). Chronic stress did not cause any significant change in AChE activity in the detergent-soluble fraction. In the salt-soluble fraction, AChE activity was significantly decreased only in the chronic stress group (0.08791 +/- 0.011) as compared to the control group (0.12051 +/- 0.011). A passive avoidance test was used to assess cognitive function. The transfer latency time (TLT) from a light to dark chamber was recorded in the control and acute stress groups (30 min after immobilization is over) on day 1 (Trial I) and the following day (Trial II). The acute stress group showed an increase (178%) in TLT from Trial I to Trial II, which was significantly higher than that of the non-stress control group (75%). In the chronic stress group, Trial I was undertaken 30 min after the last immobilization, i.e. on day 5 and 24 hr later, Trial II. However, the chronically stressed mice showed an increase (70%) in TLT similar to the control group. Thus this study shows that acute immobilization stress may enhance cognitive function in mice which may be attributed to a decrease in AChE activity leading to an increase in cholinergic activity in the brain.
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PMID:Immobilization stress-induced changes in brain acetylcholinesterase activity and cognitive function in mice. 1094 25

Type IV collagen, one of the serum markers for hepatic fibrosis, was measured perioperatively in patients with and without chronic liver damage to investigate whether this parameter changes in response to acute stress to the liver and can predict the surgical risk of hepatic resection. The serum type IV collagen level was significantly elevated in patients with liver cirrhosis. There were significant correlations between serum type IV collagen levels and the indocyanine green clearance test and cholinesterase activity, although the correlation coefficients were not high. The size of the resected hepatic mass was not the primary factor to influence the postoperative serum type IV collagen level. In patients with liver cirrhosis, the postoperative serum type IV collagen level increased significantly compared to that in patients with normal liver or chronic hepatitis. Postoperative liver failure occurred in 0%, 11.6%, and 44.4% of patients with preoperative serum type IV collagen levels of <150, < or = 150 to 300, and > or = 300 ng/ml, respectively. In those with postoperative liver failure, the serum type IV collagen levels were significantly higher both pre- and postoperatively compared to those in patients with uneventful courses. Several preoperative liver function tests indicated that type IV collagen is an independent risk factor for postoperative liver failure. Thus perioperative measurement of the serum type IV collagen levels seemed to be useful for predicting the risk of hepatic resection in patients with chronic liver damage.
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PMID:Significance of serum type IV collagen level of hepatectomized patients with chronic liver damage. 1191 Apr 79

Mental stress modifies both cholinergic neurotransmission and alternative splicing in the brain, via incompletely understood mechanisms. Here, we report that stress changes brain microRNA (miR) expression and that some of these stress-regulated miRs regulate alternative splicing. Acute and chronic immobilization stress differentially altered the expression of numerous miRs in two stress-responsive regions of the rat brain, the hippocampal CA1 region and the central nucleus of the amygdala. miR-134 and miR-183 levels both increased in the amygdala following acute stress, compared to unstressed controls. Chronic stress decreased miR-134 levels, whereas miR-183 remained unchanged in both the amygdala and CA1. Importantly, miR-134 and miR-183 share a common predicted mRNA target, encoding the splicing factor SC35. Stress was previously shown to upregulate SC35, which promotes the alternative splicing of acetylcholinesterase (AChE) from the synapse-associated isoform AChE-S to the, normally rare, soluble AChE-R protein. Knockdown of miR-183 expression increased SC35 protein levels in vitro, whereas overexpression of miR-183 reduced SC35 protein levels, suggesting a physiological role for miR-183 regulation under stress. We show stress-induced changes in miR-183 and miR-134 and suggest that, by regulating splicing factors and their targets, these changes modify both alternative splicing and cholinergic neurotransmission in the stressed brain.
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PMID:Changes in brain MicroRNAs contribute to cholinergic stress reactions. 1971 Dec 2

A single i.p. administration of 1.0 mg/kg of chlorphenvinphos (CVP), an organophosphorus pesticide, results in an acute stress response, evidenced by a marked (6-7 fold) rise in plasma corticosterone (CORT) concentration, and a diminished behavioural sensitivity to amphetamine (AMPH) three weeks postexposure. Surprisingly, in rats subjected to a single series of inescapable electric footshocks (60 10 msec triplets of 3.0 mA, 2 msec, square pulses during 20 min - IF ) two weeks prior to the CVP exposure, these effects are not observed. It has been assumed that the reduced effectiveness of CVP might be related to some persisting alterations in the functional state of the cholinergic system. The aim of the present work was to discover whether and in what way the IF pretreatment affects i) the cholinesterase activity in blood, and ii) the dynamics of the alterations in the cholinesterase (ChE) activity following the CVP exposure. The experiments were performed on 3 mo. old, male Wistar rats. In the first experiment, the blood samples were taken from the tail vein 15, 60 and 180 min after the IF. In the second experiment, the rats were pretreated with IF and 14 days later given 1.0 mg/kg of CVP i.p. Blood samples were taken 15 min, 60 min, 180 min, 24 h, 7 days, and 14 days after the CVP exposure. In the first experiment no differences in the ChE activity in plasma (pChE) and erythrocytes (rbcChE) were found between the shocked and control rats. In the second experiment, however, in rats pretreated with IF the rbcChE activity of was reduced by CVP less and pChE activity returned to normal faster than in rats not pretreated with IF. The results confirm that exposure to IF, a nonchemical stressor, induces some long-lasting adaptive changes which render the cholinergic system less susceptible to the harmful action of ChE inhibitors. It has been hypothesized that the changes consist in an increase of the antioxidant potential in blood and possibly other tissues.
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PMID:Effects of stress pretreatment on the dynamics of blood cholinesterase activity after exposure to an organophosphorus pesticide in the rat. 2068 82


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