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Query: UMLS:C0848237 (
acute stress
)
4,619
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The hippocampus plays an important role in central stress integration. The present study tests the hypothesis that the ventral subiculum, as a principal source of hippocampal efferents, is involved in co-ordination of hypothalamo-pituitary-adrenocortical and behavioural responses to cognitively-processed information. Basal hypothalamo-pituitary-adrenocortical activation appears to be normal in ventral subiculum lesion rats, as basal corticosterone and adrenocorticotropic hormone secretion, anterior pituitary pro-opiomelanocortin and type 1 corticotropin-releasing hormone receptor messenger RNA expression, adrenal and thymus weight, and splenic mitogen activity are not affected by lesion. Lesions of the ventral subiculum induce glucocorticoid hypersecretion following restraint stress or open field exposure, whereas responses to ether inhalation are unaffected. Interestingly, ventral subiculum lesion does not affect fast glucocorticoid negative feedback inhibition of restraint-induced adrenocorticotropic hormone release. Corticotropin-releasing hormone immunoreactivity is increased in the hypothalamic paraventricular nucleus of ventral subiculum lesion rats, and is differentially depleted by
acute stress
exposure (relative to sham-lesion rats). However, ventral subiculum lesion does not affect basal and stress-induced corticotropin-releasing hormone, arginine vasopressin and cFOS messenger RNA expression in paraventricular nucleus neurons. Behavioural analysis reveals that ventral subiculum lesion rats are hyper-responsive to open field exposure, showing decreased total ambulation and reduced incidence of central square entry. The results suggest that the ventral subiculum plays a specific role in integrating cognitively-processed stimuli (e.g., restraint and open field exposure) into appropriate neuroendocrine and behavioural responses to stress. Enhanced stress-induced glucocorticoid secretion and increased corticotropin-releasing hormone biosynthesis are likely due to removal of oligosynaptic inhibitory input to the paraventricular nucleus subsequent to ventral subiculum lesion.
Neuroscience 1998
Sep
PMID:Ventral subiculum regulates hypothalamo-pituitary-adrenocortical and behavioural responses to cognitive stressors. 988 60
Gonadal hormones may modulate analgesia responses induced by
acute stress
in humans and rats. To evaluate the effects of gonadal hormones in modifying neuropathic pain, we measured autotomy changes following sciatic nerve resection in ovariectomized rats and in the presence of estrogen replacement. Two groups of female rats were subjected to ovariectomy and sham surgery. Each group was then divided into two subgroups receiving subcutaneously sesame oil with or without estradiol benzoate (5 microg/day/rat). All rats then underwent sciatic nerve resection in one hindlimb. Degree of self-mutilation was measured daily for 8 weeks. Estradiol treatment resulted in significantly lower autotomy scores in ovariectomized rats (3.6 +/- 0.6 vs. 5.5 +/- 0.3, p < 0.01) and in sham-operated rats (3.4 +/- 0.7 vs. 5.1 +/- 0.4, p < 0.05). The results of this study indicate that estrogen can modify the autotomy behavior, an indicator of neuropathic pain, in rats after nerve injury.
Pharmacology 1999
Sep
PMID:Effects of estrogen on autotomy in normal and ovariectomized rats. 1045 69
Multiple neurochemical estimates were used to examine peripheral corticosterone (CORT) effects in dopaminergic terminal regions. Acute CORT administration, which elevated plasma CORT (5 h), slightly decreased dihydroxyphenylacetic acid (DOPAC) to dopamine (DA) ratios in the striatum but not in other regions examined. Two weeks of adrenalectomy (ADX) increased both medial prefrontal cortex DOPAC/DA and homovanillic acid (HVA)/DA and striatal HVA/DA. A reciprocal pattern of changes was observed with CORT replacement in ADX animals. In contrast, CORT replacement in ADX animals did not significantly influence tyrosine hydroxylase content, basal dihydroxyphenylalanine (DOPA) accumulation after NSD 1015 treatment or the decline in DA after alpha-methyl-para-tyrosine, suggesting that neither DA neuronal activity nor release are altered by CORT. Moreover, neither gamma-hydroxybutyric acid lactone-induced increases in DOPA accumulation or stress-induced increases in DA utilization were influenced by CORT replacement, indicating that neither autoreceptor regulation of DA synthesis nor
acute stress
regulation of DA utilization are changed by CORT. The findings are most consistent with direct inhibition of basal DA metabolism in the medial prefrontal cortex and striatum. The possible physiological and behavioral significance of this inhibition is being further explored.
Neuropsychopharmacology 1999
Sep
PMID:Glucocorticoid effects on mesotelencephalic dopamine neurotransmission. 1045 37
Neuronal mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) proteins are glucocorticoid-activated transcription factors that bind identical DNA response elements yet transduce distinct physiological/transcriptional actions. The present study assessed regulation of adrenocorticosteroid receptor RNA and protein following intermittent stress exposure, using Sprague Dawley (S-D) and stress-hyperresponsive Fischer 344 (F344) rat strains. The F344 (but not S-D) strain showed enhanced
acute stress
responsivity and enhanced corticosterone secretion following prolonged stress. F344 rats also showed reduced responsiveness to a novel stressor after prolonged stress exposure, suggestive of enhanced glucocorticoid negative feed-back. Upon prolonged stress, F344 rats down-regulated MR hnRNA in CA1, CA3, and dentate gyrus. Transcriptional changes were accompanied by decreased expression of the alpha 5' messenger RNA (mRNA) form, consistent with altered promoter utilization. In contrast, alpha 5' splice variant, full-length mRNA, and MR protein expression were not affected by stress in either strain, implying that transcriptional changes do not affect overall mRNA or protein expression. GR protein was increased in pyramidal and granule cell somata/nuclei of F344 rats despite lack of a change in mRNA expression. These data suggest that prolonged stress elicits restricted changes in MR and GR expression in the F344 strain only. Overall, stable expression of adrenocorticosteroid receptors is rigorously defended in hippocampal neurons, apparently through transcriptional and posttranscriptional mechanisms.
Endocrinology 1999
Sep
PMID:Defense of adrenocorticosteroid receptor expression in rat hippocampus: effects of stress and strain. 1046 67
The cAMP signalling pathway plays a key role in the regulation of the hypothalamic-pituitary-adrenal axis. Transcription factor CREM (cAMP response element modulator) is implicated in the modulation of a number of neuroendocrine functions. By virtue of an alternative, intronic promoter CREM generates the powerful transcriptional repressor ICER (inducible cAMP early repressor), which displays a pronounced neuroendocrine-specific expression. Here we document a remarkable induction of ICER in response to
acute stress
in the intermediate lobe (IL) of the pituitary gland. The induction is transient and is preceded by CREB phosphorylation. Adrenergic stimulation directs ICER induction in the IL through the activation of both beta2-adrenergic and corticotrophin-releasing hormone receptors. These receptors are positively coupled to the adenylate cyclase signalling pathway, which regulates hormone release from the IL, implicating ICER in the modulation of peptide secretion. We show that targeted ablation of the CREM gene in the mouse causes a chronic increase of beta-endorphin levels. Altered hormonal production occurs both in basal conditions and after stress. Thus, early ICER induction in the IL may be involved in the modulation of gene expression in response to stress.
Mol Cell Endocrinol 1999
Sep
10
PMID:The inducible cyclic adenosine monophosphate early repressor (ICER) in the pituitary intermediate lobe: role in the stress response. 1058 Aug 43
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.
Pharmacol Res 2000
Sep
PMID:Immobilization stress-induced changes in brain acetylcholinesterase activity and cognitive function in mice. 1094 25
This study investigated the influence of attempted suppression and thought control strategies on traumatic memories. Survivors of civilian trauma with
acute stress
disorder (ASD; n = 20) and without ASD (n = 20) monitored their trauma-related thoughts for three 24-h periods. In period 1, participants were instructed to think about anything. In period 2, participants were administered suppression or nonsuppression instructions relating to thoughts of the trauma. In period 3, participants were again instructed to think about anything. The results revealed no evidence for an increase in trauma-related thoughts following suppression instructions. Punishment and worry thought control strategies correlated significantly with both anxiety and suppression ratings. Frequency of intrusions was associated with a distraction cognitive strategy. These findings point to the importance of traumatised individuals' cognitive strategies in mediating the management and occurrence of posttraumatic intrusions.
Behav Res Ther 2000
Sep
PMID:Attempting suppression of traumatic memories over extended periods in acute stress disorder. 1095 24
The present study aimed to index the accuracy of memory for acute trauma symptoms by comparing the symptoms reported by motor vehicle accident (MVA) victims within 1 month posttrauma with the recall of these symptoms at 2 years posttrauma. Ninety-two consecutive MVA admissions were assessed for the presence of
acute stress
disorder (ASD) within 1 month posttrauma. At 2 years posttrauma, 61% (N = 56) of the sample were reassessed for posttraumatic stress disorder (PTSD) and for accuracy of recall of the symptoms reported during the first assessment. At least one of the four ASD diagnostic clusters was recalled inaccurately by 75% of patients. High levels of posttraumatic stress severity and high subjective ratings of injury severity at 2 years posttrauma were associated with errors of addition (i.e., recalling the presence of acute symptoms 2 years posttrauma that were not reported during the first assessment). Low levels of posttraumatic stress severity and low subjective ratings of injury severity at 2 years posttrauma were associated with errors of omission (i.e., omitting to recall acute symptoms 2 years posttrauma that were reported during the first assessment). These results suggest that retrospective reports of
acute stress
symptoms should be interpreted cautiously because of the influence of current symptoms on recall of acute symptoms.
J Nerv Ment Dis 2000
Sep
PMID:Memory for acute stress disorder symptoms: a two-year prospective study. 1100 34
Chorioamnionitis represents the leading cause of preterm birth and related pathologic conditions as well as of fetal death and frequently occurs in symptom-free mothers. Recent radiologic findings have indicated that thymus size is significantly reduced in preterm infants born to mothers with subclinical, histologically proven chorioamnionitis. However, an accurate morphologic description of the thymus gland in fetuses and neonates with chorioamnionitis is lacking, although it is known that infection and other stress processes may cause lymphocyte depletion in the thymuses of infants and older babies (
acute stress
involution). We describe morphologic modifications in the thymus of fetuses with histologically proven chorioamnionitis and newborn infants with chorioamnionitis and proven sepsis. The main findings included (1) decreased organ volume (ANOVA, P < .0024); (2) reduced corticomedullary ratio (P < 10(-6)); (3) significant changes in the relationship between thymic parenchyma and thymic interstitial tissue with resulting increased organ complexity (P = .03); (4) severe reduction of thymocytes; and (5) other degenerative processes such as monocyte/macrophage infiltration of Hassall's bodies. These results indicate that chorioamnionitis, with or without sepsis, is associated with significant morphologic modifications in the thymus. We wish to note that the described thymic pathology is only one aspect of the fetal systemic inflammatory response syndrome with which chorioamnionitis is associated.
Hum Pathol 2000
Sep
PMID:Acute thymic involution in fetuses and neonates with chorioamnionitis. 1101 81
A powerful motivation for clinicians working in the field of trauma is the wish to prevent or minimize chronic posttraumatic reactions by early interventions. This paper illustrates the process and the elements of important programs that have been introduced into the psychological or psychiatric literature. Studies that have been done to evaluate these programs are discussed. With regard to early interventions given to traumatized victims regardless of whether they suffer from posttraumatic stress or not, it is clearly shown that the evidence that these programs have a substantial positive benefit is disappointingly scarce. However, with regard to the treatment of
acute stress
disorder, a brief cognitive-behavioral program appears to effectively prevent the development of chronic posttraumatic stress disorders. In summary, it has to be noted that much more research on this issue is needed.
Fortschr Neurol Psychiatr 2000
Sep
PMID:[Early intervention following trauma. An overview of programs and their effectiveness]. 1103 40
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