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

Acute stress affects NMDA receptor (NMDAR)-dependent synaptic plasticity in the CA1 region of the hippocampus, with long-term potentiation and long-term depression (LTD) being, respectively, diminished and facilitated by acute exposure to stress. Here, we examined whether this facilitatory effect of stress on NMDAR-dependent LTD extends to metabotropic glutamate receptor (mGluR)-dependent LTD at Schaffer collateral-CA1 synapses. Application of a low dose (50 microM) of the selective group 1 mGluR agonist (RS)-3,5-dihydroxyphenylglycine (DHPG) promoted LTD in slices from stressed, but not from control, rats. Pretreatment of stressed rats with the glucocorticoid receptor (GR) antagonist RU38486 prevented the facilitation of DHPG-induced LTD (DHPG-LTD), indicating the involvement of corticosterone secretion and, in turn, stimulation of GRs. Finally, pretreatment of slices with an mGluR1, but not an mGluR5, antagonist blunted the sensitizing effect of stress on DHPG-LTD. These results indicate that acute stress, through corticosterone stimulation of GRs, facilitates the expression of mGluR1-dependent DHPG-LTD in the hippocampal CA1 region.
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PMID:Acute stress facilitates hippocampal CA1 metabotropic glutamate receptor-dependent long-term depression. 1761 Dec 66

Stress strongly alters the physiology and behavior of some individuals, while others are little or not affected. The causes of this individual variability have remained unknown. Here, we hypothesize that epigenetically induced levels of trait anxiety predict the stress response of individual mice in a genetically homogeneous population. Inbred C57BL/6 male mice were selected for their latency to freely enter from their home cage into an unfamiliar arena and classified as having high or low levels of trait anxiety. Mice were then exposed to acute stress (1-h olfactory contact with a rat) or control conditions. After 24 h, acute stress enhanced state anxiety measured in the elevated-plus maze test only in mice previously classified as having high levels of trait anxiety. This anxiogenic effect of acute stress was paralleled by enhanced novelty-induced plasma corticosterone secretion and increased messenger RNA (mRNA) expression for glucocorticoid and mineralocorticoid receptors in the hippocampus. No effects of acute stress were observed in mice classified as having low levels of trait anxiety. Under unstressed control conditions, mice only differed in basal levels of hippocampal mRNA for the glucocorticoid receptor, which were higher in mice with high trait anxiety than in mice with low trait anxiety. In summary, inbred C57BL/6 mice display a remarkably high interindividual variability in their trait anxiety that predicts the behavioral and neuroendocrine response to an acute stressor, indicating that expression of extremely different coping strategies can develop also between genetically identical individuals.
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PMID:Individual variability in the stress response of C57BL/6J male mice correlates with trait anxiety. 1768 Aug 3

We previously communicated that long-term hypoxia (LTH) resulted in a selective reduction in plasma epinephrine following acute stress in fetal sheep. The present study tested the hypothesis that LTH selectively reduces adrenomedullary expression of phenylethanolamine-N-methyltransferase (PNMT), the rate-limiting enzyme for epinephrine synthesis. We also examined the effect of LTH on adrenomedullary nicotinic, muscarinic, and glucocorticoid receptor (GR) expression. Ewes were maintained at high altitude (3,820 m) from 30 to 138 days gestation (dGA); adrenomedullary tissue was collected from LTH and age-matched, normoxic control fetuses at 139-141 dGA. Contrary to our hypothesis, in addition to PNMT, adrenomedullary expression (mRNA, protein) of tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) were reduced in the LTH fetus. Immunocytochemistry indicated that TH and DBH expression was lower throughout the medulla, while PNMT appeared to reflect a reduction in PNMT-expressing cells. Nicotinic receptor alpha 1, 2, 3, 5, 6, 7, beta 1, 2, and 4 subunits were expressed in the medulla of LTH and control fetuses. Messenger RNA for alpha 1 and 7 and beta 1 and 2 subunits was lower in LTH fetuses. Muscarinic receptors M1, M2, and M3 as well as the GR were also expressed, and no differences were noted between groups. In summary, LTH in fetal sheep has a profound effect on expression of key enzymes mediating adrenomedullary catecholamine synthesis. Further, LTH impacts nicotinic receptor subunit expression potentially altering cholinergic neurotransmission within the medulla. These findings have important implications regarding fetal cardiovascular and metabolic responses to stress in the LTH fetus.
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PMID:Long-term hypoxia modulates expression of key genes regulating adrenomedullary function in the late gestation ovine fetus. 1769 66

Stressful events before or just after parturition alter the subsequent phenotypical response to stress in a general process termed programming. Hypoxia during the period before and during parturition, and in the postnatal period, is one of the most common causes of perinatal distress, morbidity, and mortality. We have found that perinatal hypoxia (prenatal day 19 to postnatal day 14) augmented the corticosterone response to stress and increased basal corticotrophin-releasing hormone (CRH) mRNA levels in the parvocellular portion of the paraventricular nucleus (PVN) in 6-month-old rats. There was no effect on the levels of hypothalamic parvocellular PVN vasopressin mRNA, anterior pituitary pro-opiomelanocortin or CRH receptor-1 mRNA, or hippocampus glucocorticoid receptor mRNA. We conclude that hypoxia spanning the period just before and for several weeks after parturition programmes the hypothalamic-pituitary-adrenal axis to hyper-respond to acute stress in adulthood, probably as a result of drive from the parvocellular CRH neurones.
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PMID:Augmented hypothalamic corticotrophin-releasing hormone mRNA and corticosterone responses to stress in adult rats exposed to perinatal hypoxia. 1792 69

We previously reported that exposure to acute and chronic stress impairs long-term potentiation (LTP) in the hippocampal-prefrontal cortex pathway and showed evidence for a fundamental role of the prefrontal cortex in maladaptive responses to stress. The goal of the current studies was to examine whether blockade of glucocorticosteroid receptors (GR), by mifepristone (a Type II glucocorticoid receptor antagonist), just after exposure to acute stress could prevent stress-induced impairment of prefrontal LTP. We further examine the effects of mifepristone on mitogen-activated protein/ERK kinase (MEK) signaling pathway in the prefrontal cortex. The data show that an acute injection of mifepristone after stress restored the stress-induced blockade of prefrontal LTP and reduction of phospho-Ser217/221-MEK. These findings have significance for the treatment of memory deficits in hypercortisolemic states, such as stress and depression.
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PMID:Protection of stress-induced impairment of hippocampal/prefrontal LTP through blockade of glucocorticoid receptors: implication of MEK signaling. 1843 12

CC-chemokine receptor 2 (CCR2) and its ligand, monocyte chemotactic protein-1 (MCP-1, also known as CCL2), are crucial for the recruitment of monocytes/macrophages to sites of inflammation. We conducted a series of experiments to investigate the relationship between stress, monocyte CCR2 expression and migration activity. First, we collected peripheral blood mononuclear cells (PBMC) from untrained subjects (n=8) and measured CCR2 expression on CD14(+) monocytes cultured with cortisol, epinephrine and norepinephrine. Second, we collected PBMC from the subjects before and after they cycled for 60 min at 70% peak O(2) uptake (VO2(peak)), and measured alterations in CCR2 expression on monocytes following exercise. Third, we cultured PBMC with serum obtained before and after exercise and the glucocorticoid antagonist RU-486 to determine the effect of cortisol on CCR2 expression in vitro. Last, we measured the ability of PBMC treated with serum or cortisol to migrate through membrane filters in response to CCL2. Cortisol (but not epinephrine or norepinephrine) increased CCR2 expression on monocytes in a dose- and time-dependent manner. Exercise did not influence CCR2 expression on PBMC, whereas incubation of PBMC with post-exercise serum significantly increased CCR2 expression. Both cortisol and post-exercise serum increased the migration of PBMC toward CCL2. The increase in CCR2 expression on PBMC following stimulation with cortisol and serum was blocked by the glucocorticoid receptor antagonist RU-486. In conclusion, cortisol released during exercise increased monocyte CCR2 expression and migration activity in vitro. These alterations may influence inflammation and regeneration of damaged tissue after acute stress.
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PMID:The effects of acute exercise-induced cortisol on CCR2 expression on human monocytes. 1847 3

Proper integration and execution of the physiological stress response is essential for maintaining homoeostasis. Stress responses are controlled in large part by the paraventricular nucleus (PVN) of the hypothalamus, which contains three functionally distinct neural populations that modulate multiple stress effectors: (1) hypophysiotrophic PVN neurons that directly control the activity of the hypothalamic-pituitary-adrenocortical (HPA) axis; (2) magnocellular neurons and their secreted neurohypophysial peptides; and (3) brainstem and spinal cord projecting neurons that regulate autonomic function. Evidence for activation of PVN neurons during acute stress exposure demonstrates extensive involvement of all three effector systems. In addition, all PVN regions appear to participate in chronic stress responses. Within the hypophysiotrophic neurons, chronic stress leads to enhanced expression of secreted products, reduced expression of glucocorticoid receptor and GABA receptor subunits and enhanced glutamate receptor expression. In addition, there is evidence for chronic stress-induced morphological plasticity in these neurons, with chronic drive causing changes in cell size and altered GABAergic and glutamatergic innervation. The response of the magnocellular system varies with different chronic exposure paradigms, with changes in neurohypophysial peptide gene expression, peptide secretion and morphology seen primarily after intense stress exposure. The preautonomic cell groups are less well studied, but are likely to be associated with chronic stress-induced changes in cardiovascular function. Overall, the PVN is uniquely situated to coordinate responses of multiple stress effector systems in the face of prolonged stimulation, and likely plays a role in both adaptation and pathology associated with chronic stress.
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PMID:Chronic stress plasticity in the hypothalamic paraventricular nucleus. 1865 95

Increasing evidence suggests that depression is characterised by impaired brain plasticity that might originate from the interaction between genetic and environmental risk factors. Hence, the aim of this study was to investigate changes in neuroplasticity following exposure to stress, an environmental condition highly relevant to psychiatric disorders, in glucocorticoid receptor-deficient mice (GR(+/-)), a genetic model of predisposition to depression. Specifically, we have analysed the neurotrophin brain-derived neurotrophic factor (BDNF) and the immediate-early gene activity-regulated cytoskeletal-associated protein (Arc), two closely related molecules that can contribute to neuroplastic and morphological changes observed in depression. We found a region-specific influence of the GR-genotype on BDNF levels both under basal and stress conditions. Steady-state levels of BDNF mRNA were unchanged in hippocampus while up-regulated in frontal lobe of GR(+/-) mice. Following exposure to an acute stress, increased processing from pro- to mature BDNF was observed in hippocampal synaptosomes of wild-type mice, but not in GR mutants. Furthermore, the stress-dependent modulation of Arc was impaired in the hippocampus of GR(+/-) mice. These results indicate that GR(+/-) mice show overt differences in the stress-induced modulation of neuroplastic proteins, which may contribute to pathologic conditions that may originate following gene x environment interaction.
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PMID:Depression-prone mice with reduced glucocorticoid receptor expression display an altered stress-dependent regulation of brain-derived neurotrophic factor and activity-regulated cytoskeleton-associated protein. 1907 32

Dysregulation of hypothalamic-pituitary-adrenal (HPA) axis activity is thought to be an important factor in pathogenesis of depression. In animals, stress or glucocorticoids given in prenatal period lead to long-lasting behavioral and neuroendocrine changes similar to those observed in depressed patients. However, molecular basis for HPA disturbances in animals exposed to prenatal stress - a model of depression - have been only partially recognized. Therefore, in the present study we investigated the effect of prenatal stress on behavioral changes, blood corticosterone level, concentrations of glucocorticoid receptor (GR) and its cochaperone, FKBP51, in the hippocampus and frontal cortex in adult rats. It has been found that prenatally stressed rats display high level of immobility in the Porsolt test and anxiety-like behavior. The HPA axis hyperactivity in theses animals was evidenced by corticosterone hypersecretion at the end of the light phase and 1h following acute stress. Western blot study revealed that GR level was significantly elevated in the hippocampus but not in the frontal cortex of prenatally stressed rats, whereas concentration of FKBP51 was decreased only in the former brain structure. Chronic treatment with imipramine, fluoxetine, mirtazapine and tianeptine have diminished both behavioral and biochemical alterations observed in this animal model of depression. These data indicate that the increase in hippocampal GR level and low concentration of FKBP51 in the frontal cortex may be responsible for enhanced glucocorticoid action in depression.
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PMID:The effect of antidepressant drugs on the HPA axis activity, glucocorticoid receptor level and FKBP51 concentration in prenatally stressed rats. 1919 90

The physiological responses to stressors, including hormonal profiles and associated tissue responsiveness have been extensively studied in teleosts, but the molecular mechanisms associated with this adaptive response are not well understood. The advent of cDNA microarray technology has transformed the field of functional genomics by revealing global gene expression changes in response to stressor exposures even in non-mammalian vertebrates, including fish. A unifying response in studies related to stressor exposure is activation of the hypothalamus-pituitary-interrenal (HPI) axis in fish, leading to cortisol release into the circulation. Here we will discuss the implications of some of the gene expression changes observed in response to acute stress in fish, while highlighting a role for cortisol in this adaptive stress response. As liver is a key organ for metabolic adjustments to stressors and also is a major target for cortisol action, the genomic studies pertaining to stress and glucocorticoid regulation have focused mainly on this tissue. The studies have identified several genes that are altered transiently after an acute stressor exposure in fish. A number of these stress-responsive genes were also modulated by glucocorticoid receptor activation, suggesting that elevation in cortisol levels during stressor exposure may be a key signal for target tissue molecular programming, essential for stress adaptation. The identification of regulatory gene networks that are stress activated, and modulated by cortisol, both in hepatic and extra-hepatic tissues, including gonads, brain, immune cells and gills, will provide a mechanistic framework to characterize the multifaceted role of cortisol during stress adaptation.
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PMID:Stress transcriptomics in fish: a role for genomic cortisol signaling. 1934 38


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