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

Acute immobilization stress increased serotonin and 5-hydroxyindoleacetic acid levels, the 5-hydroxyindoleacetic/serotonin ratio, and the number of [3H]ketanserin binding sites, representing serotonin-2 type receptors, in the rat frontal cortex. Peripheral administration of propranolol or central administration of 6-hydroxydopamine abolished the stress induced elevation of [3H]ketanserin binding sites. Treatment with 6-hydroxydopamine did not affect the increase in serotonin and 5-hydroxyindoleacetic acid levels, and enhanced the increase in the 5-hydroxyindoleacetic acid/serotonin ratio produced by stress. Conversely, chemical serotoninergic denervation with 5,7-dihydroxytryptamine had no influence on the stress-induced elevation of [3H]ketanserin binding sites, but abolished the serotonin and 5-hydroxyindoleacetic acid increase produced by stress. These results suggest that an intact serotoninergic system is not essential for serotonin-2 type receptor regulation during stress. Instead, the noradrenergic system, most probably through stimulation of beta-adrenoreceptors, may control the regulation of [3H]ketanserin binding sites in the rat frontal cortex during acute stress.
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PMID:Adrenergic regulation of [3H]ketanserin binding sites during immobilization stress in the rat frontal cortex. 170 36

Using a chronic stress model of depression, the biochemical, hormonal, and neurochemical effects of chronic stress were determined in male CD-1 mice. The effects of chronic administration of three tricyclic antidepressants (TCA): chlorimipramine, amitriptyline and desmethylimipramine, as well as fluoxetine, a specific serotonin uptake inhibitor, were also evaluated. Exposure to acute noise/light stress dramatically increased motor activity (behavioral activation) in comparison with basal (unstressed) activity. However, animals with a history of chronic stress exhibited reduced basal activity levels as well as a decreased behavioral activation response to acute stress. There was also exaggerated corticosterone (CS) responding in both of these behavioral test situations attributable to prior chronic stress exposure. Chronic treatment with any of the TCAs significantly restored the behavioral activation response to acute stress and normalized CS responding in chronically stressed animals. Chronic fluoxetine treatment was ineffective. In chronically stressed, but behaviorally untested (quiescent) mice, there were no changes in CS levels, but norepinephrine (NE) and 5-hydroxyindoleacetic acid (5-HIAA) levels were increased. However, chronically stressed mice tested for basal motor activity showed large NE decreases, while those receiving acute stress exposure prior to testing showed large NE decreases and further 5-HIAA increases. There were no alterations on neurochemical parameters due to any drug treatment which could be correlated with a possible mechanism for their efficacy, although evidence suggested NE involvement. It was further proposed that the chronic stress paradigm induced conditioned neuroendocrine and neurochemical responses.
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PMID:Biochemical and behavioral correlates of chronic stress: effects of tricyclic antidepressants. 242 79

The effects of 1 h/day restraint in plastic tubes for 24 days on the levels of serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), tryptophan (TP), and noradrenaline (NA) in six regions of rat brain 20 h after the last restraint period were investigated. The levels of 5-HT, 5-HIAA, and NA but not TP increased in several regions. The effects of 1 h of immobilization on both control and chronically restrained rats were also studied. Immobilization per se did not alter brain 5-HT, 5-HIAA, and TP levels, but decreased NA in the pons plus medulla oblongata and hypothalamus. However, immobilization after chronic restraint decreased 5-HT, increased 5-HIAA, and decreased NA in most brain regions in comparison with values for the chronically restrained rats. We suggest that chronic restraint leads to compensatory increases of brain 5-HT and NA synthesis and sensitizes both monoaminergic systems to an additional acute stress. These changes may affect coping with stress demands.
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PMID:Chronic stress increases serotonin and noradrenaline in rat brain and sensitizes their responses to a further acute stress. 245 9

The effects of different kinds of acute stress on collagen-induced whole blood platelet aggregation and fibrinolysis in relation to blood serotonergic measures were studied. In rats water-immersion restraint stress resulted in a shortening of euglobulin clot lysis time (ECLT), an increase in tissue plasminogen activator (tPA) activity with a concurrent fall in its inhibitor activity. Footshock caused rather a suppression in fibrinolysis with a prolongation of ECLT and a decline in tPA activity as well as a reduction in whole blood platelet aggregation induced by collagen. Serotonin (5-HT) level, a marker of a severity of stress, increased after footshock application with a concomitant rise in its major metabolite-5-hydroxyindoleacetic acid (5-HIAA). This indicates an enhanced 5-HT metabolism. Following water-immersion restraint stress 5-HT and 5-HIAA levels did not differ from controls. In both groups of stressed animals an inverse correlation between tPA activity and blood serotonin was observed. Our data indicate that these types of stress may influence either fibrinolysis or peripheral serotonergic mechanism in different ways. Acute and severe stress such as footshock by causing an impairment in fibrinolysis and a rise in 5-HT may contribute to the pathogenesis of thrombosis and henceforth to the development of atherosclerosis.
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PMID:Stress-dependent changes in fibrinolysis, serotonin and platelet aggregation in rats. 751 40

Since stress can alter serotonin (5-hydroxytryptamine, 5-HT) turnover in the brain and the periphery, the effects of different types of acute stress on serotonin and related substances in the whole blood and various brain areas in rats pretreated with tranylcypromine (TCP) were studied. TCP administered alone caused a rise in 5-HT, a fall in its metabolite (5-hydroxyindoleacetic acid, 5-HIAA) in the whole blood and in every part of the brain analyzed relative to controls. In rats given TCP and subjected to footshock or water-immersion restraint stress similar changes, but to a different extent, were observed. 5-HT level remained essentially constant except in the blood and the limbic system, whereas 5-HIAA level was found to be increased in the blood and the brain, mainly in the limbic system and the brainstem following footshock. Water-immersion restraint stress caused an increase in 5-HT only in the limbic system without any changes in 5-HT and 5-HIAA in the blood. Relative to controls, an increase in total tryptophan concentration in the whole blood and in every part of the brain was found only after footshock application with or without pretreatment with TCP. In conclusion, responses to stress in rats may depend upon the type of stimulus applied as well as of a concurrent administration of TCP. Some regional differences may account for an altered in vivo efficacy of this drug.
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PMID:Stress and/or tranylcypromine treatment affects serotonergic measures in blood and brain in rats. 752 9

1. Clinical data suggest that valproate (VPA) may be useful in prophylaxis of affective disorders, which show disturbances of the serotoninergic system. On the other hand, chronic stress has an adverse effect on affective disorders, those with disturbances of the serotonergic system, especially. 2. In order to study the effects of VPA on brain monoamines and acute stress, 200 mgr VPA/Kgr was administered intraperitoneal (ip) to juvenile male rats; the control group was treated with NaCL 0.9% ip. After 30 min, all animals were evoked on predictable neurogenic or systemic stress (30 min foot shock, or 15 min ether stress, respectively), and 48 hours later, VPA or NaCL were administered ip again; 30 min afterwards, the rats were decapitated. Rats without stress were also sacrificed 30 min after VPA or NaCL administration. 3. Measurements of brain monoamines noradrenaline (NA), dopamine (DA), 5-hydroxytryptamine (5-HT), and their metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), and 5-hydroxyindoleacetic acid (5-HIAA), were done in Frontal Cortex (FC), Hypothalamus (HY) and Striatum (S), by High Performance Liquid Chromatography (HPLC). 4. Compared with the control stress group the level of 5-HIAA in the FC was significantly increased (P < 0.01) in VPA stress rats; in the HY and in S the increase of 5-HIAA was not significant. No remarkable differences were observed in NA, DA, 5-HT and DOPAC concentrations, in any of the brain regions. No changes in brain monoamine levels were found in non stress rats, either. 5. The augmentation of 5-HIAA level after VPA administration and after stress, in correlation with the decrease of 5-HIAA that is observed in depression, support the hypothesis that VPA may be effective in affective disorders by influencing the serotoninergic system.
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PMID:The effects of valproate in brain monoamines of juvenile rats after stress. 843 Feb 20

The influence of chronic stress (footshock combined with randomized light flashes) on acute stress-induced (immobilization) release of noradrenaline, dopamine and serotonin in rat lateral hypothalamus was assessed by microdialysis. The chronic stress resulted in an increase and prolongation of the acute stress-induced release of noradrenaline but not of dopamine and serotonin. The increased rate of accumulation of dioxyphenylacetic acid and unchanged accumulation of homovanillic acid (dopamine metabolites) and dopamine during and after the acute stress in chronically stressed animals reflect a rise of synthetic activity of catecholaminergic systems in response to acute stress and reuptake increase. Marked stress-induced increase in hydroxyindoleacetic acid in chronically stressed rats without any changes in the ST dynamics may be regarded in a similar way. A significant increase in potassium-stimulated release of all the studied monoamines was found while their basal level remained unchanged. The conclusions was made that the hyperergic release of neurotransmitters may be the basis of an inadequate response of animals to acute stress, i.e., one of the neurotic symptoms.
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PMID:[The activity of the monoaminergic systems of the rat hypothalamus in acute stress after chronic stressing]. 1048

Environmental influences during early life periods, particularly those provided by the mother or parents, are generally considered to have a strong impact on the development of brain and behaviour of the offspring. In the semi-precocial South American species Octodon degus, a rodent becoming increasingly popular in different laboratory research fields, the present study aimed to examine the consequences of the disturbance of the parent-offspring interaction induced by parental separation on the serotonergic neurotransmission. Based on a quantitative neurochemical approach using brain homogenates obtained from cortical regions and the hippocampus our results revealed that (i) the tissue levels of serotonin and 5-hydroxyindoleacetic acid showed in both sexes a moderate, around two-fold increase until adulthood, indicating relatively matured cortical and hippocampal serotonergic systems at birth. In addition, we found an age-, region- and sex-specific pattern of changes in the serotonergic system induced by (ii) an acute stress challenge early in life (1-h parental separation at the postnatal day 3, 8, 14 or 21) with the most pronounced effects at earlier ages (between postnatal days 3 and 14) in the female cortex and (iii) repeated stress exposure (1h daily) during the first 3 weeks of life affecting cortical regions of both sexes. Taken together, these data indicate that early life stress (i.e. parental separation) influences the developing serotonergic system in the semi-precocial O. degus, even if the brain is relatively well matured at the early stages of postnatal development.
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PMID:Epigenetic modulation of the developing serotonergic neurotransmission in the semi-precocial rodent Octodon degus. 1642 27

We have investigated if treatment with two different PAHs such as naphthalene (NAP) and benzo(a)pyrene (BaP), and the PAH-like compound beta-naphthoflavone (BNF), may modify the stress responses elicited in rainbow trout by acute or prolonged stress stimuli, and the possible involvement of brain monoamines in those responses. Two experiments (acute and prolonged stress) were performed. In the acute stress experiment, fish were i.p. injected with vegetable oil alone (control) or oil containing NAP, BNF or BaP (10 mg kg(-1)), and 72 h after injection fish were acutely stressed by chasing for 15 min. In the prolonged stress experiment, a similar group-design and injection protocol were followed, but fish were submitted to severe confinement stress by maintaining fish under high stock density (70 kg fish mass m(-3)) for 72 h. The levels of cortisol, glucose and lactate were assayed in plasma. In addition, the contents of dopamine (DA), noradrenaline (NA) and serotonin (5HT), as well as their oxidized amine metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxy-3-indoleacetic acid (5HIAA) were assayed in telencephalon, hypothalamus, preoptic region, optic tectum and brain stem, as well as the pituitary. Both acute and prolonged stress stimuli increased plasma levels of cortisol, which further increase with NAP and BNF treatments after acute stress. In contrast, cortisol levels of fish exposed to prolonged stress showed a clear tendency to decrease after the treatment with BNF and BaP. Stress stimuli also increased plasma glucose levels, which were not affected by PAHs in acute stressed fish but decreased in fish exposed to prolonged stress. Increased plasma levels of lactate in fish exposed to stress decreased after PAHs treatment in acute stress but not in prolonged stress. With respect to monoaminergic systems, major changes induced by both acute and prolonged stress were increases of the metabolites DOPAC and 5HIAA and DOPAC/DA or 5HIAA/5HT ratios in several brain regions. PAHs induced alterations in the normal responses of monoaminergic systems to stress, with dopaminergic system being the most affected after acute stress, and serotonergic system after prolonged stress. Those alterations, especially after prolonged stress, showed certain parallelism with alterations of plasma cortisol levels. Thus, results suggest that in stressed fish PAH effects on plasma cortisol levels (and its derived metabolic actions) could be in part mediated by alterations on the monoaminergic systems at the CNS of rainbow trout.
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PMID:Acute and prolonged stress responses of brain monoaminergic activity and plasma cortisol levels in rainbow trout are modified by PAHs (naphthalene, beta-naphthoflavone and benzo(a)pyrene) treatment. 1818 48

The urocortin (Ucn) family of neuropeptides is suggested to be involved in homeostatic coping mechanisms of the central stress response through the activation of corticotropin-releasing factor receptor type 2 (CRFR2). The neuropeptides, Ucn1 and Ucn2, serve as endogenous ligands for the CRFR2, which is highly expressed by the dorsal raphe serotonergic neurons and is suggested to be involved in regulating major component of the central stress response. Here, we describe genetically modified mice in which both Ucn1 and Ucn2 are developmentally deleted. The double knockout mice showed a robust anxiolytic phenotype and altered hypothalamic-pituitary-adrenal axis activity compared with wild-type mice. The significant reduction in anxiety-like behavior observed in these mice was further enhanced after exposure to acute stress, and was correlated with the levels of serotonin and 5-hydroxyindoleacetic acid measured in brain regions associated with anxiety circuits. Thus, we propose that the Ucn/CRFR2 serotonergic system has an important role in regulating homeostatic equilibrium under challenge conditions.
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PMID:Urocortin-1 and -2 double-deficient mice show robust anxiolytic phenotype and modified serotonergic activity in anxiety circuits. 2001 Aug 91


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