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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of acute footshock stress on the sensitivity of the isolated rat tail artery were studied. Footshock stress applied to male Wistar rats (200-300 g) causes subsensitivity to the vasoconstrictor effects of phenylephrine and epinephrine. No significant changes in the pA2 values of prazosin were detected, using epinephrine as the agonist. Footshock stress-induced subsensitivity to epinephrine was not affected by the calcium entry blocker nifedipine. However, nifedipine significantly depressed the maximum response to epinephrine in tail arteries isolated from acute footshock-stressed rats. The present results suggest that acute footshock stress-induced reduced sensitivity to phenylephrine and epinephrine may not be only related to events at the alpha-adrenoceptor level. The nifedipine-induced depression of the maximum response to epinephrine suggests a role for the calcium mobilization processes in the vascular responsiveness during acute stress.
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PMID:Effect of acute footshock stress on the responsiveness of the isolated rat tail artery to phenylephrine and epinephrine. 133 28

Stressors generally induce a depression of the hypothalamus-pituitary-testis (HPT) system, mediated by the activated hypothalamus-pituitary-adrenocortical (HPA) system, resulting in a fall in plasma luteinising hormone (LH) and testosterone levels. Hypothalamic gonadotrophin-releasing hormone (GnRH) secretion may be suppressed by endogenous opioid peptides (EOP) and/or corticosteroids. The latter dramatically enhance the negative feedback effects of testosterone on both the hypothalamus and pituitary. Pituitary gonadotrophin secretion may be reduced by adrenocorticotrophic hormone or by EOP of hypothalamic or pituitary origin. Decreases in plasma concentrations of testosterone, independent of gonadotrophins, can be induced by corticosteroids. These hormones might reduce the number of Leydig-cell LH-receptors or occupation of LH-receptors. Testicular steroidogenesis may also be inhibited by pro-opiomelanocortin-derived (opioid) peptides secreted by the Leydig cells. There are some indications of increases in LH and testosterone during acute stress and, in dominant male animals, during the stress of social conflict. The latter finding indicates a difference in stress response between dominant and subordinate males. In subordinate males, decreased feedback sensitivity may allow hypersecretion throughout the HPA system. As a result, corticotrophin releasing hormone may induce the release of EOP from the hypothalamus, which inhibit the HPT axis. This inhibition may be enhanced by a corticosteroid-induced decrease in testosterone feedback.
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PMID:Stress and the endocrine hypothalamus-pituitary-testis system: a review. 188 89

Although life events continue to be the major focus of stress research, recent studies suggest that chronic stress should be a more central focus. An evaluation of this issue is presented using data from a large community survey of married men (n = 819) and women (n = 936). Results show that chronic stresses are more strongly related to depressive symptoms than acute stresses in all but one life domain. The interaction patterns exhibited by chronic and acute stresses are predominantly associated with lower levels of depression than those predicted by a main effects model. This pattern suggests that chronic stresses may reduce the emotional effects of acute stresses. Although the processes through which this effect occurs are not clear, it is suggested that anticipation and reappraisal reduce the stressfulness of an event by making its meaning more benign. Implications for future research on chronic and acute stress effects are discussed.
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PMID:Chronic stress, acute stress, and depressive symptoms. 207 97

The present study contrasted the widely cited "buffer" model of social support with an alternative mediator model. Distinctions were drawn between the functions of social support under chronic vs. acute stress conditions, and between situation-specific stressors and major life events. Ongoing parenting stress was assessed in 96 mothers of deaf children and 118 matched controls. Tests of the competing models showed no moderating effects for social support. However, path analyses suggested that social support mediated the relationship between stressors and outcomes. Chronic parenting stress was associated with lowered perceptions of emotional support, and greater symptoms of depression and anxiety. Furthermore, parenting stress accounted for a substantial proportion of the variance in psychological distress scores in contrast to life event stress, which was only weakly related to psychological outcomes. The implications of mediational models for understanding adaptation to chronic stress are discussed.
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PMID:Chronic parenting stress: moderating versus mediating effects of social support. 228 93

An influence of early stimulation on sensitivity to acute stress in adulthood has been reported. The purpose of the present work was to determine the effect of exposure of male and female rats to three models of chronic stress (unpredictable stress, cold stress and handling) from day 2 to day 15 of life on behavioral and endocrine sensitivity to chronic stresses in adulthood. The chronic stresses applied in adulthood were a model of intermittent cold stress (daily 30-min sessions at -20 degrees C for 15 days) and the Katz's model of unpredictable chronic stress (15 days). Forced swim behavior and serum concentration of the stress-sensitive hormones, corticosterone and prolactin, were chosen to investigate stress sensitivity. It was found that all neonatal treatments stimulated body weight gain, did not cause infant mortality and did not affect forced swim behavior as adult. The repetitive exposure to cold stress in adulthood did not cause major impairment of forced swim behavior and did not affect basal levels of serum corticosterone and prolactin in either control or experimental rats. These findings support the view that repeated stressors can induce behavioral and endocrine adaptation in rats. The neonatal treatments did not affect this characteristic. The exposure of control rats to the unpredictable stress model severely impaired forced swim behavior and increased basal levels of serum corticosterone and prolactin. This observation conforms to the view that standard laboratory rats cannot adapt to unpredictable chronic stress. This has been reported to cause a behavioral depression syndrome comprising forced swim deficit and endocrine alterations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neonatal chronic stress induces subsensitivity to chronic stress in adult rats. I. Effects on forced swim behavior and endocrine responses. 238 47

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

Regulation of zinc metabolism by dibutyryl cAMP, glucagon, and epinephrine was examined in rats fed adequate amounts of zinc. Dibutyryl cAMP, epinephrine, and glucagon each produced an increase in liver metallothionein levels by 10 h after they were first administered. The increase in liver metallothionein was inversely related to the serum zinc concentration. Treatment with dexamethasone, a glucocorticoid, accentuated these effects to some extent. Both metallothionein I and II were induced by dibutyryl cAMP and glucagon. Levels of metallothionein mRNA in total liver RNA extracts were measured by dot blot hybridization using a synthetic 21-base oligonucleotide complimentary to the 5' region of both the metallothionein I and II genes. Individual administration of dibutyryl cAMP, glucagon, and epinephrine increased the number of metallothionein mRNA molecules per cell by up to fourfold. The data suggest that glucagon and epinephrine are primary regulators of metallothionein gene expression acting at least in part via cAMP. In adrenalectomized rats, glucagon, dibutyryl cAMP, and epinephrine had a less potent effect in terms of metallothionein induction and depression of serum zinc concentrations. These effects were largely restored when dexamethasone was also given. Collectively these data suggest that changes in zinc metabolism associated with acute stress involve coordinate regulation mediated by many factors, including glucocorticoids and cAMP.
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PMID:Coordinate regulation of zinc metabolism and metallothionein gene expression in rats. 302 99

Depression is the most common psychiatric problem encountered among patients with cancer. The acute stress response, which occurs at pivotal points during the course of illness, is normal. However, severe or protracted depressive symptoms should be evaluated and treated. The treatment of depression, which often involves a combined regimen of psychotherapy and psychopharmacologic intervention, can result in improved compliance with therapy, a greater tolerance for the disease and its outcome, and an improved quality of life.
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PMID:Managing depression in the patient with cancer. 311 69

The effect of two different types of acute stress (immobilization and fasting) on the polymorphonuclear leukocyte phagocytic function has been studied in male and female rats. With this aim, a subgroup of rats was under immobilization and fasting, another under complete energy deprivation and a third one (controls), exposed to the normal activity of the animal room, for 15 hours. The stress induction was assessed by controlling weight variations and gastric ulcers generation. Both stressors induced weight loss but only immobilization resulted in the development of gastric ulcer in all the animals studied. Phagocytosis was increased in male rats stressed by fasting and in immobilized female rats. In the remaining subgroups polymorphonuclear leukocyte cells showed a phagocytic capacity within the range of control values. Only comparison of the males group stressed by fasting with the male group stressed by fasting and immobilization showed a significant depression in phagocytosis.
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PMID:Effects of fasting and immobilization stresses on the phagocytic capacity of rat polymorphonuclear phagocyte monolayers. 359 41

Psychological factors have long been thought to play a contributing role in either the predisposition, onset or course of various physical illnesses. Recently, rapid advances in immunology have created interest in the interaction between psychosocial factors, behaviour and the immune system. This paper reviews some of the models proposed to explain the relationship between psychological variables and physical illness and presents evidence for a contribution of psychological factors to certain illnesses in which abnormalities in immunologic state are thought to be important. From a somewhat different perspective, animal studies have demonstrated complex effects of stress, on disease susceptibility. Recent human studies have demonstrated consistent immunologic changes in people undergoing acute naturally occurring psychological stress such as bereavement or an important examination. In humans, the effects of chronic stress may be different from acute stress, corresponding to the findings in animals. Abnormalities in immunologic functioning and physical illness are reviewed for different psychiatric disorders--depression, anorexia nervosa and schizophrenia; depression is the only disorder which consistently demonstrated immunologic changes. Possible mechanisms for the stress/immune-change relationship are suggested.
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PMID:Stress, immunity and illness--a review. 360 31


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