Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study evaluates and describes disease-related distress in parents, with particular focus on the association between the time elapsed since the child's cancer diagnosis and a number of indicators of distress. In a cross-sectional design, 264 mothers and fathers of children with various malignancies completed a multidimensional questionnaire focusing on 11 illness-specific and general indicators of distress. Parents were assessed from 4 weeks to 14 years after the child's diagnosis, and age of children at onset of illness ranged from newly born to 21 years (mean approximately 6 years). The levels of distress related to loss of control, self-esteem, anxiety, depression, sleep disturbances, and psychological and physical distress were lower among parents for whom a longer period of time had elapsed from the time of diagnosis. However, the time elapsed could not explain all of the variation in these stress reactions, or any of the variation in uncertainty, disease-related fear and loneliness. The child's age at diagnosis and treatment situation at assessment were surpassed by time elapsed since diagnosis as predictors of variance in parental distress. The pattern observed indicates the presence of disease-related distress even years after the completion of medical treatment. The findings point to the need for research to identify parents at particular risk of suffering long-term harmful consequences from the prolonged stress of parenting a child with cancer. The necessity of longitudinal studies to evaluate the proportion of acute stress in relation to chronic or cumulative parental stress is emphasized.
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PMID:Disease-related distress in parents of children with cancer at various stages after the time of diagnosis. 1280 Nov 32

Accumulating evidence indicates that neural activity in the lateral septum (LS) influences the pathophysiology of depression and therapeutic effectiveness of antidepressant drugs. For example, the development of behavioral deficits in animal screens for antidepressant drug activity corresponds with a blunting of LS activity, whereas chronic treatment with antidepressants enhances cell firing in the LS; however, the molecular mechanisms underlying such behavioral functions of the LS have not been determined. The nonreceptor tyrosine kinase Pyk2 is highly expressed in the LS and plays important roles in regulating cellular excitability and synaptic plasticity, making it an attractive candidate for regulating the effects of stress and antidepressants on LS functioning and behavior. We provide evidence that stress decreases Pyk2 phosphorylation in the LS, whereas enhancing Pyk2 expression in LS neurons has an antidepressant effect behaviorally.Pyk2 messenger ribonucleic acid (mRNA) expression in the rat forebrain was detected by in situ hybridization, and a brief description of the distribution of Pyk2 mRNA in selected areas is presented. Levels of total Pyk2 protein and phosphorylated Pyk2 were subsequently measured in the LS and hippocampus following stress exposure, as were levels of extracellular stimuli-regulated kinase (Erk) and phospho-Erk. Herpes simplex virus (HSV)-mediated gene transfer was then used to enhance Pyk2 expression in the LS, and the effect this had on behavior in the learned helplessness model of depression was evaluated. High levels of Pyk2 mRNA were detected in a number of forebrain regions, including the hippocampus and LS. Following acute stress exposure, subjects showed a decrease in phosphorylated Pyk2 and Erk in the LS but not in the hippocampus. Total levels of Pyk2 and Erk remained unchanged following stress. In the learned helplessness paradigm, injection of HSV-Pyk2 into the LS prevented the active avoidance deficit caused by exposure to inescapable shock, indicative of an antidepressant effect. These results indicate that following acute stress, Pyk2 and Erk activity in the LS are decreased, whereas experimentally increasing Pyk2 activity in LS neurons reverses the behavioral deficits of acute, inescapable stress. These findings establish a role for the tyrosine kinase Pyk2 in the biochemical and behavioral responses to stress and suggest a possible role in the pathophysiology of depression, particularly notable considering Pyk2's role in promoting synaptic plasticity.
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PMID:Antidepressant effect of the calcium-activated tyrosine kinase Pyk2 in the lateral septum. 1294 83

We studied the effects of single peroral treatment with antibodies against S100 protein and delta sleep-inducing peptide in ultralow doses on behavioral characteristics of rats with anxious depression produced by acute stress (unavoidable electrical shock). Stress-produced behavioral changes and anxiolytic activity of antibodies were determined using the elevated plus-maze, open field, and tail suspension tests. High efficiency of the mixture of antibodies against S100 protein and delta sleep-inducing peptide was observed in all tests. Anxiolytic activity of anti-S100 antibodies (although less pronounced than that of the mixture of antibodies) was revealed in the elevated plus-maze and tail suspension test.
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PMID:Efficiency of ultralow doses of antibodies to S100 protein and delta sleep-inducing peptide in rats with anxious depression. 1294 37

This study examined the prevalence of peritraumatic and persistent panic symptoms following trauma. Survivors of civilian trauma (n=30) with either acute stress disorder (ASD) or no acute stress disorder (non-ASD) were administered the Panic Module of the Structured Clinical Interview for DSM-IV (SCID). Participants also completed the Impact of Event Scale, Acute Stress Disorder Scale, Beck Depression Inventory, Beck Anxiety Inventory, and the Anxiety Sensitivity Index. Panic attacks were experienced by 77% of participants during their trauma, and 47% reported recurrent panic attacks post-trauma. ASD participants demonstrated more panic symptoms during and after their trauma than non-ASD participants. Posttraumatic panic was most strongly associated with anxiety sensitivity. These findings are discussed in terms of cognitive factors that may mediate posttrauma panic and treatment implications for managing posttraumatic anxiety. There is increasing evidence that panic attacks play a role in psychopathological response to trauma. A significant proportion of people with panic disorder report a history of trauma (). Moreover, two-thirds of trauma survivors report panic attacks within the previous 2 weeks (). There is also evidence that people with posttraumatic stress disorder (PTSD) display elevated levels of anxiety sensitivity (). Recent attention has focused on acute panic reactions because of proposals that panic during trauma may condition trauma-related cues to subsequent panic (). There is evidence that panic attacks occur in 53-90% of trauma survivors during the traumatic experience (). Further, people with acute stress disorder (ASD) are more likely to report peritraumatic panic attacks than non-ASD individuals. ASD is a useful framework in which to investigate the role of panic in posttraumatic stress because ASD describes acute responses to trauma that are strongly predictive of chronic PTSD (). This study investigated the relationship between peritraumatic panic and ongoing panic attacks following trauma. Specifically, we indexed panic attacks during trauma and subsequent to trauma in trauma survivors with and without ASD. We also indexed the extent to which distorted interpretations about somatic sensations may be associated with panic attacks following trauma. We considered that the strong evidence that maladaptive appraisals of somatic sensations mediate panic () is directly relevant to posttraumatic panic. We hypothesized that ASD participants would report more peritraumatic and persistent panic than non-ASD participants, and that this panic would be associated with dysfunctional interpretations about somatic stimuli.
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PMID:Peritraumatic and persistent panic attacks in acute stress disorder. 1297 43

Nerve growth factor (NGF) has several effects on the central nervous system; on the one hand NGF fosters survival and function of cholinergic neurons of the basal forebrain, on the other hand this protein is implicated in the stress response of the hypothalamic-pituitary-adrenocortical axis (HPAA). In this study we tested the influence of threatening and painful stress treatments in three different intensities as well as forced motoric activity on NGF content in different brain areas in adult rats. We found that threatening treatment with or without painful stimuli was followed by a significant decrease of NGF concentration in the amygdala (44.5%; P=0.03) and the frontal cortex (-45.5%; P=0.02). We also observed that after stress of forced motoric activity NGF content in the frontal cortex (-32%; P=0.01) and the hippocampus (-32%; P=0.006) was significantly reduced. Thus, NGF content in distinct brain regions is decreased, following different forms of acute stress. This might be relevant for the pathophysiological understanding of psychiatric diseases, such as depression, which are associated with stress.
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PMID:Effects of different kinds of acute stress on nerve growth factor content in rat brain. 1449 65

Gestational stress (GS) produces profound behavioural impairments in the offspring and may permanently programme hypothalamic-pituitary-adrenal (HPA) axis function. We investigated whether or not GS produced changes in the maternal behaviour of rat dams, and measured depression-like behaviour in the dam, which might contribute to effects in the progeny. We used the Porsolt test, which measures immobility in a forced-swim task, and models depression in rodents, while monitoring maternal care (arched-back nursing, licking/grooming, nesting/grouping pups). Pregnant rats underwent daily restraint stress (1 h/day, days 10-20 of gestation), or were left undisturbed (control). On post-parturition days 3 and 4, dams were placed into a swim tank, and time spent immobile was measured. GS significantly elevated immobility scores by approximately 25% above control values on the second test day. Maternal behaviours, in particular arched-back nursing and nesting/grouping pups, were reduced in GS dams over post-natal days 1-10. Adult offspring showed increased immobility in the Porsolt test, and also hypersecreted ACTH and CORT in response to an acute stress challenge. These data show that GS can alter maternal behaviour in mothers, and this might contribute to alterations in the offspring. GS may be an important factor in maternal post-natal depression, which may in turn detrimentally effect the offspring because depressed mothers do not sufficiently care for their offspring.
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PMID:Gestational stress induces post-partum depression-like behaviour and alters maternal care in rats. 1460 3

Mental stress and depression are characterized by a hypercoagulable state, which might mediate the increased coronary risk in individuals who feel stressed or depressed. Changes in blood coagulation and fibrinolysis with stress and depression are largely mediated by the sympathetic nervous system via catecholamine and adrenergic receptor activity. Stress might also affect coagulation activity via an influence on the regulation of genes coding for coagulation and fibrinolysis molecules. There is some evidence that non-selective beta-blocking agents decrease hypercoagulability elicited by acute stress. The selective serotonin reuptake inhibitors appear to normalize increased platelet activity in depression. Prospective studies need to show whether there is an association between coagulation abnormalities in stress and depression with hard cardiovascular end-points and whether such an association is favorably affected by therapeutic interventions (e.g., medication, psychotherapy, stress management).
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PMID:[Changes in blood coagulation in stress and depression--from evolution to gene regulation]. 1466 6

Acute stress suppresses new cell birth in the hippocampus in several species. Relatively little is known, however, on how chronic stress affects the turnover, i.e. proliferation and apoptosis, of the rat dentate gyrus (DG) cells, and whether the stress effects are lasting. We investigated how 3 weeks of chronic unpredictable stress would influence the structural dynamic plasticity of the rat DG, and studied newborn cell proliferation, survival, apoptosis, volume and cell number in 10-week-old animals. To study lasting effects, another group of animals was allowed to recover for 3 weeks. Based on two independent parameters, bromodeoxyuridine (BrdU) and Ki-67 immunocytochemistry, our results show that both chronic and acute stress decrease new cell proliferation rate. The reduced proliferation after acute stress normalized within 24 h. Interestingly, chronically stressed animals showed recovery after 3 weeks, albeit with still fewer proliferating cells than controls. Apoptosis, by contrast, increased after acute but decreased after chronic stress. These results demonstrate that, although chronic stress suppresses proliferation and apoptosis, 3 weeks of recovery again normalized most of these alterations. This may have important implications for our understanding of the reversibility of stress-related hippocampal volume changes, such as occur, for example, in depression.
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PMID:Suppressed proliferation and apoptotic changes in the rat dentate gyrus after acute and chronic stress are reversible. 1475 Sep 71

The hippocampus, being sensitive to stress and glucocorticoids, plays significant roles in certain types of learning and memory. Therefore, the hippocampus is probably involved in the increasing drug use, drug seeking, and relapse caused by stress. We have studied the effect of stress with morphine on synaptic plasticity in the CA1 region of the hippocampus in vivo and on a delayed-escape paradigm of the Morris water maze. Our results reveal that acute stress enables long-term depression (LTD) induction by low-frequency stimulation (LFS) but acute morphine causes synaptic potentiation. Remarkably, exposure to an acute stressor reverses the effect of morphine from synaptic potentiation (approximately 20%) to synaptic depression (approximately 40%), precluding further LTD induction by LFS. The synaptic depression caused by stress with morphine is blocked either by the glucocorticoid receptor antagonist RU38486 or by the NMDA-receptor antagonist D-APV. Chronic morphine attenuates the ability of acute morphine to cause synaptic potentiation, and stress to enable LTD induction, but not the ability of stress in tandem with morphine to cause synaptic depression. Furthermore, corticosterone with morphine during the initial phase of drug use promotes later delayed-escape behavior, as indicated by the morphine-reinforced longer latencies to escape, leading to persistent morphine-seeking after withdrawal. These results suggest that hippocampal synaptic plasticity may play a significant role in the effects of stress or glucocorticoids on opiate addiction.
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PMID:Stress enables synaptic depression in CA1 synapses by acute and chronic morphine: possible mechanisms for corticosterone on opiate addiction. 1501 16

Activation of the brain noradrenergic system during acute stress is thought to play an important integrative function in coping and stress adaptation by facilitating transmission in many brain regions involved in regulating behavioral and physiologic components of the stress response. Compared with outbred control Sprague-Dawley (SD) rats, inbred Wistar-Kyoto (WKY) rats exhibit an exaggerated hypothalamic-pituitary-adrenal (HPA) response as well as increased susceptibility to certain forms of stress-related pathology. However, we have also shown previously that WKY rats exhibit reduced anxiety-like behavioral reactivity to acute stress, associated with reduced activation of the brain noradrenergic system. Thus, to understand better the possible neurobiological mechanisms underlying dysregulation of the stress response in WKY rats, we investigated potential strain differences in stress-induced neuronal activation in brain regions that are both involved in regulating behavioral and neuroendocrine stress responses, and are related to the noradrenergic system, either as targets of noradrenergic modulation or as sources of afferent innervation of noradrenergic neurons. This was accomplished by visualizing stress-induced expression of Fos immunoreactivity in the paraventricular nucleus of the hypothalamus, lateral bed nucleus of the stria terminalis, central nucleus of the amygdala, and medial nucleus of the amygdala (MeA), as well as the noradrenergic nucleus locus coeruleus (LC). Stress-induced Fos expression was found to be decreased in the LC and MeA of WKY rats compared with similarly stressed SD rats, whereas no strain differences were observed in any of the other brain regions. This suggests that strain-related differences in activation of the MeA may be involved in the abnormal neuroendocrine and behavioral stress responses exhibited by WKY rats. Moreover, as the MeA is both an afferent as well as an efferent target of the brainstem noradrenergic system, reduced MeA activation may either be a source of reduced noradrenergic reactivity seen in WKY rats, or possibly a consequence. Nonetheless, understanding the mechanisms underlying altered stress reactivity in models such as the WKY rat may contribute to a better understanding of stress-related psychopathologies such as depression, post-traumatic stress disorder or other anxiety disorders.
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PMID:Induction of FOS expression by acute immobilization stress is reduced in locus coeruleus and medial amygdala of Wistar-Kyoto rats compared to Sprague-Dawley rats. 1502 36


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