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)

The assessment of cortisol in saliva has been proven a valid and reliable reflection of the respective unbound hormone in blood. In the present study, a standard dexamethasone suppression test (DST) with measures of salivary cortisol levels was performed in bulimic women without depression (DSM-IV; N=48) and healthy controls (N=24) matched for age. Feedback sensitivity was assessed using the standard DST with pre- and post-measures of salivary cortisol. Subjects were divided into suppressors and nonsuppressors according to their post-DST levels. Bulimic suppressors and nonsuppressors were compared for their basal cortisol levels, body weight (body mass index, BMI), previous episodes of anorexia nervosa, and their results in psychometric tests. A total of 16 (33.3%) out of 48 women with bulimia nervosa (BN) failed to suppress in the DST. Basal salivary cortisol levels were elevated in bulimic nonsuppressors. Significant differences between suppressors and nonsuppressors were found for body weight and previous episodes of anorexia nervosa. The results are in accordance with recent findings. They support the hypothesized association between low body weight and DST nonsuppression. Using saliva cortisol in the standard DST could be advantageous for studying bulimic patients. Furthermore, the results show the importance of determining HPA reagibility when measuring cortisol in bulimic patients.
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PMID:Dexamethasone suppression test using saliva cortisol measurement in bulimia nervosa. 1123 85

To explore the mechanisms mediating the effects of acute morphine on the immune system, effects of ganglionic blockade with chlorisondamine on acute high dose morphine-induced alterations in blood lymphocyte proliferation, white blood cell counts, spleen lymphocyte proliferation and splenic natural killer (NK) cell cytolytic activity were examined in male Sprague--Dawley rats. Two hours after morphine (30 mg/kg, s.c.) administration, blood lymphocyte proliferation (ConA) was decreased 85%; this effect was antagonized by chlorisondamine (5 mg/kg, i.p.). Notably, however, such morphine exposure did not significantly decrease splenic lymphocyte proliferation, although depression of NK cell activity was also evident and appeared to be chlorisondamine-sensitive. Immune effects of morphine 1 h after treatment were somewhat different. In this case, blood lymphocyte proliferation decreased and plasma levels of corticosterone increased, with ED(50) values of 2.2 and 7.8 mg/kg, respectively. Splenic lymphocyte proliferation and NK activity were also significantly depressed in the 1-h exposure paradigm, but only after administration of 30 mg/kg morphine. These results indicate that chlorisondamine blocks the effects of relatively high doses of morphine on blood lymphocyte activity and indicate that blood lymphocyte proliferation is more sensitive to effects of acute morphine exposure than splenic lymphocyte proliferation, NK cell cytolytic activity and activation of the HPA axis.
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PMID:Reversal of acute effects of high dose morphine on lymphocyte activity by chlorisondamine. 1124 70

Neuroendocrinology of chronic stress seems to be characterized by HPA axis hyperactivity and early childhood stressors have been hypothesized to predispose individuals to adult onset depression by means of dysregulation of the HPA axis. Pivagabine (PVG), a hydrophobic 4-aminobutyric acid derivative, has been used experimentally recently in the treatment of different disorders related to stress-maladaptation, because of its possible inhibitory action on corticotrophin releasing factor secretion and HPA axis function. In the present study, 20 healthy male subjects were each exposed twice to the same psychosocial stressor (stroop color-word interference task, public speaking and mental arithmetic in front of an audience) during a first session (day 1) and a second session (day 8). Plasma concentrations of norepinephrine (NE), epinephrine (EPI), adrenocorticotropic hormone (ACTH) and cortisol (CORT), heart rate (HR) and systolic blood pressure (SBP) were measured immediately before the beginning of the tests and at their end, 30 min later, on both experimental days. Utilizing a double blind schedule, the subjects received pivagabine (900 mg, twice a day)(PVG group: nine subjects) or placebo (PBO group: 11 subjects) during the 7 days between the two stress sessions. NE, EPI, ACTH, and CORT levels were significantly elevated after stress exposure on day 1 and day 8 in PBO group subjects. After PVG treatment, on day 8, ACTH, CORT, NE and EPI responses to stress were significantly blunted, together with HR and SBP, in PVG group subjects. These results add to the evidence concerning PVG capacity to inhibit the HPA axis in humans, in response to stressful stimuli, and suggest that the action of PVG may be mediated not only by GABAergic receptors, but also by the suppression of catecholamines response. PVG treatment could modulate HPA hyper-responsiveness to stress in subjects with negative affectivity and depressive traits.
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PMID:Pivagabine effects on neuroendocrine responses to experimentally-induced psychological stress in humans. 1128 80

Corticotropin-releasing hormone (CRH) has been implicated in the regulation of a wide range of behaviors including arousal, motor function, feeding, and reproduction. Because depressed patients are often hypercortisolemic and intracerebroventricular administration of CRH to experimental animals produces a syndrome reminiscent of depression, dysregulation of this compound has been suggested to be involved in the pathogenesis of depressive and anxiety disorders. Studies of cerebrospinal fluid CRH levels and clinical neuroendocrine tests in patients with anxiety and affective disorders have supported this hypothesis. This review discusses these neuroendocrine findings in melancholic and atypical depression as well as post-traumatic stress disorder (PTSD). Overall, the data suggest that melancholic depression is characterized by hyperactive central CRH systems with overactivity of the pituitary-adrenal (HPA) axis. On the other hand, atypical depression is characterized by hypoactive central CRH systems and accompanying underactivity of the hypothalamic-pituitary-adrenal axis. Furthermore, the neuroendocrinology of PTSD appears to be unique, in that patients have hyperactive central CRH systems with underactivity of the pituitary-adrenal axis.
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PMID:Corticotropin-releasing hormone in depression and post-traumatic stress disorder. 1133 99

In depression and aging an increase in nocturnal cortisol secretion and a blunted nocturnal growth hormone (GH) surge have been described. In normal young men, growth hormone-releasing hormone (GHRH) promotes GH release and reduces plasma cortisol. Here, we examined whether GHRH could help to restore sleep-endocrine regulation in patients with depression and aging. GHRH (4x50 microgram, at 2200, 2300, 2400 and 0100 h) or saline (placebo) was injected intravenously to 42 patients with depression (19 females, 23 males) and matched controls (age range 19-76 years). Blood samples were withdrawn at 20 min intervals between 2200-0700 h and analysed using Manova (D.F. 1, 72). Patients compared to controls had significantly higher levels of ACTH and cortisol, particularly during the first half of the night (F=9 and F=11.8, each p<0.05). GHRH reduced ACTH during the first and cortisol secretion during the second half of the night in males, regardless of diagnosis, but enhanced it in females (F=5.1 and F=4.0, each p<0.05). ACTH and cortisol secretion were inversely related to NREM and stage 2 sleep in patients (r= -0.42, -0.42 and r= -0.36, -0.39, respectively, each p<0.05) but not in controls. Our data suggest that: 1) female gender, depression and aging add-on to enhance HPA activity, and 2) hyperactivity of the HPA system and the decrease in NREM and in particular stage 2 sleep in depression are interrelated. In men, GHRH can restore some of the sleep-endocrine alterations associated with depression and aging.
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PMID:Sexually dimorphic effects of GHRH on sleep-endocrine activity in patients with depression and normal controls - part II: hormone secretion. 1138 95

Increased plasma cortisol in patients with major depression is a well documented finding, although it is present in only 25-30% of subjects with major depression. However, ACTH and cortisol are secreted in a pulsatile manner, so it is unclear if increased ACTH secretion occurs in depression and if there are changes in the pulsatile components of ACTH secretion. Ten-minute sampling for ACTH and cortisol was performed for 24 hr in 25 premenopausal depressed women, whose age and menstrual cycle day matched control women. As a group, the depressed women demonstrated a trend to increase cortisol secretion (p = 0.089). There was no difference in mean cortisol between the patient group as a whole (8.36 +/- 2.9 microg/dl) and those patients meeting criteria for atypical depression (8.38 +/- 1.9 microg/dl), but patients meeting criteria for endogenous showed increased cortisol (12.17 +/- 4 microg/dl) Mean ACTH was not significantly different between patients and controls. Pulse analyses revealed similar number of secretory events and similar amplitudes for cortisol secretory bursts in patients and controls. The baseline component area under the curve of cortisol secretion was increased at a trend level (p =.064) in depressed patients, and the baseline AUC for ACTH was significantly increased in depressed patients (p =.045). No differences were found in pulsatile components of ACTH secretion between patients and matched controls. Harmonic analyses indicated no significant differences between patients and controls on any detected rhythm for ACTH or cortisol. These data suggest that the pulsatile and circadian components of the HPA axis are normal in premenopausal depressed women and that only 24% of depressed women demonstrate hypercortisolemia.
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PMID:Twenty-four-hour ACTH and cortisol pulsatility in depressed women. 1185 Jan 57

The mother in this case study had numerous known risk factors for postpartum depression and was in rehabilitation for drug abuse. She was crying at 2 hours postbirth and expressing feelings of sadness as her baby was being unwrapped for her first kangaroo care (KC) experience. Thereafter, during our research protocol, her self-reported depression scores decreased rapidly and had disappeared by 32 hours postbirth. A benefit of KC requiring systematic study is that KC may lessen maternal depression. There is new knowledge that some functions of the maternal HPA axis become dampened during the last trimester of pregnancy as the placenta increases its secretion of corticotrophin-releasing hormone. The sudden loss of the placenta following delivery, accompanied by a suppressed HPA axis, may have an effect on mood during the immediate postpartum period. Perhaps appropriate reactivation of the maternal HPA axis can be triggered following birth by the stimulation inherent in KC, thereby minimizing risk for postpartum depression.
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PMID:Kangaroo (skin-to-skin) care with a postpartum woman who felt depressed. 1145 67

There is considerable evidence for a unitary and dimensional view of the genetic vulnerability to symptoms of anxiety and depression. The GENESiS (Genetic Environmental-Nature of Emotional States in Siblings) Study aims to use a multivariate approach to detect genetic loci that contribute to individual differences in this vulnerability dimension. The study used the UK General Practice Research Framework to generate a community-based sample of siblings. Questionnaire measures of anxiety/depression included the short form of the neuroticism scale from the revised Eysenck Personality Questionnaire (EPQ-N), the General Health Questionnaire (GHQ-12), and the anxious arousal and high positive affect subscales from the Mood and Anxiety Symptoms Questionnaire (MASQ-AA and MASQ-HPA). Genetic model-fitting of 2658 unselected sibships provided evidence for a single common genetic (familial) factor that accounted for a substantial proportion of the genetic variances and covariances of these four measures. Using the parameter estimates of this model, we constructed a composite index of this common genetic factor. This index, which has a sib correlation of 0.22, will be used as a quantitative phenotype in the molecular genetic phase of GENESiS.
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PMID:GENESiS: creating a composite index of the vulnerability to anxiety and depression in a community-based sample of siblings. 1146 53

Corticotropin-releasing hormone (CRH) is a key neuroendocrine factor implementing endocrine, immune and behavioral responses to stress. CRH exerts its action through two major receptors, CRH-R1 and CRH-R2. Recently novel non-peptidic antagonists directed against CRH-R1 or CRH-R2 have been proposed as promising agents in the treatment of depression, anxiety and eating disorder. However, so far the CRH-receptor system has not been widely studied in humans. Therefore, we employed quantitative TaqMan PCR to analyze the expression and distribution of both CRH-R1 and CRH-R2 in human brain tissue and peripheral organs. Furthermore the expression of CRH receptors was analyzed for the first time in pituitaries of suicide victims by in situ hybridization and quantitative PCR. Our data demonstrated a different expression pattern in humans as compared to rodents. Both CRH-R1 and CRH-R2 were expressed in high amounts in the brain with the strongest expression in the pituitary. As described in rodents, however the CRH-R1 in human was the predominant receptor in the brain (82.7 +/- 11.0%), whilst CRH-R2 was the predominant receptor in peripheral organs (77.0 +/- 15.8%). There was a shift in the ratio of CRH-R1/R2 in the pituitaries of suicide victims. In conclusion, both CRH-R1 and CRH-R2 are widely expressed in human tissues with a distribution substantially different from rodents. Strong expression of both CRH-R1 and CRH-R2 in human pituitaries suggests that particularly under stress, activation of the HPA axis can be maintained through both receptors.
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PMID:Expression of corticotropin releasing hormone receptors type I and type II mRNA in suicide victims and controls. 1152 68

In the present study we investigated HPA axis activity in depressed patients treated with partial sleep deprivation (PSD) in order to identify endocrinological characteristics related to PSD responsiveness. Thirty-three drug-free patients (14 men, 19 women) suffering from major depression according to DSM-IV criteria were treated with PSD. Response to PSD was defined as a reduction of at least 30% according to the 6-item version of the Hamilton Depression Scale (6-HAMD). Subsequently, the combined dexamethasone-suppression/CRH-stimulation test (DEX/CRH test) was performed. Patients were pretreated with 1.5 mg dexamethasone (DEX) at 23:00 h and challenged with 100 microg corticotropin-releasing hormone (CRH) the following day. Postdexamethasone cortisol concentrations (before CRH administration) served as parameters for the DST status (dexamethasone suppression test). The cortisol stimulation after CRH was used as measurement for the DEX/CRH test status. Of the depressive patients, 54.5% (18 out of 33) responded to PSD. DST suppressors (postdexamethasone cortisol levels < 15 ng/ml) showed a significantly greater reduction in 6-HAMD scores after PSD than DST nonsuppressors. Furthermore, a significant negative correlation between postdexamethasone cortisol levels and reduction in 6-HAMD scores after PSD could be established. However, there was no relationship between the cortisol stimulation following CRH challenge and response to PSD. Although the combined DEX/CRH challenge test is a more sensitive marker for HPA axis dysregulation in depression than the standard DST, the negative feedback of the HPA system reflected by the DST status is apparently more closely associated with response to partial sleep deprivation in major depressive disorder.
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PMID:Sleep deprivation and hypothalamic-pituitary-adrenal (HPA) axis activity in depressed patients. 1157 42


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