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

Recent evidence has suggested the involvement of the GABAergic system in depression and in the mechanism of action of somatic antidepressant treatments. In particular, GABAB receptors have been found to be increased in the rat frontal cortex following chronic antidepressant therapies. In the present study, the sensitivity of GABAB binding sites was assessed in nine healthy men and 10 depressed patients via the plasma growth hormone (GH) response to acute baclofen administration (20 mg p.o.). Depressed subjects were tested before and after 15 and 35 days of treatment with amitriptyline (100 mg/day), imipramine (100 mg/day) and fluoxetine (20 mg/day). GH response to acute GABAB receptor activation did not differ between depressed subjects and healthy controls. Moreover, chronic antidepressant treatment did not significantly modify this response, even when a clear therapeutic effect was obtained. These results do not support the idea that GABAergic mechanisms are involved in the pathophysiology of depression and in the mechanism of action of antidepressant drugs.
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PMID:GABA, depression and the mechanism of action of antidepressant drugs: a neuroendocrine approach. 217 69

Abnormal growth hormone (GH) responses have been observed after several neuroendocrine challenge tests. In the present study, we examined the relationship between GH response after clonidine and insulin administration within the same subject to see if consistent response patterns were evident. Though there was a significant reduction in the mean GH response after clonidine (p = 0.0002), similar differences were not observed after insulin (p = 0.10). Furthermore, there were no apparent within-subject correlations for GH response between the clonidine and insulin challenge tests. Although the present findings indicate an inherent variability in GH response patterns after different neuroendocrine challenge tests, it appears from prior studies that GH may be more consistently blunted after clonidine in depression when compared to other GH provocative tests.
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PMID:Comparison of growth hormone response after clonidine and insulin hypoglycemia in affective illness. 220 33

To investigate whether depression is a consequence of disturbed function in 5HT systems, neuroendocrine responses to infusions of the 5HT precursor L-tryptophan (LTP) were studied in patients and controls. After an overnight fast and 60 min bed rest, a solution of LTP (10 g/l) was infused intravenously to a dose of 100 mg/kg over 30 min. Circulating growth hormone (GH), prolactin (PRL), cortisol and tryptophan concentrations were followed from 60 min pre-infusion to 60 min post-infusion. GH responses were attenuated in 23 major depressives (DSM-III) compared with 22 controls and were almost absent in endogenous depressives (New-castle criteria). PRL responses were normal in depressives who had lost more than 3 kg body weight but attenuated in those who had not. GH and PRL responses did not correlate with each other. Reduced basal tryptophan concentrations and more rapid tryptophan clearance were observed in the depressives, but there were no correlations with GH or PRL responses. However, basal cortisol concentrations, which were raised in depressives with chronic psychosocial difficulties, were strongly and inversely predictive of PRL responses in depressives and controls. Blunted GH and PRL responses to LTP appear to be distinct abnormalities in depression which may relate to two processes; (1), an endogenous mechanism indicated by reduced GH responses, and (2), an impairment in 5HT systems, indicated by blunted PRL responses and perhaps caused by raised circulating cortisol or reduced tryptophan concentrations.
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PMID:A neuroendocrine study of 5HT function in depression: evidence for biological mechanisms of endogenous and psychosocial causation. 234 77

Biological research in depression has concentrated on 'endogenous' depressions and over the past 30 years has been guided by the amine theory. Neuroendocrine abnormalities in depression have been reported for over 20 years and include changes in the hypothalamic-pituitary-adrenal and thyroid axes, in growth hormone and prolactin secretion. As neurotransmitters regulate neuroendocrine secretion, inter-relationships between neurochemical and neuroendocrine abnormalities may provide a window for understanding the pathophysiology of depression. The availability of these biological markers for depression opens new possibilities for research in psychiatric diagnosis and for management.
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PMID:Neuroendocrine changes in depression. 241 36

Plasma levels of growth hormone (GH), free fatty acids (FFA) and glucose were measured in vagotomized (VgX) and sham-operated (VgS) control pigeons. In VgX pigeons, GH level was significantly lower whereas FFA and glucose levels were higher than in VgS pigeons. The depression in GH level in VgX pigeons has been attributed to the significantly high levels of norepinephrine (NE) and corticosterone in these Birds. The higher plasma FFA concentration in VgX pigeons was therefore due to adipokinetic hormonal action other than of GH. It has been suggested that the adrenocorticotrophic hormone (ACTH) and/or NE could have produced the increase in plasma FFA in VgX pigeons. The pronounced hyperglycemia seen in VgX pigeons has been attributed to catecholamine action in the absence of the vagal tone.
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PMID:Effect of vagotomy on plasma levels of growth hormone, free fatty acids and glucose in the pigeon. 241 92

Abnormalities in neuroendocrine regulation are widespread in depressive illness. In this article, abnormalities found in five different endocrine systems are evaluated. There has been a wide-spread use of the dexamethasone suppression test in investigation of depressed patients. Use of this test as a diagnostic test for melancholia may be confounded because abnormalities are found in overlapping illnesses such as Alzheimer's disease or anorexia nervosa as well as in a variety of other conditions such as fasting. However, this test has promise in monitoring clinical status in patients who have an abnormal DST. Abnormalities found in the TRH test and in growth hormone regulation are of limited use clinically, but point to underlying biologic abnormalities. Aberrent regulation of prolactin is now well established, but this hormone has been investigated to a limited extent and warrants further investigation. There is currently a good deal of interest in the pineal hormone melatonin. Reduction in the normal nocturnal peak is found in depressed patients and there is an increase in nocturnal melatonin levels found in patients during treatment with desipramine. Bipolar patients are reported to be abnormally sensitive to melatonin suppression by light. This finding points to the abnormality in the photoperiodic regulation of the pineal output in these patients. Further refinement of neuroendocrine approaches to the investigation of depression should be very productive.
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PMID:Psychoneuroendocrinology of depression. 250 40

The neuroendocrinology of bulimia nervosa has only recently been investigated, with initial research suggesting some biological overlap with both anorexia nervosa (AN) and depression. Similarities among AN, depression, and bulimia include a nonsuppressed Dexamethasone Suppression Test and an abnormal growth hormone (GH) response to thyrotropin-releasing hormone (TRH). Bulimics and anorectics both tend to have a delayed thyrotropin (TSH) response to TRH and elevated basal GH levels. Bulimics, however, have a normal GH response to clonidine, a nonblunted TSH response to TRH, low basal prolactin (PRL) levels, and may have an exaggerated PRL response to TRH. Unpublished data suggest bulimics may have a gonadotropin profile distinct from either AN or depression, as well as a variety of other endocrinopathies. Although many of these abnormalities may reflect malnutrition despite normal weight, other factors that are as yet unidentified are likely to be contributing to the neuroendocrine abnormalities seen in bulimia.
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PMID:Neuroendocrine profile in bulimia nervosa. 252 54

In order to evaluate the possible effect of glucocorticoids as neuromodulators of the hypothalamic-pituitary-somatotropic system in depression, cortisol, growth hormone (GH), and insulin-like growth factor I (IGF-I) concentrations were studied before and after oral administration of 1 mg dexamethasone at 11 p.m. in 16 patients during depression and after recovery and in 28 healthy controls. While there were no significant differences in GH and IGF-I levels between depressed, recovered and control subjects, GH and IGF-I concentrations of cortisol non-suppressors were significantly elevated compared to suppressors. Moreover, post-dexamethasone cortisol, GH, and IGF-I levels were positively correlated. Dexamethasone had a stimulating effect on GH and IGF-I values in patients during depression and in cortisol non-suppressors only; this effect was absent in recovered and in control subjects and in cortisol suppressors. Thus, hypercortisolemia may be of great importance for the dysregulation of the hypothalamic-pituitary-somatotropic system reported in depression.
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PMID:Effects of glucocorticoids on the regulation of the hypothalamic-pituitary-somatotropic system in depression. 252 80

Growth hormone (GH) response to clonidine and growth hormone-releasing hormone (GHRH) stimulation, together with baseline somatomedin C (SmC) levels, were examined in parallel in a group of 21 patients with anorexia nervosa (AN) and in 10 controls. In addition, the Hamilton Rating Scale for Depression (HRS) was administered to the patients. Clonidine (2.5 micrograms/kg body weight, iv) induced GH elevations that were not significantly different between patients and controls. In contrast, GHRH (1 microgram/kg body weight, iv) produced a significantly higher GH response in anorectics than in controls. The ratio between GH responses (area under the curve, or AUC) to GHRH and to clonidine was significantly higher in patients than in controls. Baseline SmC levels (6 patients) were significantly lower in anorectics than in controls. Minor depressive symptomatology was present in all patients. When viewed in relation to the GH hyperresponsiveness to GHRH, the apparent normality of the response to clonidine in anorectics reflects the existence of an actual alpha 2-adrenoceptor subsensitivity. As clonidine reportedly acts via release of endogenous GHRH, an excessive, rather than a normal, GH response to clonidine was to be anticipated.
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PMID:Alpha 2-adrenoceptor sensitivity in anorexia nervosa: GH response to clonidine or GHRH stimulation. 253 61

Alterations in peripheral blood leukocyte distribution in major depression, including leukocytosis, neurotrophilia and lymphopenia, have been described. To assess peripheral white blood cells and the hypothalamic-pituitary (HP) axis in drug-free patients with major depression, we measured the total white blood cell count (WBC), and percentage of lymphocytes, and the plasma levels of cortisol, adrenocorticotropic hormone (ACTH), growth hormone (GH) and prolactin (PRL). Twenty male patients with major depression had relative lymphopenia and leukocytosis when compared with 20 age, sex and racematched control subjects. Elevated Beck and Hamilton depression scores correlated with a decreased percentage of lymphocytes, in a group of all subjects combined. There was a weak tendency for elevated growth hormone to correlate with relative lymphopenia in the control subjects only. Relative lymphopenia and leukocytosis may be a part of the psychobiology of major depression.
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PMID:Peripheral white blood cells and HPA axis neurohormones in major depression. 254 Oct 94


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