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

Late-onset ethanol (EtOH) consumption is related to life and social stressors of aging. The stress system (hypothalamic-pituitary-adrenal, HPA, axis) coordinates the adaptive response of the organism to stressors, but age-related deficits in HPA function seem to be associated with disorders such as late-onset EtOH consumption, anxiety and depression. In the present study, we examined whether HPA dysfunction is associated with stress-related EtOH consumption in aged rats and whether the treatment with nefazodone hydrochloride, a phenylpiperazine antidepressant, partially reverses the adverse effects of isolation (ISOL) stress. The animals were offered two-bottle choice consumption of 0.2% saccharin and 10% EtOH/0.2% saccharin, and then exposed to 4 days of ISOL stress on an irregular, unpredictable schedule. ISOL stress-induced increases in corticosterone secretion and EtOH consumption both during and following the stress (recovery period) in aged rats. Nevertheless, this effect at the recovery period was not evident in young stressed rats. Nefazodone caused a significant decrease in plasma corticosterone levels and EtOH consumption. The attenuation of stress-induced corticosterone by nefazodone was correlated with reduced EtOH consumption. These findings link the effect of ISOL stress to the induction of voluntary EtOH consumption following the end of the stressor and the limitation of aged HPA to down-regulated corticosterone.
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PMID:Effects of nefazodone on voluntary ethanol consumption induced by isolation stress in young and aged rats. 1215 Oct 45

Cushing's syndrome is due to chronic glucocorticoid excess that may have various etiologies. The most common endogenous form is pituitary-dependent bilateral adrenal hyperplasia, which is termed Cushing's disease. Major depression occurs in more than half of the cases. The presence of depressive symptoms connotes severity of clinical presentation and, in patients with hypothalamic-pituitary forms, entails prognostic value. Medical treatment may be used while awaiting more definitive solutions for the illness by surgery. The inhibitors of steroid production (e.g., ketoconazole, metyrapone and aminoglutethimide), rather than antidepressant drugs, are generally successful in lifting depression as well as other disabling symptoms. Since central serotonergic regulation could have a role in the course of Cushing's disease, serotonin antagonists (e.g., cyproheptadine, ritanserin and ketanserin) have been employed. Findings related to the pharmacological response of depression in Cushing's disease were found to have implications for the pathophysiology of depression and the potential involvement of the hypothalamic-pituitary-adrenal axis (HPA axis) in resistance and tolerance to antidepressant drugs. The use of serotonergic drugs in Cushing's disease may yield important insights in the understanding of serotonergic regulation both in Cushing's disease and in the HPA axis in nonendocrine major depression.
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PMID:Residual symptoms in depression an emerging therapeutic concept. 1236 51

From the author's direct involvement in clinical research, the conclusion has been drawn that clinically relevant long-term pain relieving effects of acupuncture (>6 months) can be seen in a proportion of patients with nociceptive pain. The mechanisms behind such effects are considered in this paper. From the existing experimental data some important conclusions can be drawn: 1. Much of the animal research only represents short-term hypoalgesia probably induced by the mechanisms behind stress-induced analgesia (SIA) and the activation of diffuse noxious inhibitory control (DNIC). 2. Almost all experimental acupuncture research has been performed with electro-acupuncture (EA) even though therapeutic acupuncture is mostly gentle manual acupuncture (MA). 3. Most of the experimental human acupuncture pain threshold (PT) research shows only fast and very short-term hypoalgesia, and, importantly, PT elevation in humans does not predict the clinical outcome. 4. The effects of acupuncture may be divided into two main components--acupuncture analgesia and therapeutic acupuncture. A hypothesis on the mechanisms of therapeutic acupuncture will include: 1. Peripheral events that might improve tissue healing and give rise to local pain relief through axon reflexes, the release of neuropeptides with trophic effects, dichotomising nerve fibres and local endorphins. 2. Spinal mechanisms, for example, gate-control, long-term depression, propriospinal inhibition and the balance between long-term depression and long-term potentiation. 3. Supraspinal mechanisms through the descending pain inhibitory system, DNIC, the sympathetic nervous system and the HPA-axis. Is oxytocin also involved in the long-term effects? 4. Cortical, psychological, "placebo" mechanisms from counselling, reassurance and anxiety reduction.
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PMID:Acupuncture mechanisms for clinically relevant long-term effects--reconsideration and a hypothesis. 1221 6

Cushing's syndrome is due to chronic glucocorticoid excess that may have various etiologies. The most common endogenous form is pituitary-dependent bilateral adrenal hyperplasia, which is termed Cushing's disease. Major depression occurs in more than half of the cases. The presence of depressive symptoms connotes severity of clinical presentation and, in patients with hypothalamic-pituitary forms, entails prognostic value. Medical treatment may be used while awaiting more definitive solutions for the illness by surgery. The inhibitors of steroid production (e.g., ketoconazole, metyrapone and aminoglutethimide), rather than antidepressant drugs, are generally successful in lifting depression as well as other disabling symptoms. Since central serotonergic regulation could have a role in the course of Cushing's disease, serotonin antagonists (e.g., cyproheptadine, ritanserin and ketanserin) have been employed. Findings related to the pharmacological response of depression in Cushing's disease were found to have implications for the pathophysiology of depression and the potential involvement of the hypothalamic-pituitary-adrenal axis (HPA axis) in resistance and tolerance to antidepressant drugs. The use of serotonergic drugs in Cushing's disease may yield important insights in the understanding of serotonergic regulation both in Cushing's disease and in the HPA axis in nonendocrine major depression.
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PMID:Erratum to "CNS drugs in Cushing's disease: pathophysiological and therapeutic implications for mood disorders" [Prog. Neuro-Psycol. Biol. Psychiatry, 26, 763 (2002)]. 1218 8

Macrophages produced proinflammatory cytokines and inflammatory responses can cause many symptoms of depression, including direct stimulation of the HPA axis and secretion of cortisol. In depressed patients, hypercortisolism has been well described as one of the major symptoms and also as the cause for hippocampal atrophy and memory impairment. In this paper, the relationships between thymectomy, increased IL-1 levels, and changes in corticosterone and neurotransmitter concentrations in rats are discussed, as well as their implications for memory impairments and depression. In thymectomized rats, deficits in both spatial and fear conditioned memory have been observed. Thymectomy decreases noradrenaline and dopamine levels, and increases serotonergic neurotransmission in limbic areas, without affecting corticosterone concentrations. In a depression model, thymopeptides or IL-2 treatment significantly attenuated changes in behavior, lymphocyte proliferation and neurotransmitters caused by bulbectomy. The reduction of thymic functions may increase IL-1 synthesis. Central IL-1beta administration impairs rat's spatial memory in the Morris water maze and 8 arms radial maze, but enhances conditioned memory in the passive avoidance. These changes can be reversed by either IL-1 receptor antagonist or a glucocorticoid receptor antagonist (RU 486). Furthermore, IL-1-induced changes in some neurotransmitter systems are similar to those observed in thymectomized rats. However, both acute and sub-chronic IL-1 administration increases plasma corticosterone concentrations. Together, these findings suggest that changes in the function of the thymus gland may play an important role in the unbalance between macrophages, cytokines, and lymphocytes, which induces neurotransmitter and neuroendocrine changes, and memory disturbances in depressive illness.
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PMID:The effect of thymectomy and IL-1 on memory: implications for the relationship between immunity and depression. 1240 69

The cytokine hypothesis of depression raises a certain number of questions. These questions include: the inability of the theory to account for the classical (Freudian) psychodynamics of depression; the role of sensitization in cytokine-induced depression; the compatibility of some of the effects of cytokines (on sleep, on cognition, on the HPA) with the hypothesis; the possibility of occurrence of depression in the absence of an increase in circulating cytokines; the nature of the relationships between cytokines, stress, and depression; the compatibility of the effects of cytokines on brain monoamines with the current monoamine hypothesis of depression; the inability of antidepressants to fully abrogate the brain effects of individual cytokines in animal experiments. Based on these limitations of the theory, it is proposed to define a new clinical entity designated as "the cytokine-associated depressive syndrome."
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PMID:Questions raised by the cytokine hypothesis of depression. 1240 76

There is increasing evidence that depression and related neurotic illnesses are associated with alterations in immune function that may contribute to their pathogenesis. For example, clinical and experimental studies have shown that abnormal HPA-axis activation and monoamine neurotransmission may be related to an increased release of proinflammatory cytokines from stimulated lymphocytes in the periphery and brain. In the present investigation, the effects of tryptophan depletion (TD) on unstimulated plasma interleukin-6 (IL-6) concentrations were investigated in order to determine whether acute changes in serotonin (5-HT) neurotransmission would induce a proinflammatory response in healthy individuals. The effects of TD were compared with the analogous procedure of tyrosine depletion (TPD), which reduces catecholamine metabolism in humans. Thirteen female participants completed three experimental sessions: TD, TPD and a balanced-control condition (B). Mood-ratings and blood sampling were performed at baseline and 5 h after the administration of the mixtures. Analyses revealed that TD and TPD markedly reduced tryptophan and tyrosine/phenylalanine levels, respectively. No changes in plasma IL-6 production or ratings of lowered mood were observed, however, subjects did report feeling more fatigued after TD. These findings indicate that a transient disruption in global monoamine function does not stimulate a proinflammatory response of IL-6 in normal volunteers.
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PMID:Effects of serotonin and catecholamine depletion on interleukin-6 activation and mood in human volunteers. 1240 74

Patients suffering from diabetes mellitus and depressive patients show a hyperactivity of the hypothalamic-pituitary-adrenocortical axis (HPA-axis) with hypercortisolemia. Hypercortisolemia is associated with cognitive dysfunction. These neuroendocrinological disturbances can cause an insulin resistance syndrome which complicates the regulation of blood glucose. Cognitive and depressive disorders in patients with diabetes mellitus might be associated with a hyperactivity of the HPA-axis. By normalising the HPA-axis both disorders could be improved. In addition, one can expect that antidepressive treatment with normalization of the HPA-axis could improve the metabolic situation and cognitive dysfunction. There is need for further research to study the associations between depression, diabetes mellitus and cognitive dysfunction.
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PMID:[The HPA-axis as a possible link between depression, diabetes mellitus and cognitive dysfunction]. 1252 32

Unlike other antidepressants, mirtazapine does not inhibit the reuptake of norepinephrine or serotonin but acts as an antagonist at presynaptic alpha(2)-receptors, at postsynaptic 5-HT2 and 5-HT3 receptors, and at histaminergic H1 receptors. Furthermore, mirtazapine has been shown to acutely inhibit cortisol secretion in healthy subjects. In the present study, the impact of mirtazapine treatment on salivary cortisol secretion was investigated in 12 patients (4 men, 8 women) suffering from major depression according to DSM-IV criteria. Patients were treated with mirtazapine for 3 weeks, receiving 15 mg mirtazapine on day 0, 30 mg on day 1 and 45 mg per day from day 2 up to the end of the study (day 21). Response to mirtazapine treatment was defined by a reduction of at least 50% in the Hamilton Rating Scale for Depression after 3 weeks of therapy. Salivary cortisol concentrations were measured before treatment (day -1), at the beginning of treatment (day 0), after 1 week (day 7) and after 3 weeks (day 21) of treatment with mirtazapine. Saliva samples were collected hourly from 08.00 until 20.00 h. The area under the curve values served as parameter for the salivary cortisol secretion. Following analysis of variance with a repeated measures design, tests with contrasts revealed a significant reduction of cortisol concentrations already after 1 day of mirtazapine treatment that was comparable in responders and nonresponders. In addition to new pharmacological approaches such as CRH1 receptor antagonists, mirtazapine therefore appears to be an effective strategy to decrease hypercortisolism and restore HPA system dysregulation in depression. However, the importance of the acute inhibitory effects of mirtazapine on cortisol secretion for its antidepressant efficacy has to be further clarified.
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PMID:Influence of mirtazapine on salivary cortisol in depressed patients. 1260 43

This paper presents a valid animal model of innate anxiety/depression: anxious (HAB) or non-anxious (LAB) rats, which show stable and robust responses in a variety of ethological tests. In addition to their extreme anxiety-related behavior, HAB animals are characterized by passive stress coping, an activated stress (HPA) axis, and increased stress vulnerability. The enhanced expression and release of arginine vasopressin (AVP) in the hypothalamus of HAB rats seem to underlie these phenomena. Accordingly, an AVP receptor antagonist attenuates anxiety-related behavior and normalizes the HPA axis and the dexamethasone/CRH test. Treatment with the antidepressive drug paroxetine reduces the overexpression of AVP and normalizes both the depression-like behavior and neuroendocrine correlates of anxiety/depression. The complex phenotyping led us to the conclusion that the AVP gene is likely to be a candidate gene of inborn anxiety. Partial genotyping of HAB animals results in the identification of polymorphisms (SNPs) in the promoter domain of the AVP gene, thus potentially leading to novel strategies of diagnosis and therapy of anxiety disorders and depression.
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PMID:[Neurobiology and genetics of anxiety in an animal model]. 1262 44


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