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

The subtypes of major depression are reviewed, and a decision tree for the acute somatic treatment of major depression, including delusional and nondelusional depression, is presented. Considerations in clinicians' decisions about initiation and selection of acute somatic treatment for patients with major depression are then discussed. Current somatic therapies for nondelusional depression are described, with emphasis on the mechanisms of action of the drugs employed, the relationship between mechanism of action and side effect profile, and the selection of a drug on the basis of its side effect profile. The three current strategies for the treatment of delusional depression--electroconvulsive therapy, the combination of an antidepressant and an antipsychotic agent, and amoxapine alone--are then reviewed.
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PMID:Recent developments in the acute somatic treatment of major depression. 134 70

To examine directly in the brain the status of the alpha 2-adrenoceptor in major depression, the specific binding of the agonists [3H]clonidine and [3H]UK 14304 was quantitated in various brain regions of suicide victims with a retrospective diagnosis of depression or other psychiatric disorders. In depressed suicides, the binding capacity of [3H]clonidine was found to be increased in the hypothalamus (Bmax 35%-55% greater), and to a lesser extent in the frontal cortex, as compared with that in matched controls, schizophrenic suicides, or suicides with various diagnosis. The binding capacity of [3H]UK 14304 also was found increased in the frontal cortex (Bmax 30% greater), and to a lesser extent in the hypothalamus, of depressed suicides. In other brain regions such as the amygdala, hippocampus, and cerebellum there also was a tendency for an increased receptor density associated with suicide. Moreover, in the frontal cortex of suicides, the potency of norepinephrine in displacing the binding of the antagonist [3H]idazoxan also was found increased (Ki decreased eight-fold). The results indicate that the density and affinity of alpha 2A-adrenoceptors in the high-affinity state are increased in the brain of depressed suicides.
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PMID:Alpha 2-adrenoceptors in the brain of suicide victims: increased receptor density associated with major depression. 134 30

1. The present study assessed the potential antidepressant action of gepirone hydrochloride, an azapirone serotonin (5-HT1A) partial agonist in patients with major depression. 2. Overall, gepirone demonstrated a significant antidepressant activity within the entire patient group (p less than 0.001). However, when subjects were stratified based upon the presence or absence of DSM III-R melancholic features, the melancholic depressives showed little change in weekly depression ratings compared to patients without melancholic symptoms (p less than 0.001). 3. Similarly, patients who were more severely ill at the pretreatment period had less improvement compared to those with more modest illness severity (p less than 0.001). 4. These observations compliment those of prior studies suggesting antidepressant activity for gepirone. 5. However, a consistent efficacy comparable to conventional neuronal reuptake inhibitor antidepressants remains to be established in patients with more severe depression characterized by melancholic features.
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PMID:Gepirone, a selective serotonin (5HT1A) partial agonist in the treatment of major depression. 135 Mar 53

Drug-induced depression which is classified as DSM-III-R is difficult for clinicians to diagnose because the cause is not easily distinguishable from adjustment disorders or nonorganic mood disorders. This review summarizes the few articles published within 20 years as searched in the Index Medicus about the clinical manifestations of organic mood syndromes from oral contraceptives (OCs), beta blockers, alcohol and sedative-hypnotic drugs, and other medications. There was a noticeable lack of articles and specific clinical features which would help differentiate causes. Oral contraception may cause depression by inducing hepatic tryptophan oxidase, which may lead to a deficiency of vitamin B6. The most common reason for discontinuing OCs is depression, i.e., there are reports of a rate of 70/1000 woman years during the 1st year of OC use. However, the rate among females examined in a catchment study was similar at 6.6%. There is some indication that depression may be dose related, i.e., low dose is related to the same prevalence as in the control group. A basic requirement of DSM-III-R is severe and persistent depression; OC-related depression does not exhibit sleep or appetite disturbances. The relationship between beta blockers and depression indicates that the prevalence and the nature of the relationship are not consistently confirmed. Depressive episodes (14) reported in 8 studies showed major depression and suicidal thoughts or attempts just after initiation of propranolol and resolution when the drug was discontinued; timing of the symptoms may be the best basis upon which to make a clinical judgement. Alcohol use is usually seen as associated with depression, but the extent to which alcohol induces depression is unknown. Symptoms are transitory and appear during bouts of heavy drinking. Studies on benzodiazepine use and depression are reported to be confounded by other factors. Other depression-causing agents for which information was unavailable are identified as psychostimulants, metoclopramide, H-2 blockers, methyldopa, and steroids.
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PMID:Can drug-induced depressions be identified by their clinical features? 135 May 3

Various classes of antidepressant drugs with distinct pharmacologic actions are differentially effective in the treatment of classic melancholic depression--characterized by pathological hyperarousal and atypical depression--associated with lethargy, hypersomnia, and hyperphagia. All antidepressant agents exert their therapeutic efficacy only after prolonged administration. In situ hybridization histochemistry was used to examine in rats the effects of short-term (2 weeks) and long-term (8 weeks) administration of 3 different classes of activating antidepressant drugs which tend to be preferentially effective in treating atypical depressions, on the expression of central nervous system genes thought to be dysregulated in major depression. Daily administration (5 mg/kg, i.p.) of the selective 5-hydroxytryptophan (5-HT) reuptake inhibitor fluoxetine, the selective alpha 2-adrenergic receptor antagonist idazoxan, and the nonspecific monoamine oxidase A and B inhibitor phenelzine increased tyrosine hydroxylase mRNA levels by 70-150% in the locus coeruleus after 2 weeks of drug and by 71-115% after 8 weeks. The 3 drugs decreased corticotropin-releasing hormone mRNA levels by 30-48% in the paraventricular nucleus of the hypothalamus. The decreases occurred at 8 weeks but not at 2 weeks. No consistent change in steroid hormone receptor mRNA levels was seen in the hippocampus with the 3 drugs, but fluoxetine and idazoxan increased the level of mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) mRNA, respectively, after 8 weeks of drug administration. Proopiomelanocortin (POMC) mRNA levels in the anterior pituitary and plasma adrenocorticotropic-hormone (ACTH) levels were not altered after 2 or 8 weeks of drug treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The antidepressants fluoxetine, idazoxan and phenelzine alter corticotropin-releasing hormone and tyrosine hydroxylase mRNA levels in rat brain: therapeutic implications. 135 83

Cerebrospinal fluid (CSF) concentrations of immunoreactive corticotropin-releasing hormone (CRH) and somatostatin (SRIF) were measured in female psychiatric inpatients with DSM-III-R diagnoses of major depression, mania, generalized anxiety and somatization disorder. In addition, elderly patients with dementia disorders, with or without concomitant major depression, were also investigated. CSF SRIF was not significantly different among these groups; on the other hand, mean CSF CRH concentrations were significantly higher in major depression and in dementia with depression as compared with neurological controls with no psychiatric disorders. CSF CRH levels in mania, simple dementia, or anxiety or somatization disorder were not significantly different from the controls. Background physical or clinical variables did not account for the differences in CRH concentrations. It is concluded that CSF CRH elevation may be present in some patients with major depression independent of age and an underlying dementia disorder.
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PMID:Cerebrospinal fluid neuropeptides in mood disorder and dementia. 135 20

Immunoreactive corticotropin-releasing hormone (CRH) and somatostatin (SRIF) were measured in the cerebrospinal fluid (CSF) of 24 female in-patients, suffering from DSM-III-R major depression, both before and after antidepressant treatment. In the total group there were no significant differences between pre- and post-treatment CSF-CRH and SRIF concentrations despite satisfactory clinical improvement in each patient. However, there was a significant post-treatment reduction of the CSF-CRH concentration in the 15 patients who remained depression-free for at least 6 months following treatment, in contrast to the tendency for elevation in those 9 subjects who relapsed within 6 months. CSF-SRIF showed no similar pattern. High, or even increasing, CSF-CRH concentration during antidepressant treatment may indicate lack of normalization of an underlying process in major depression despite symptomatic improvement and predicted early relapse.
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PMID:CSF corticotropin-releasing hormone and somatostatin in major depression: response to antidepressant treatment and relapse. 135 99

We ascertained 8 multigenerational pedigrees afflicted with multiple cases of bipolar and recurrent major depressive disorder. Alterations in dopaminergic and noradrenergic neurotransmission have been implicated in the pathogenesis of this disease, and tyrosine hydroxylase (TH) is the rate-limiting enzyme in the synthesis of these two catecholamines. As TH mutations could underlie susceptibility to manic-depression, we carried out a linkage analysis between this disease in 8 families and two RFLP probes that map to the TH gene region on the short arm of chromosome 11. Evidence of linkage was not found in 7 of 8 kindreds.
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PMID:Tyrosine hydroxylase gene not linked to manic-depression in seven of eight pedigrees. 135 73

Somatostatin (somatotropin release-inhibiting factor, SRIF) was originally discovered (1) during the purification of growth hormone-releasing factor from rat hypothalamus and was subsequently isolated and characterized (2) in 1972 from ovine hypothalamus. Since its initial characterization, SRIF has been shown to fulfill criteria for a neurotransmitter and to directly modulate neuronal activity as well as acting as an inhibitory factor regulating endocrine and exocrine secretion. Alterations in cerebrospinal fluid (CSF) concentrations of SRIF have been reported in several diseases exhibiting prominent cognitive dysfunction, including Alzheimer's disease (AD), major depression, Huntington's chorea, multiple sclerosis, schizophrenia and Parkinson's disease, while evidence for regional brain tissue concentration deficits in SRIF are more specific for AD. This mini-review will focus on the studies reporting alterations in CSF and postmortem tissue concentrations of SRIF in AD and depression.
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PMID:Somatostatin in Alzheimer's disease and depression. 135 21

Dopamine autoreceptor agonists reduce the firing rate, synthesis, and release of dopamine in dopaminergic neurons by means of a negative feedback mechanism via stimulation of autoreceptors. Moreover, dopamine autoreceptor agonists are able to stimulate supersensitive but not normosensitive postsynaptic receptors. For dopamine autoreceptor agonists, therapeutic effects by readjustment of excessive or deficient dopaminergic function have been postulated for positive and negative schizophrenic symptomatology as well as for subtypes of depressive disorders. Investigations on the therapeutic effects of autoreceptor-nonselective dopamine agonists in schizophrenia or depression have yielded inconsistent results. In order to reduce the excess of central dopaminergic activity postulated by the dopamine hypothesis of schizophrenia, dopamine autoreceptor agonists have been tested in open clinical trials in positive schizophrenic symptomatology. However, administration of selective dopamine autoreceptor agonists like talipexole or roxindole did not result in a significant improvement of positive psychotic symptoms. In negative schizophrenic symptomatology, a dopamine deficit rather than an excess has been hypothesized. Current evidence from pilot studies suggests that dopamine autoreceptor agonists like roxindole may produce a minor to moderate improvement of symptoms like affective flattening, depressed mood, alogia, and avolition, possibly by stimulation of supersensitive postsynaptic dopamine receptors. For certain subgroups of depression, a reduction of functional dopamine activity has been postulated. In an open pilot study in patients with a major depression, roxindole demonstrated antidepressive properties comparable to those of standard antidepressants, justifying further double-blind controlled trials against reference drugs.
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PMID:Dopamine autoreceptor agonists in the treatment of schizophrenia and major depression. 136 97


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