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

We investigated the ameliorating effects of DN-1417 (a TRH analog) on the changes of behavior, EEG, neurochemical parameters and regional cerebral blood flow (rCBF) in rats with global cerebral ischemia. Global cerebral ischemia was produced by 10-min occlusion of both common carotid arteries 24 hr after the permanent electrocauterization of bilateral vertebral arteries. DN-1417 was administered intraperitoneally as soon as possible, following recirculation of carotid blood flow. DN-1417 shortened significantly the recovery times of righting reflex (RR) and spontaneous movement (SM) at 2.5 mg/kg and higher doses, and it recovered effectively the EEG activity at 10 mg/kg during recirculation after 10-min cerebral ischemia. In addition, DN-1417 (10 mg/kg) recovered the various changes such as decrease of 5-hydroxytryptamine (5-HT) levels, increase of cyclic AMP (cAMP) levels, inhibition of [3H]-choline uptake, depression of choline acetyltransferase (CAT) and acetylcholine esterase (AChE) activities, and shortened the durations of hyperperfusion and hypoperfusion of rCBF. As a result, it is identified that DN-1417 ameliorates the disturbance of consciousness supposedly caused by behavioral and EEG abnormalities during recirculation following the temporary cerebral ischemia, and the effect of DN-1417 seems to be mediated by normalizing of alterations in the brain monoaminergic and cholinergic systems, as well as rCBF, and the effectiveness for disturbance of consciousness in clinical situations would be expected.
 ...
PMID:[Pharmacological study of the temporary cerebral ischemic rats produced by bilateral vertebral and carotid artery occlusion. Effects of DN-1417]. 286 Nov 49

The finding of a diminished TSH response to exogenously administered TRH in a significant proportion of depressed patients has now been established as one of the most reproducible findings in biological psychiatry. More than 50 reports, in which more than 1000 patients have been studied, reveal that the TSH response is blunted in approximately 25% of patients with major depression. TSH blunting is clearly not specific for depression, because it also has been observed in mania, alcoholism, and borderline personality disorder. It is doubtful that TSH blunting represents a non-specific response to mental stress: it was found only rarely in schizophrenic patients, and the TSH response to in vivo flooding therapy in phobic patients was normal. In both depression and alcoholism, TSH blunting has been reported to be sometimes a state marker and sometimes a trait marker, i.e. the fault was found to persist into remission in more than half the patients. In both conditions, TSH blunting was unrelated to the patients' age, body weight, height, body surface, thyroid status, and serum cortisol concentrations. It also is unlikely that TSH blunting was due to increased dopaminergic inhibition of thyrotroph cells: serum prolactin concentrations in TSH blunters were found to be normal, and pretreatment with haloperidol had no effect on either basal TSH levels or TSH blunting. In depression, TSH blunting was not associated with previous drug intake, dexamethasone suppression test abnormalities, or variables of biogenic amine metabolism, nor did it usefully segregate between primary and secondary depression or between unipolar and bipolar subgroups. Preliminary evidence suggests that TSH blunting in depression may be related to duration of illness, history of violent suicide attempts, and a reduced 24 h TSH secretion. In alcoholism, TSH blunting was unrelated to family or personal history of depression and duration of abstinence. With reference to clinical utility, TSH blunting may aid in assessing the response to antidepressant treatment, predicting outcome to such treatment, assessing the risk for violent suicide attempts, and describing relationships between different psychiatric populations (e.g. depression and alcoholism).
 ...
PMID:The TRH-induced TSH response in psychiatric patients: a possible neuroendocrine marker. 286 65

Neuroendocrine abnormalities in depression have been regarded, by many authors, as relatively specific markers of nosological subtypes of the disorder, e.g. primary vs. secondary, endogenous vs. non-endogenous or unipolar vs. bipolar depression. They should reflect the same changes in central neurotransmitters (e.g. noradrenergic insufficiency and/or cholinergic hyperactivity) that were hypothesized as the cause of clinical symptoms. This view is challenged on the basis of our own neuroendocrine investigations in 317 psychiatric patients and 103 normal controls. According to these studies the abnormalities are nosologically rather unspecific. They are induced by a large variety of factors, e.g. emotional stress associated with the clinical symptomatology, weight loss due to malnutrition as a consequence of reduced appetite, medication and drug withdrawal. Stress-induced hypercortisolism appears to be the most common abnormality that may trigger other neuroendocrine dysfunctions, such as a blunted TSH response to TRH. Differences in neuroendocrine abnormalities of depressives are probably due to variations in the manifold factors influencing the hormonal axes involved, to temporal changes in hormonal patterns (e.g. one abnormality triggering another) and to individual differences in the basic activity and the responsiveness of the various axes.
 ...
PMID:The nature of neuroendocrine abnormalities in depression: a controversial issue in contemporary psychiatry. 288 Mar 46

Chronic pain has been considered as a variant of depression or as a masked depression. In an attempt to unravel the complex relationship between chronic pain and depression, we administered the TRH stimulation test to a uniform group of chronic pain patients classified into those with and without major depression using DSM-III criteria. Eighteen percent showed blunting of TSH response to TRH. There was no significant difference between the two groups.
 ...
PMID:Preliminary study of thyrotrophin releasing hormone stimulation test in chronic low back pain patients. 294 31

Despite a lack of documented efficacy in controlled trials, triiodothyronine (T3) is frequently administered as an adjunctive therapy for tricyclic resistant depressions. In this study, we tested the efficacy of T3 as an adjunctive treatment using a double-blind, placebo-controlled crossover design. Sixteen depressed patients who were unresponsive to 4 weeks of imipramine therapy (mean dose = 206 +/- 54 mg daily, mean combined blood level = 220 +/- 132 ng/dl) received T3 25 micrograms and placebo for 2 weeks each. There was no evidence of a T3 effect using both Hamilton depression scores and global improvement. No subgroup of responders using baseline TRH stimulation tests could be identified. T3 treatment lowered plasma free T4 (P = 0.001) and TSH (P greater than 0.02) while raising plasma T3 levels (P less than 0.01), indicating the physiological effect of the drug.
 ...
PMID:Failure of T3 to potentiate tricyclic antidepressant response. 296 Jul 19

We studied the prolactin response to TRH in 53 unmedicated psychiatric inpatients. The prolactin response of females was significantly greater than the response of male subjects. There was no significant difference in the prolactin response to TRH between depressed patients and those with other psychiatric diagnoses. There was no significant relationship between the prolactin response to TRH and the severity of depression, the TSH response to TRH or the resistance to suppression of cortisol secretion by dexamethasone.
 ...
PMID:Prolactin response to TRH in depression. 308 43

TRH-induced thyrotropin (TSH), prolactin (PRL), and growth hormone (GH) responses were investigated together with a dexamethasone suppression test in female psychiatric inpatients with major melancholic depression (n = 21), schizophrenic disorder (n = 20), alcohol dependence (n = 11), and adjustment disorder with predominantly depressed mood (n = 13), as well as in 15 healthy women. Abnormal responses for all four endocrine variables were noted most frequently in melancholia; however, a significant number of the non-depressed patients also had abnormal hormonal responses in the individual test. The association of two or three abnormalities proved to be quite specific for the melancholic group. There were no statistically significant differences in TRH-induced TSH responses among the patient subgroups. Non-suppression of cortisol after dexamethasone was associated with blunted TSH-responses only in melancholia. There was a tendency for non-suppressor schizophrenics to show more abnormal GH-responses to TRH administration.
 ...
PMID:Associations among dexamethasone non-suppression and TRH-induced hormonal responses: increased specificity for melancholia? 309 67

TRH tests were performed on 131 patients with RDC diagnoses of major depressive disorders to study altered endocrine control mechanisms in subtypes of depression. The TSH response to TRH was measured in all patients. In more than a third of the sample the prolactin (PRL) and growth hormone (GH) responses were also analysed. There were no differences between bipolar, primary unipolar and secondary unipolar patients in means of any endocrine variable. However, the expected positive correlation between baseline TSH and delta TSH was absent in the secondary unipolar group, indicating a dysregulation of pituitary TRH receptor sensitivity in this depressive subtype. Only delta TSH was dependent on depressive state, being lower in currently ill primary unipolar patients only. Patients with melancholic features (endogeneity scores high) had blunted TSH responses. Weight loss was connected with TSH blunting in all depressive subtypes. Among patients with blunted delta TSH (less than 5 mU/l) there was no relationship between degree of weight loss and delta TSH. Further, examination of partial correlation coefficients suggests weight loss of affect delta TSH by virtue of its being part of the melancholic syndrome. A significant correlation between blunted delta TSH and nonsuppression of cortisol in the DST was found only among primary unipolar patients, arguing for some independence of the TRH test and the DST in mirroring disturbed endocrine controls in depression.
 ...
PMID:TRH tests with analyses of TSH, prolactin, and GH responses in subtypes of patients with major depressive disorders. 309 81

The aims of the present study were to investigate the value of adding DSM-III diagnosis and Newcastle Scale Rating to the ICD-8 diagnosis currently used and to investigate the association between Dexamethasone Suppression Test (DST) and the Thyrotropine Releasing Hormone- Thyroid Stimulating Hormone (TRH-TSH) test and the three classification systems for depression. Twenty-six depressed in-patients were included, 17 women and 9 men, with a mean age of 51.5 years. Fourteen patients were psychotic depressed. DST and Newcastle Scale Rating were performed on 18 patients and TRH-TSH test was performed on 16 patients. The addition of DSM-III diagnosis on the 4-digit level did not have any value compared to the ICD-8 diagnosis. However, DSM-III diagnosis on the 5-digit level added important clinical information which corresponded better to Newcastle Scale scores and DST and TRH-TSH test results than ICD-8 diagnosis. The main advantage of the DSM-III classification of depression on the 5-digit level compared to ICD-8 concerns depression on the border between psychosis and neurosis. In clinical practice there is a risk of underestimating the severity of a depression if ICD-8/9 is used as the only criterion for severity. This may have tragic consequences for the patient. This study suggests that rating of the depression on the Newcastle Scale or provision of a DSM-III diagnosis on the 5-digit level are valuable assessment procedures of severity.
 ...
PMID:A comparison of DSM-III and ICD-8 diagnoses for major affective disorders and the use of biological markers for depression. 309 84

In an evaluation of the possible role of dopamine on TRH test results, 21 depressed patients were given TRH before and after one week of treatment with a low dose of haloperidol. Haloperidol significantly increased serum prolactin (both basal and after TRH) and cortisol levels, decreased body temperature, and had no effect on serum TSH, growth hormone, or thyroid hormone levels. Five of six patients with initial TSH blunting were retested with TRH; in four patients the TSH response remained blunted. These data render it unlikely that dopamine exerts a major inhibitory input on TSH secretion in depression.
 ...
PMID:The TRH test during dopamine receptor blockade in depressed patients. 309 92


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>