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)

Leukotriene D4 (LTD4) is the major constituent of slow-reacting substance of anaphylaxis (SRS-A). Cardiovascular depression and hypotensive shock represent the major manifestations that attend systemic anaphylaxis. To further evaluate the hemodynamic effects of LTD4, we measured blood pressure (BP), heart rate (HR) and blood flow (BF) (directional pulsed Doppler flowmeter) to different vascular beds (hindquarter, mesenteric and renal) of the urethane-anesthetized rat. LTD4 (3, 10 and 30 micrograms/kg, i.v.) caused a dose-dependent increase in BP: 15 +/- 3, 20 +/- 4 and 24 +/- 2 mm Hg, respectively, which was maximum after 2 min and returned to control level at 10 min; HR was not significantly altered. BF to different vascular beds was differentially altered: mesenteric (-59%) greater than hindquarter (-38%) greater than renal (-10%). Vascular resistance (VR) increased by 195, 85 and 40% in mesenteric, hindquarter and renal beds, respectively. Thyrotropin-releasing hormone (TRH) (2-5 mg/kg, i.v.) injected after LTD4 increased BP, reversed the decrease in BF and the increase in VR in the mesenteric and hindquarter vascular beds. These data suggest that LTD4 receptors are unevenly distributed in various vascular beds and that the splanchnic area is particularly vulnerable to anaphylaxis-induced ischemia. Furthermore, Thyrotropin Releasing Hormone (TRH) might be useful to antagonize the hemodynamic consequences mediated by SRS-A or leukotriene.
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PMID:Differential hemodynamic effects of leukotriene D4 in anesthetized rats: evaluation by directional pulsed Doppler technique. 385 95

Investigations were undertaken with 5,7-dihydroxytryptamine and 6-hydroxydopamine treated rats to see whether activity changes induced by TRH, ethanol and the TRH-ethanol combination would be affected after reduced monoamine function. In keeping with earlier results, TRH increased activity, ethanol reduced activity and the TRH-ethanol combination produced activity counts greater than those for TRH alone. Neither the 5,7-dihydroxytryptamine-induced reduction of brain serotonin nor the 6-hydroxydopamine treatments which reduced brain catecholamines altered the hyperactivity induced by TRH or the TRH-ethanol combination. While reduction of brain serotonin did not affect the ethanol-induced changes in activity, preferential reduction of dopamine as well as reduction of both norepinephrine and dopamine significantly antagonized this measure of ethanol-induced depression. The reduction of dopamine alone produced the greatest effect on this action of ethanol. It can be concluded from the data that the increased locomotion induced by TRH and the TRH-ethanol combination does not depend upon endogenous monoamines, whereas the sedative effects of ethanol are apparently influenced by alterations in brain catecholamine function.
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PMID:Effects of TRH, ethanol, and TRH-ethanol combination on activity in rats with altered monoamine content. 392 22

Baseline and TRH-induced changes of thyroid stimulating hormone (TSH), prolactin (PRL), and growth hormone (GH) were measured in 15 healthy control subjects and 63 psychiatric inpatients with DSM-III diagnoses of major depression (n = 19), schizophrenic disorder (n = 20), alcohol dependence (n = 10), and adjustment disorder (n = 14); baseline and postdexamethasone cortisol (CS) were also determined 3-6 days after the TRH-challenge. All patients and controls were women of similar mean age, weight, height, and they were free from interfering illness or drugs. Baseline TSH and PRL were lower in depression, TRH-induced TSH and PRL responses were lower in the whole patient group, but most markedly in depression and alcohol dependence. Postdexamethasone CS was significantly higher in depression, schizophrenia and alcohol dependence. Basal GH did not differentiate the subgroups; TRH-induced pathological GH responses were sometimes found in the patient groups. The differences were most marked quantitatively in major depression: a multivariate analysis of variance showed that delta TSH, postdexamethasone CS and delta PRL were the most important variables in separating patients from controls. A discriminant function derived from these variables classified all controls and 18 of 19 depressed patients correctly; however, 25 of the 44 other patients were also classified with depression. It was confirmed that psychiatric patients show significantly more endocrine disturbances than controls, and this was seen not only in major depression but also in at least three other conditions. Further work is needed to identify other neuroendocrine patterns more specific to depressive disorder.
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PMID:Dexamethasone suppression and multiple hormonal responses (TSH, prolactin and growth hormone) to TRH in some psychiatric disorders. 393 Feb 50

In recent years, several neuropeptides were tested in psychiatric populations, particularly depression, as to their possible use as diagnostic tools. To date, results of most of these "tests" are equivocal and preliminary in nature. The measurement of serum TSH after administration of TRH, however, has revealed that approximately 25% of depressed patients show a blunted TSH response after TRH. TSH blunting, although not being specific for depression, may aid in assessing the response to antidepressant treatment, predicting outcome to such treatment, and assessing the risk of violent suicide attempts.
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PMID:The use of neuropeptide challenge tests as diagnostic adjuncts in psychiatry. 393 54

Studies of depression carried out for over 10 years have led to the discovery of biological tracers for depression. The authors have performed numerous TRH and dexamethasone tests and in their opinion, the present enthusiasm for these tests should be tempered. In several aspects the various values attributed to them seem to be questionable. Owing to the difficulty in codifying these tests, the authors question their diagnostic, pronostic, therapeutic and predictive values. The authors' own experience as well as the evolution of the publications throughout the world have been taken into consideration. Finally, the problem of interferences and the doubtful specificity of endocrine tests for depression have been dealt with.
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PMID:[Several critical aspects of the value of peripheral markers in depression (TRH test and dexamethasone depression)]. 393 96

Male Sprague-Dawley rats were given a single electroconvulsive shock (ECS) on alternate days and sacrificed 48 hrs after 1, 3, or 5 seizures. The content of TRH in hippocampus, pyriform cortex and amygdala was increased 2.5-fold, 5.4-fold and 4.3-fold respectively, 48 hrs. after 3 alternate-day electroconvulsive shocks (ECS) and remained unchanged after 2 additional shocks. Pyriform cortex exhibited a significant intermediate increase (1.7-fold) after only 1 ECS. In a second study, rats were sacrificed 48 hrs after a series of 5 alternate-day ECS vs. subconvulsive shocks (SCS). SCS had no significant effect in these same regions, but was seen to alter TRH in striatum. These results provide an interesting parallel to several aspects of clinical electroconvulsive treatment (ECT) of depression. Together with other findings, these data suggest also, that endogenous TRH may play a role in the modulation of convulsive seizures.
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PMID:Effects of subconvulsive and repeated electroconvulsive shock on thyrotropin-releasing hormone in rat brain. 396 50

Nowadays the diagnosis of depression can be made through two neuroendocrine tests, which tend to become common: the TRH test and the Dexamethasone Suppression Test which have a wide diagnostic accuracy. Any abnormal finding could implicate a dysfunction of neurotransmitter systems. They are of diagnostic assistance in endogenous depressions supposed to be responsive to antidepressants. They might also be a practical monitor of treatment response since the test results reverting to normal seems to indicate recovery whereas persisting abnormal results are a possible predictor of relapse.
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PMID:[Biologic diagnosis of depression by the TRH and dexamethasone tests]. 613 96

The interactions of thyrotropin releasing hormone, its metabolites and synthetic analogues with acute and chronic effects of endogenous and exogenous opiates have been described. The endogenous and exogenous opiates are represented by beta-endorphin and morphine, respectively. The pharmacological effects of opiates include analgesia, temperature effects, respiratory depression, catalepsy, locomotor activity, opiate receptor binding, tolerance, and physical dependence. Thyrotropin releasing hormone and related compounds appear to (a) antagonize hypothermia, respiratory depression, locomotor depression and catalepsy but not the analgesia induced by opiates, (b) inhibit the development of tolerance to the analgesic effect but not to the hypothermic effect of opiates, (c) inhibit the development of physical dependence on opiates as evidenced by the inhibition of development of certain withdrawal symptoms, and (d) suppress the abstinence syndrome in opiate dependent rodents. Thyrotropin releasing hormone does not interact with the opiate receptors in the brain. Potential therapeutic applications of thyrotropin releasing hormone and its synthetic analogues in counteracting some of the undesirable effects of opiates are discussed.
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PMID:Interactions of thyrotropin releasing hormone, its metabolites and analogues with endogenous and exogenous opiates. 614 Nov 21

Distorted biorhythms and altered neuroendocrine function may accompany depressive disorders. Restoration of the above derangements occurs with effective therapy, whereas persistence of the biological abnormalities is found in patients incompletely cured and may be predictive of early relapse. The commonest hormonal abnormalities are: decreased suppressibility of the ACTH-cortisol axis to dexamethasone, subnormal thyrotropin response to TRH and growth hormone release to hypoglycemia; attenuated gonadotropin production and abnormal light-dark entrained melatonin secretion. The observed hormonal derangements seem to be epiphenomena of the primary disorder. The reversibility of the disordered neuroendocrine control with treatment of the depressive syndrome suggests that the hormonal abnormalities represent a state rather than trait disorders. Finally, the lack of similar neuroendocrine derangements in schizophrenia or secondary exogenous depression suggests that different neurochemical alterations underlie these disorders.
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PMID:Depression: biological and neuroendocrine aspects. 614 19

The authors performed dexamethasone suppression tests (DST), TRH infusions, 72-hour urine collections, and lumbar punctures on a group of male depressed patients. Approximately 60% of the patients were DST positive and 33% had a blunted TSH response. Two biologic variables, the 8 a.m. postdexamethasone cortisol and the postprobenecid CSF 5-hydroxyindoleacetic acid (5-HIAA), accounted for over half of the variance in the behavioral measure, the Hamilton score. Plasma cortisol elevation was associated with high 3-methoxy-4-hydroxyphenyl glycol (MHPG) excretion; TSH blunting was associated with low urinary MHPG excretion. Comprehensive biologic measures showed certain significant interrelationships and correlations with the severity of depression.
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PMID:Neuroendocrine and neurochemical measurements in depression. 617 Nov 69


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