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)

Biological tests may help clarify the relationship of schizoaffective disorder to major depressive disorder (MDD) and schizophrenia (SCZ). Thyrotropin-releasing hormone (TRH), 500 micrograms, was administered intravenously to eight schizoaffective depressed (SD), ten SCZ, 23 MDD patients and 43 healthy controls (HC), all males, ages 20-66 years and drug-free. Research Diagnostic Criteria (RDC) were utilized for establishing diagnoses, Hamilton Rating Scale for Depression (HRSD) total scores were used for assessing depressive symptoms. There were no differences in dmax PRL (post-TRH prolactin peak minus baseline, mean +/- SD) amongst SD, SCZ and HC groups (27.3 +/- 5.2, 28.8 +/- 5.4 and 31.5 +/- 5.6 ng/ml respectively). Mean dmax PRL in MDD was significantly lower than each of the other three groups (17.1 +/- 2.2 ng/ml, P less than 0.05 for all). The essentially normal PRL response to TRH in SD, significantly different from MDD but similar to SCZ parallels our previous observations on the pattern of thyrotropin (TSH) response to TRH in the same diagnostic groups. These biological findings may be taken to indicate that schizoaffective disorder, depressed subtype, is closer to schizophrenia than to major depressive disorder. However, they cannot be considered definitive evidence to that effect since schizoaffective disorders are known to be quite heterogeneous, and since the utilized biological tests lack specificity.
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PMID:Prolactin response to thyrotropin-releasing hormone in schizoaffective depressed compared to depressed and schizophrenic men and healthy controls. 212 54

With a highly sensitive time-resolved fluorometric immunoassay (TR-FIA), serum thyrotropin (TSH) levels were determined in various conditions in healthy subjects. In addition, we compared the thyroid function in 10 depressed female patients with that in 27 female controls. 1) We evaluated a highly sensitive time-resolved fluorometric immunoassay kit for serum TSH. The lower limit of detection of TSH in serum was 0.008 less than U/ml. The intraassay and interassay variances were 3.0 greater than 3.6% and 3.4 greater than 5.1%, respectively. There was a significant correlation between basal TSH levels and maximum TSH values after TRH administration (r = 0.797, p less than 0.01). 2) The mean TSH levels in 31 healthy controls of both sexes was 1.26 +/- 0.96 less than U/ml, but TSH levels in women were significantly higher than in men (p less than 0.01). A large intra-individual variation of serum TSH levels determined on different days was found equally in both men and women. The nyctohemeral elevation of TSH levels was not clearly seen prior to the onset of normal sleep, but the nocturnal rise of TSH levels was remarkably accentuated by sleep deprivation. 3) The serum TSH levels in depressed female patients were significantly lower than those in healthy female controls when the post-menopausal subjects were excluded. For the serum thyroid hormone concentrations, serum T4 levels were normal. Serum free T3 levels tended to be lower, although the reduction was not significant. The serum levels of these 3 thyroid hormones were not related to serum TSH values. The present study demonstrated a large variation of TSH levels in various conditions, even in the same individuals, indicating the necessity of strictly controlled conditions in the study of TSH secretion. A significant reduction in TSH levels was observed in the depressed female patients when the post-menopausal subjects were excluded. Our results suggest that the dysfunction of the regulating mechanism of the pituitary-thyroid axis in depression may occur at a pituitary or a suprapituitary level.
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PMID:[Studies on the factors affecting serum thyrotropin levels in healthy controls and on the thyroid function in depressed patients using a highly sensitive immunoassay]. 228 57

The effect of DSP4 [N-(2-chloroethyl)-N-ethyl-2 bromobenzylamine], a neurotoxin which selectively lesions noradrenergic projections from the locus coeruleus, on thyrotropin (TSH) secretion was investigated in the rat. DSP4 treatment (60 mg/kg injected i.p. 10 days prior to experimentation) significantly decreased the noradrenaline (NA) content of the hippocampus, frontal cortex and hypothalamus of the rat brain. DSP4 treatment did not affect the clonidine (250 micrograms/kg, i.p ) or TSH-releasing-hormone (TRH 5 micrograms/kg i.v.) induced stimulation or the isoproterenol induced inhibition of TSH secretion in the rat. These results suggest that the noradrenergic projection from the locus coeruleus to the hypothalamus does not play a significant role in the regulation of TSH secretion. Furthermore, the noradrenergic deficiency did not give rise to the development of the abnormal TSH response to TRH administration which is frequently observed in depression.
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PMID:The effect of selective noradrenergic denervation on thyrotropin secretion in the rat. 232 21

The present investigation sought to examine the importance of substance P in the altered respiratory activity after neonatal capsaicin administration. Halothane-anesthetized adult rats given capsaicin neonatally exhibit a decreased basal minute ventilation with PaCO2 equal to and PaO2 greater than vehicle injected controls. In addition, the minute ventilation-PaCO2 curve was displaced to the right. Acute bilateral cervical vagotomy severely blunted the minute ventilation response to PaCO2 and abolished the differences in ventilation between capsaicin treated and control rats. Neonatal capsaicin significantly reduced pons-medulla substance P content but not TRH, serotonin or 5-hydroxyindole acetic acid. Immunohistochemical studies revealed that substance P fibers of the trigeminal spinal nucleus were the most severely affected in the brain stem and that substance P fibers in the lung were totally absent. The intracerebroventricular administration of substance P increased minute ventilation similarly in both control and capsaicin treated rats, largely as a result of increases in tidal volume. The minute ventilation-PaCO2 curve was similar in both groups after substance P administration. Simultaneous administration of the peptidase inhibitor captopril with substance P increased the respiratory response to substance P in normal rats. Administration of captopril to capsaicin treated rats restored the ventilation-PaCO2 curve to the position observed in normal rats. The hypotensive response to intracerebroventricular captopril alone in control rats was less profound in rats given neonatal capsaicin. These results are consistent with the thesis that respiratory depression after capsaicin treatment is at least in part due to the loss of substance P primary afferent nerve terminals in the brain stem, suggesting that substance P fibers in the brain stem may participate in the normal modulation of respiratory activity.
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PMID:Altered respiratory response to substance P in capsaicin-treated rats. 241 26

The effect of maternal diabetes (induced by i.p. injections of 40-50 mg/kg BW Streptozotocin on the day of mating) on TRH in the pancreas of newborn rats was studied. Determination of peptide alpha amidation activity and TRH precursor level on the day of birth revealed decreased biosynthesis of TRH resulting in profoundly (10 times) lower pancreatic TRH and TRH-OH concentrations in pups of diabetic rats. Pancreatic His-Pro-diketopiperazine (His-Pro-DKP) remained unaffected by maternal diabetes. The depression of pancreatic TRH was less profound 24 h later, and even elevated TRH was measured in the pancreas of pups of diabetic mothers on postnatal day 5. Short term postnatal starvation or nursing of intact pups by the diabetic foster mother did not affect pancreatic TRH. It could be postulated that postnatal TRH development in the rat pancreas is retarded by maternal diabetes, while His-Pro-DKP remains unaltered.
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PMID:Thyrotropin releasing hormone in the pancreas of newborn rats from streptozotocin-treated mothers. 249 94

Thyrotropin-releasing hormone (TRH) possesses significant arousing and cardio-respiratory stimulant actions. The effects of a 2 mg/kg i.v. bolus dose of TRH on respiration and systemic hemodynamics were compared in conscious, freely-moving rats and during anesthesia with 4 different anesthetics. Fifty-four male Sprague-Dawley rats weighing 285 +/- 4 g (mean +/- S.E.M.) were divided into 5 groups: conscious, enflurane (2%), isoflurane (1.4%), pentobarbital (8 mg/kg/h i.v.), and ketamine (60 mg/kg/h i.v.). Anesthetized rats were intubated and breathed oxygen or anesthetic/oxygen spontaneously. Aortic blood pressure, heart rate, cardiac output, respiratory rate, arterial blood pH, blood gases, lactate and glucose were measured, and data were collected over a 20 min baseline period and for 130 min post-TRH. TRH increased respiratory rate in all groups; concomitant changes in arterial PCO2 indicated increased minute ventilation in the inhalation agent groups but not in the i.v. anesthetic groups or in the awake group. Significant respiratory depression in the enflurane group was rapidly reversed by TRH. The respiratory stimulant and arousing effects of TRH were smallest with ketamine anesthesia. The hemodynamic responses to TRH were consistent with a pattern of sympathoadrenalmedullary activation and were relatively uniform across groups despite anesthetic-induced alterations in baseline values. TRH or its analogues may prove useful as an analeptic in clinical anesthesia.
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PMID:Respiratory and cardiovascular effects of thyrotropin-releasing hormone as modified by isoflurane, enflurane, pentobarbital and ketamine. 249 39

We measured serum thyroid hormone levels, and pre- and post-TRH administration serum thyrotropin (TSH) in 46 psychiatric inpatients with major depression (n = 20), anxiety disorder (n = 9), and anxious depression (n = 17), and in 56 healthy subjects. Basal serum triiodothyronine was lower in female patients with major depression and anxious depression than in healthy women (P less than 0.05). Basal serum thyroxine was lower in female patients with anxious depression than in controls; all patients showed lower basal serum TSH than controls. In healthy subjects, basal triiodothyronine and thyroxine, basal TSH, and delta TSH (the increment of TSH after TRH administration) correlated, whereas no correlation was found between triiodothyronine and thyroxine in male patients with major depression, or between TSH and delta TSH in female patients with major depression or anxious depression. In female patients, 45% with major depression, 25% with anxiety disorder, and 35% with anxious depression showed a blunted TSH response. We also investigated pre- and post-dexamethasone administration cortisol levels in these patients. The sensitivity obtained by the combination of the results of the TRH and dexamethasone suppression tests for major depression, anxiety disorder, and anxious depression was 45%, 55%, and 65%, respectively.
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PMID:Thyroid function in anxious and depressed patients. 249 74

The effects of low doses of thyrotropin-releasing hormone (TRH, 50 and 200 micrograms) on thyrotropin (TSH) and prolactin levels have been studied in depressed women and compared with the depressive condition and with the results of the dexamethasone suppression test (DST). TRH administration elicited blunted hormonal responses that were not correlated either with the age of the patients or with DST results. Different effects were observed in subgroups of depressive patients classified according to DSM III and ICD. No correlation was found between hormone responses and the scores of Hamilton Rating Scale and Montgomery Depression Scale. The effects of 50 micrograms on TSH were significant and inversely correlated with Anxiety Rating Scale scores. No dose-response effect was apparent of prolactin and TSH in depressed patients, suggesting an impaired function of pituitary TRH receptors.
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PMID:Thyrotropin and prolactin responses to different doses of thyrotropin-releasing hormone in depression. 250 67

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

Abnormal neuroendocrine responses have been found in depression and eating disorders. It remains unclear whether these reflect an underlying shared biology or epiphenomena. To evaluate this further, we conducted the 1 mg DST and the TSH response to 500 micrograms i.v. TRH in normal-weight bulimics and controls. Bulimics (n = 18) demonstrated significantly more DST non-suppression (45%) than controls (18%; n = 20). In the bulimic group, non-suppressors were significantly thinner than suppressors, but did not differ from them on any measure of depression. Bulimics (n = 19) and controls (n = 12) responded similarly without blunting on the TSH response to TRH. These data suggest that DST non-suppression may be related to non-specific variables such as weight. Bulimics do not demonstrate TSH blunting as found in some depressed patients. These tests do not support evidence for a biological link between these disorders.
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PMID:The DST and TRH test in bulimia nervosa. 250 82


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