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)

Changes in thyroid activity and variations in the hypthalamo-pituitary-thyroid hormone levels were examined in rats exposed to heat (34 degrees C)for3 weeks. Thyroid activity evaluated histologically (epithelium/colloid ratio, nuclear size) by radioiodine exploration (24 hrs 125 I uptake, ratio of mono- to di-125 iodotyrosines - MIT/DIT, ratio of tri- to tetra-125 iodothyronines-T3/T4, and plasma 125I-T4 and assay of plasma T4, evolves in a triphasic manner. 1.a depression phase between day 0 and day 2.5. 2. a rebound of thyroid activity between day 2.5 and day 9.3 a stabilization of thyroid parameters from day 9 to day 24. These results indicate adaptation of thyroid function to heat after 3 weeks. In phase i, plasma TSH )MeKenzie bioassay) fell to undectable levels concurrent with a 50% decrease in hypothalamic TRH (in vitro assay). Plasma TSH peaked on day 4.5, fell on day 9.5 and returned progressively to initial levels. Hypothalamic TRH returned to initial levels after 6.5 days. The rapid and simultaneous decrease in hypothalamic TRH, plasma TSH, plasma T4 and thyroid activity by the 36th hour of heat exposure (34 degrees C) suggests initiation at the hypothalamic level. In the secound phase, the rebound in thyroid activity is presumably due to the peak in circulating TSH in ralation to the marked decrease in plasma T4. The oscillations of phase 2 and the stabilization of all the thyroid parameters in phase 3 may be the reflection of an apparent discrepancy remains between a low plasma T4 and a normal or subnormal plasma TSH. A modification in the "set point" for the control of TSH secretion is discussed.
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PMID:Variations of rat thyroid activity during exposure to high environmental temperature (34 degrees C). Relation between hypothalamic pituitary and thyroid hormone levels. 80 54

Both oral and intravenous TRH produce systematic alterations in brain function of depressive patients as determined by scalp-recorded computerized cerebral biopotentials (computer EEG). The computer EEG (CEEG) profiles of both formulations are not only very similar to each other, but also resemble the CEEG profiles of psychostimulant compounds (Bio-availability). As in CEEG findings, TSH plasma levels also indicate that oral TRH is indeed an active compound. Although some "antidepressive" effects were observed after both formulations, they were not present in every patient, and it was not always the case after repetitive TRH administration, nor were the effects on depressed mood too impressive. On the other hand, in almost all patients certain behavioral effects of TRH were seen which related to "life instincts" and "life performance". The increase of interest, desire and drive for work, food and sex was one of the most striking findings, particularly after intravenous TRH. This may be responsible for the "antidepressive" effects of TRH in patients in whom depression may be the result of an inhibition of "instinctive" functions.
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PMID:Clinical and CNS effects of oral and I.V. Thyrotropin-releasing hormone in depressed patients. 80 53

Thyroid levels were estimated in 15 patients with endogenous depressions. Before electroconvulsive treatment (ECT), serum thyroxine (T4) and free T4 index values were elevated (P less than .02). After recovery from depression, the levels were normal. Serum triiodothyronine (T3) and free T3 index were normal both before and after ECT. Serum thyrotropin (TSH) levels were also normal and not substantially altered by the ECT procedure. The mean maximal TSH response to protirelin (thyrotropin-releasing hormone) was diminished in the depressed patients and normal after recovery. In three patients, the increase in TSH response to protirelin after recovery did not occur and they relapsed within six months, while in seven patients with increased TSH response to protirelin after recovery only one relapse occurred. The disturbances in the free T4 index, T4, and the protirelin test may in some depressed patients resemble hyperthyroidism, but this condition can be excluded by means of serum, T3 and free T3 index.
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PMID:Protirelin stimulation test and thyroid function during treatment of depression. 81 Jan 13

A young woman, whose psychiatric history covered 16 years, has been treated several times as in-patient for psychotic depression, which were finally cured with thyroid replacement therapy. Recent reports of the connection between depression and disturbances in the hypothalamic-pituitary-thyroid axis are discussed. The authors question the suggestion that selective pituitary insufficiency and a defect in TSH release on TRF loading are rare phenomena.
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PMID:Myxedematous madness without myxedema. Selective defect of TSH release on TRF loading in a young woman with a history of severe depressive illness cured with thryoid hormone replacement therapy. 81 76

Plasma thyrotropin (TSH) levels varied relatively little over minutes to days in the same individual not subjected to challenge with thyrotropin-releasing hormone (TRH). Thus, the TSH response to stimulation with TRH is not likely to be confounded by spontaneous changes of comparable degree. Variable numbers of depressed patients showed a blunted response to TRH stimulation of the pituitary, but the exact prevalence of this phenomenon remains to be clearly defined. In any case, the pituitary response to TRH stimulation was not correlated with the prevailing level of depression, nor did this response to an initial TRH challenge predict the degree of clinical change during a 15-day treatment during which three intravenous doses of 600 mug of TRH were given. Depressed patients, as do schizophrenics and normal patients, show diminished TSH responses to repeated challenges with TRH. Whether or not these three groups differ in regard to the rate at which the pituitary response can be abolished remains to be determined.
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PMID:Pituitary response to thyrotropin-releasing hormone in depression. 82 76

The influence of thyroid deficiency and the administration of thyroxine on pituitary-testicular function were studied in male albino rats from weaning age (22 days old) up to 82 days of age. The results showed that the hyperthyroid state induced by a daily injection of 2.5 or 5 microng L-thyroxine resulted in acceleration of growth, a comparative increase in size and number of spermatogenic and interstitial cells, an increase in the STH cells, particularly at the earlier age (42 days old), and in a decrease in the number and size of TSH cells. Gonadotrophic FSH and LH and prolactin cells exhibited an increase in their granular content. The hypothyroid state induced by thyroidectomy or thiourea feeding, at the levels of 0.1 and 0.2% resulted in the depression of growth rate, destructive changes of the spermatogenic and interstitial cells and also in the lumen of the seminiferous tubules. A decrease in the STH, gonadotrophic FSH and LH and prolactin cells and hypertrophy of TSH cells accompanied by degranulation were also observed.
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PMID:Pituitary-testicular function changes in hypo- and hyperthyroid male rats. 86 Jun 35

The effect of long-term diphenylhydantoin (DPH) treatment on thyroid hormone concentrations and protein binding was determined in a randomized controlled trial. As has been demonstrated previously, total thyroxine (T4) concentrations were significantly depressed in patients on DPH. There was no significant effect on indirect indices of protein binding of thyroid hormones, and the free thyroxine index (FTI) was also significantly depressed. Triiodothyronine (T3) and thyrotrophin (TSH) concentrations were either unaffected, or only very slightly affected by DPH. Significant effects on the FTI were still apparent 4 weeks after discontinuing treatment. It is concluded that the depression of total T4 levels observed in vivo is not due solely to diminished protein binding, but may instead be largely explained by reports suggesting enhanced degradation of T4 following DPH therapy.
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PMID:Thyroid hormone levels and protein binding in patients on long-term diphenylhydantoin treatment. 87 45

Thyroid glands of normal, TSH-treated and Thyradin (powdered thyroid)-treated mice were examined by means of the freeze-etching method. Intramembranous particles on the PF (= A face) face of the apical plasma membrane often form aggregates especially in TSH-treated mice. Each aggregate, about 200 nm in diameter, and consisting of 15-25 large particles, corresponds to a depression of the apical cytoplasm, and the particles sometimes form rosettes. Particle-aggregates are very rare in the apical plasma membrane of the thyroid follicular cell of the Thyradin-treated animal. In the cytoplasm just beneath the particle-aggregate no secretory granules, reabsorbed colloid droplets or other special structures are found. From these facts, the aggregate is considered closely related to an initial site for the micropinocytosis of the luminal colloid.
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PMID:Freeze-etching observations on the characteristic arrangement of intramembranous particles in the apical plasma membrane of the thyroid follicular cell in TSH-treated mice. 97 14

The effect of short-term dexamethasone administration (8 mg daily for 3 days) on thyroid hormone response to exogenous TSH (bovine TSH, 5 IU i.m.) was studied in 16 euthyroid volunteers. Serum T3 and T4 concentrations were measured by radio-immunoassay prior to and 2, 6, 12, 24, and 49 hr after bTSH injection, both under basal conditions and during dexamethasone treatment. In all subjects bTSH administration raised both T3 and T4 concentrations significantly. Dexamethasone treatment induced a slight depression of endogenous TSH (m +/- SEM = 2.0 +/- 0.4 versus 1.6 +/- 0.3 muU/ml) and T4 (6.8 +/- 0.4 versus 6.1 +/- 0.2 mug/100 ml) basal values and a significant decrease in T3 value (1.16 +/- 0.09 versus 0.64 +/- 0.06 ng/ml, p = 0.005). The mean increment of both T3 and T4 after bTSH injection was percentually unchanged during dexamethasone treatment but, due to lowered basal value, T3 levels at each time interval after TSH + dexamethasone were significantly lower than the corresponding values observed after TSH alone. The present data show that high dexamethasone doses decrease T3 serum levels significantly without inhibiting T3 response to TSH stimulation. Only a slight lowering was observed in T4 levels.
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PMID:Effect of dexamethasone on thyroid hormone response to TSH. 118 94

Rats fed a Purina or low-iodine diet (LID) for varying periods were serially sampled before and after a single iv injection of T4, T3, iodide or saline. Suboptimal replacement doses of T4 and T3 were given to rats fed LID for 2 months or 1 year (basal TSH, approximately 1000 and 2000 muU/ml, respectively). Both 1 mug T4 and 0.25 mug T3/100 g BW dropped plasma TSH to 70% of the initial level at 15 min and to 10--20% at 4 h. By 12 h TSH had begun to rise in 2-month LID rats, followed by a secondary decline 3--5 days after injection. Statistical comparison of the slopes of the initial TSH decline indicated there was no significant difference between the effect of T4 and T3. There effect of graded doses of T3 (0.01--0.3 mug/100 g) was also examined. There was a highly significant correlation of the magnitude of TSH suppression with the dose of T3 administered. Saline had no effect but 0.65 mug iodide/100 g BW (equal to that in 1 mug T4) had a delayed effect, depressing TSH to a minimum of 25% of the initial value at 48 h in 2-month LID rats. There was no difference in the effect of these doses of T4, T3, or saline in purina-fed rats (basal TSH, 170 muU/ml). T4 or T3 in physiologically equivalent doses thus produces an identical prompt rate of decrease in plasma TSH, indicating that both hormones possess intrinsic hormonal activity. The delayed effect of iodide is presumably because it must first be incorporated into T4 and T3 and secreted by the thyroid gland. The similarity of depression of plasma TSH by thyroid hormones or saline injection in Purina-fed rats is believed due to a nonspecific stress effect in these animals with a low basal rate of TSH secretion. The non-specific inhibition of TSH secretion is minimal in the iodine-deficient rats with a much higher basal rate of TSH secretion, presumably because of relative vectorial influences.
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PMID:Acute effects of thyroxine, triiodothyronine, and iodide on thyrotropin secretion. 119 14


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