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)

The mechanism of action of adiphenine on in vitro rat anterior pituitary TSH release was compared to that of the physiological stimulator TRH. The comparative study showed that adiphenine and TRH were able to increase TSH release in a dose-dependent manner, had similar time courses of action for equipotent stimulating concentrations and produced similar aspects of stimulated TSH cells. However, there were several differences between the effects of adiphenine and TRH. Adiphenine action was inhibited by 20 mM K+; was not calcium dependent; was inhibited by neither thyroid hormones nor somatostatin; was little affected by energy depression. It is concluded that adiphenine probably acts near the ultimate steps of the TSH release pathway and could be a useful pharmacological tool for studying the mechanism of TSH release.
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PMID:Comparison of adiphenine and TRH effects on TSH release by rat pituitary in vitro. 1 85

Thyrotropin-releasing hormone tartrate (TRH-T) was administered in 17 cases of organic brain lesions and 2 cases of disturbed mental activity (psychical depression), and its effect, mainly on the level of consciousness and electroencephalogram, was examined. Ten consecutive administrations of 0.5--1.0 mg/day TRH-T, as TRH, resulted in improvement of disturbance of consciousness in 8 of 16 cases. This effect was not necessarily correlated with the degree of disturbance or the site of the lesion. Improvement was seen even in those cases where disturbance of consciousness had been fixed over a long period. The effect on the electroencephalogram was small and did not parallel the degree of improvement of the level of consciousness. Abnormal TSH and thyroid hormone values were not seen despite the continued administration of TRH-T. These results would appear to indicate that the continuous administration of TRH-T has a mild activating effect directly on the central nervous system, and not through the endocrine mechanism, and exerts no damage on the internal environment in vivo.
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PMID:Clinical studies of thyrotropin-releasing hormone tartrate (TRH-T) as a direct stimulant to the central nervous system. 3 57

The effects of the ergoline derivative, lergotrile mesylate, on the serum levels of PRL, GH, TSH, LH, FSH, cortisol, and blood sugar were studied in six normal males. The effects of lergotrile mesylate on the serum levels of GH and PRL were also studied in eight patients with acromegaly and in two with idiopathic hyperprolactinemia. In the normal subjects, 2 mg oral lergotrile lowered basal PRL levels after 90 min and markedly impaired the PRL response to TRH (200 micrograms iv); the mean peak value +/- SE was 8.3 +/- 1.1 micrograms/liter, compared to the control value of 66.6 /+- 11.3 micrograms/liter. Lergotrile raised serum GH levels in five of the six subjects to peaks of 8-49 micrograms/liter, compared to 2-8 micrograms/liter after placebo. In three subjects, the GH response to lergotrile was attenuated by the prior administration of the dopamine antagonist, metoclopramide (10 mg orally). Lergotrile had no effect on FSH and LH levels under basal conditions or after the gonadotrophin-releasing hormone (GnRH; 100 micrograms iv). Circulating TSH levels were unaltered basally but impaired after TRH. Blood sugar levels were unaltered; serum cortisol was elevated in five of six subjects; there was a brief depression of diastolic blood pressure, but no change in pulse rate. The side effects after lergotrile were variable, with drowsiness as a consistent feature. These actions are similar to those of bromocriptine (an ergot derivative treatment of hyperprolactinemia and acromegaly, to suppress PRL and GH secretion, and in parkinsonism. Therefore, it may be expected that lergotrile could fulfill these clinical uses; however, in the studies comparing the effects of single oral doses of lergotrile (2 mg) and bromocriptine (2.5 mg) on GH and PRL secretion in patients with acromegaly and hyperprolactinemia, lergotrile in the dose used has been found to have an earlier onset and shorter duration of action.
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PMID:Effect of the dopamine agonist, lergotrile mesylate, on circulating anterior pituitary hormones in man. 4 63

Small doses of iodide (2 times 3.2 mug at 12 h interval), below those capable of inducing Wolff-Chaikoff effect, were injected into rats kept on a moderately low iodine diet. By means of a 125I equilibration technique as well as by direct measurement of cold T4, it was demonstrated that the level of circulating PB125I (representing iodothyronines as confirmed by column chromatography) increased by a mean of 40% within 24 h following the first iodide injection. The serum TSH concentration (measured by radioimmunoassay) was simultaneously depressed. Thus, in stimulated thyroid glands, a biologically significant fraction of an iodide load escapes autoregulatory control of iodothyronine synthesis. A small, transient increase of hormone release is likely to represent the physiological response of a normal gland to a sudden supplement of iodide supply. The ensuing depression of TSH secretion may be necessary for final adjustment of thyroid function. It is considered to be the last step in a cascade of mechanisms whose interaction keeps the thyroidal hormone output within narrow limits in the face of a fluctuating iodide supply. Failure of one or several of these mechanisms in the goitrous human gland could conceivable explain the phenomenon of "Jod Basedow".
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PMID:A transient rise of hormone secretion: a response of the stimulated rat thyroid gland to small increments of iodide supply. 5 15

Eleven cases are reported of subacute thyroiditis with histopathological study; there were 9 females and 2 males. Bacteriological studies were inconclusive. Different stages of pathological involvement were observed at the same time in all patients. The clinical course followed the classical pattern in most cases: hyperthyroid-like, hypothyroid-like phase and recovery. Blood TSH assessment before and after TRH stimulation revealed an early phase of depression unresponsive to TRH, followed by high levels with marked stimulation; during the first phase, radioiodine uptake was low, but was enhanced by exogenous TSH administration; accordingly the low uptake seems to be due to low TSH levels and not to complete destruction of the thyroid gland. Failure of TSH levels to rise after TRH stimulation is typical of this stage of the disease. Although the final outcome is not yet predictable in some patients, definitive myxoedema appears to be probable in two cases.
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PMID:Subacute thyroiditis. Eleven cases with histological confirmation and thyrotrophic response to thyrotrophin releasing hormone. 5 65

Administration of antiserum to synthetic thyrotropin-releasing hormone (TRH) to thyroidectomized rats caused a significant depression of serum thyrotropin (TSH). Serum TSH and triiodothyronine (T3) responses to cold exposure (4 +/- 1 C) were abolished by administration of anti-TRH serum. In addition, synthetic TRH lost its biological activity when bound to the gamma globulin fraction from the anti-TRH serum. These observations provide evidence that TRH is involved in the mechanism of enhanced TSH secretion from the pituitary following thyroidectomy and cold exposure.
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PMID:Suppression of serum thyrotropin (TSH) concentrations following thyroidectomy and cold exposure by passive immunization with antiserum to thyrotropin-releasing hormone (TRH) in rats. 8 Jul 34

Since there are some patient groups whos symptoms do not improve despite the fact that the use of the antidepressants will alleviate the symptoms to some extent, we have conducted a TRH test for depression and found that there are not a few cases who show a low TSH response. We therefore used a small amount of T3 together with the antidepressants in these cases and have found that the therapy is useful for improvement of tye symptoms. When the TRH test is made at the time of improvement of the symptoms due to the combined use of these two drugs and compared with the state at pre-treatment, it has been confirmed that the TSH response will go back to normal. Hence, we would like to present here two markedly improved cases due to the combined use of imipramine and clomipramine plus T, and to refer to the result of the TRH test.
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PMID:Combined therapy of T3, and antidepressants in depression. 11 69

15 patients with formerly endogenous recurrent depression or manic-depressive illness free of psychotic symptoms, who are under lithium prophylaxis about 3,9 years, and 16 healthy controls with approximately the same age and sex were tested with 0,1 U Insulin/kg, 200 micrograms TRH and 50 micrograms LHRH for their hGH-, TSH-, hPRL-, FSH-, LH-and Cortisol levels about 2 hours. hPRL, FSH and LH did not show any change under lithium salts. All patients under lithium showed elevated TSH-levels under basal conditions and after stimulation compared with the control groups. For the young women before menopause the difference was highly significant. Men and praemenopausal women had significantly higher hGH-levels after stimulation under lithium than the normal controls. However postmenopausal women did not show this lithium effect on their hGH levels.
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PMID:[Neuroendocrinological changes under longterm therapy with lithium salts (author's transl)]. 11 22

Follicular cells isolated from normal human thyroid tissue have been cultured for up to 140 h with bovine thyrotrophin (TSH) or dibutyryl cyclic AMP (DBcAMP). Both compounds induced marked reorganization of the cells into three-dimensional follicular structures, whilst non-supplemented cells assumed a monolayer form. Cultures treated initially with TSH or DBcAMP showed a greater iodide uptake capacity, in comparison with unsupplemented cultures, in which iodide uptake was markedly diminished after 24 h. The release of tri-iodothyronine (T3) and thyroxine (T4) into the medium was determined by radioimmunoassay. Both TSH- and DBcAMP-treated cells showed a significant increase in iodothyronine output compared with unsupplemented control cells. In contrast to the "classical" TSH-induced depression of the T4:T3 ratio in vivo, an increase in the ratio was observed for both TSH- and DBcAMP-supplemented cells in vitro. The ratio was also significantly greater after TSH than after DBcAMP, and possible implications of this findings are discussed.
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PMID:In-vitro studies of normal human thyroid cells: responses to thyrotrophin and dibutyryl cyclic AMP. 18 67

Carbamylcholine and acetylcholine through a muscarinic type of receptor, KCl, ionophore A-23187 and NaF increased cyclic GMP accumulation in dog-thyroid slices. These effects were abolished in calcium-depleted slices, which findings confirm that Ca2+ is required for cyclic GMP accumulation. All these agents depressed the accumulation of cyclic AMP in TSH-stimulated slices. KCl and NaF depressed cyclic AMP accumulation in TSH-treated slices even when they had been depleted of Ca2+. This suggests a cyclic GMP- and Ca2+-independent mechanism. The absence of inhibition of the effects of the ionophore, NaF and KCl in the presence of atropine suggests that these drugs do not act by inducing the release of acetylcholine in the slices. The effects of carbamylcholine and ionophore A-23187 on cyclic GMP accumulation and protein iodination were reversible; the inhibitions of TSH-induced cyclic AMP accumulation and secretion were non-competitive and were not accompanied by a depression of ATP levels. All these effects were greatly decreased in the absence of extracellular Ca2+. These data suggest that carbamylcholine and ionophore A-23187 act mainly by increasing the influx of extracellular Ca2+ in thyroid cells. However, the persistence of some carbamylcholine effect in the absence of Ca2+ in the medium suggests that this agent may also trigger the release of Ca2+ from an intrafollicular pool. The kinetics of action of carbamylcholine are compatible with a role of cyclic GMP in the inhibition of cyclic AMP accumulation. However, with the ionophore, the depression of cyclic AMP accumulation was much longer than the rise of cyclic GMP, which suggests a mechanism independent of cyclic GMP.
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PMID:Effects of carbamylcholine and ionophore A-23187 on cyclic 3',5'-AMP and cyclic 3',5'-GMP accumulation in dog-thyroid slices. 22 40


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