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)

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

The effects of thyrotropin-releasing hormone (TRH) on growth hormone (GH) and prolactin (Prl) secretion have been investigated in vitro and in vivo in domestic fowl. In both conscious and anaesthetized immature chickens the administration (i.v.) of TRH (2.5 and 25 microgram/kg) significantly increased the concentration of plasma GH. The simultaneous administration of somatostatin (GHRIH), 2.5 microgram/kg, to conscious birds significantly reduced the magnitude of the GH response to TRH treatment, but had no effect on the basal levels of plasma GH. The repeated injection of TRH (10 microgram/kg) every 20 min over a 100-min period failed to maintain the concentration of plasma GH at a high level. Prl secretion was not stimulated in any of these experiments, and in anaesthetized birds TRH (2.5 and 25 microgram/kg) treatment was followed by a depression in the level of plasma Prl. The effects of TRH and GHRIH on GH secretion by an in vitro dispersed pituitary cell suspension system were very similar to the in vivo studies. TRH stimulated Prl release in vitro, in contrast to the in vivo studies, and the response was dose related. GHRIH had no effect on the basal release of Prl in vitro but significantly inhibited the response to TRH treatment.
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PMID:The effect of thyrotropin-releasing hormone (TRH) and somatostatin (GHRIH) on growth hormone and prolactin secretion in vitro and in vivo in the domestic fowl (Gallus domesticus). 9 25

The mechanism of stimulatory action of thyrotropin-releasing hormone (TRH) on spontaneous motor activity was investigated in rats. TRH produced a significant hyperactivity with intraperitoneal administration of 20 mg/kg or bilateral injection of 10 micrograms into the nucleus accumbens septi (NAS). Following bilateral injection of 6-hydroxydopamine into the mesolimbic dopamine (DA) pathway, the hyperactivity induced by TRH was not altered, whereas the response to apomorphine given intraperitoneally or DA injected into the NAS was clearly enhanced. The TRH-induced hyperactivity was remarkably suppressed by alpha-methyltyrosine and in contrast, augmented by pargyline. Systemic injection of aminooxyacetic acid in a dose producing behavioral depression reduced markedly the TRH-induced hyperactivity. Bilateral injection of ethanolamine O-sulphate (100 micrograms) into the NAS produced no behavioral depression per se, but remarkably attenuated the hyperactivity response to TRH or DA (20 micrograms) given intraperitoneally or into the NAS. Both TRH (10(-5) and 10(-4) M) and methamphetamine (10(-6)--10(-4) M increased the spontaneous release of 14C-DA from rat NAS slices. These findings suggest that TRH induces hyperactivity by enhancing DA release from nerve terminals in the NAS without a direct stimulation of the post-synaptic DA recptors. TRH and GABA, independently or via interaction between them, may play a reciprocal regulatory role in the activity of the mesolimbic DA system.
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PMID:Thyrotropin-releasing hormone: hyperactivity and mesolimbic dopamine system in rats. 11 87

In order to determine the role of thyroid hormone in prolactin (PRL) secretion in patients with amenorrhea-galactorrhae, PRL response to 500 mug of iv thyrotropin-releasing hormone (TRH) was studied before and after the administration of triiodothyronine (T3) in 10 patients with amenorrhea-galactorrhea. Seven of these patients were euthyroid and the other 3 had hypothyroidism. The patients in the euthyroid group received 50 mug of T3 daily for 7 days and 75 mug q.d. for the ensuing 14 days. The hypothyroid patients received T3 at progressively increasing doses from 10 mug q.d. to 75 mug q.d. during 34 to 68 days. In the initial test, the elevated basal levels of PRL, 61.9 +/- 9.8 ng/ml (Mean +/- SE) exhibited a slight but insignificant net increase (7.7 +/- 2.1 ng/ml) after TRH injection in the euthyroid group. However, a marked response to TRH with a net increase of 147.2 +/- 26.3 ng/ml from the basal level of 47.3 +/- 11.2 ng/ml was observed in the hypothyroid patients. After treatment with T3, both the basal level (56.9 +/- 8.3 ng/ml) and the net increase (9.9 +/- 3.6 ng/ml) of PRL following TRH stimulation remained virtually unchanged in the euthyroid group. The hypothyroid group, in contrast, displayed a significant depression of both the basal level (26.1 +/- 13.0 ng/ml) and the net increase (33.8 +/- 6.5 ng/ml) of PRL to TRH stimulation. The diminution of the basal levels and responses of thyroid-stimulating hormone (TSH) to TRH stimulation was observed in all cases of both groups. These results suggest that the level of thyroid hormone has little pathogenic role in PRL secretion in euthyroid patients with amenorrhea-galactorrhea, in contrast to its marked effect in hypothyroid patients with amenorrhea-galactorrhea.
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PMID:Effect of triiodothyronine treatment on prolactin secretion in patients with amenorrhea-galactorrhea. 40 25

The biochemical research of depression did not gain in before the exploration of the nodes of effect of the antidepressants. For the present the point of research was the search for disturbances in metabolism of the biogenic amines in brain. The noradrenalin and serotonin-hypothesis was propounded postulating a disturbance in noradrenalin, or serotonin regulation, respectively at the receptor in depression. Until now experimental results did not support this hypothesis, just as the investigations of electrolytic changes in depression did not lead to homogeneous results. On the contrary the neuroendocrinological research showed important results; In endogenous depressive patients an increased cortisol-secretion was ascertained, and in about 65% of the patients a missing or strongly reduced cortisol-suppression after injection of dexamethason was noted, moreover, the growth-hormone-secretion after insulin-hypoglycemia is reduced in a part of depressive women in the menopause. Finally the thyrotropin-secretion stopped in 20--40% of the endogenous depressive patients after injection of thyrotropin-releasing hormone.
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PMID:[Biochemical research in depression (author's transl)]. 48 Aug 57

The effects of thyrotropin-releasing hormone (TRH) on the release of growth hormone (GH), prolactin (PRL) and thyrotropin (TSH) were investigated in patients with depression. Intravenous injection of synthetic TRH (500 mug) caused a significant increase in plasma GH (peak value: 7.7 minus 35.0 ng/ml) in 8 of 13 patients with mental depression. After clinical recovery these patients had no response of plasma GH to TRH. TRH administration did not raise plasma GH in normal subjects examined. Plasma PRL responses to TRH were significantly enchanced (P smaller than 0.05) in depressed patients compared with control subjects. Plasma TSH responses to TRH were significantly blunted in patients with depression (P smaller than 0.05). These results suggest disorders in the hypothalamo-pituitary function in depression.
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PMID:Growth hormone and prolactin release after injection of thyrotropin-releasing hormone in patients with depression. 80 76

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

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

To test the effect of thyrotropin-releasing hormone (TRH) on serum arginine vasopressin (AVP) in euthyroid and hypothyroid individuals, 500 mug of TRH was administered to four euthyroid subjects and three patients with primary hypothyroidism. Serum AVP was significantly depressed below basal levels from 30 to 60 min in the euthyroid and hypothyroid subjects after administering the releasing agent. The basal serum AVP in the hypothyroid subjects (3.1 +/- 1.1 muU/ml) was not significantly greater than the basal serum AVP in the euthyroid subjects (2.8 +/- 1.2 muU/ml). The maximal incremental depression in serum AVP after TRH in the hypothyroid subjects (1.4 +/- 0.7 muU/ml) was similar to the depression observed in the euthyroid subjects (1.8 +/- 0.9 muU/ml). These data suggest that TRH may have a physiologic role in modulation of AVP release in man.
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PMID:Effect of TRH on serum arginine vasopressin in euthyroid and hypothyroid subjects. 82 36

The respiratory effects of pymadin, amiridine, thyrotropin-releasing hormone (TRH), its analog RGH 2202, and pentetrazol and their interaction with morphine were studied in anesthesized rats. During intravenous injection or local application to the medulla oblongata, pymadin, amiridine, TRH and RGH 2202 were shown to enhance the respiratory activity of the diaphragm and to abolish its morphine-induced inhibition. TRH and RGH 2202 proved to be the most potent and safe antagonists of morphine-induced respiratory depression. These agents given in the doses sufficient to completely abolish morphine-induced respiratory depression unchanged its antinociceptive activity. Pentetrazol in the tested dose range failed to increase diaphragmatic respiratory activity or to eliminate its depression induced by morphine.
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PMID:[Central nervous system stimulants as nonspecific antagonists of morphine-induced respiratory depression]. 130 43


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