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)

Ram "rete testis" fluid (RTF) routinely collected throughout the year has been used as a source of inhibin. The mean flow rate and mean concentration of spermatozoa in the fluid remained constant during the first 12 days of cannulation. More than 50 castrated or cryptorchid rams have been treated with low doses of steroid-free RTF over a 25-h blood sampling period. Human serum albumin was injected as a control. RTF depressed both FSH and LH plasma levels although the pattern was different for each hormone. There was no change in prolactin secretion. LH secretion was affected first while FSH remained unchanged in castrated and in cryptorchid rams. Thereafter, the maximum depression of FSH plasma levels occurred at a time when LH started to return or had returned to preinjection levels in the cryptorchid and castrated animals respectively. In the cryptorchid rams, RTF suppressed pulsatile LH secretion which was present before treatment but in the castrated animals, RTF lowered LH plasma levels which were constant and showed no pulsatile changes before treatment. Both FSH and LH inhibitory activities have been found in all active fractions obtained by purification of RTF. These activities are papain-sensitive and active fractions have a high apparent molecular weight (greater than or equal to 100 000) as shown by gel filtration and ultrafiltration. These and other results in the literature have lead to a re-definition of inhibin as a protein factor of gonadal origin able to depress plasma levels of FSH and LH, even at low doses.
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PMID:Inhibin activity in ram rete testis fluid: depression of plasma FSH and LH in the castrated and cryptorchid ram. 4 91

Amineptine is a tricyclic derivative with a 7-carbon chain of aminoacids. Chemical alterations of the aminoacid chain have revealed its importance in the shaping of the pharmacological effects. The drug is rapidly absorbed. Amineptine is metabolised principally by beta-hydroxylation of the chain. The pharmacological profile at different doses is as follows: a. 0.1 mg/kg: reduction of exploratory behaviour, b. 1 mg/kg: reduction of serum prolactin level, c. 5 mg/kg: potentiation of L-5 HTP, d. 10 mg/kg: antagonism of the effects of reserpine and of tetrabenazine, e. increased activity and social behaviour, EEG alerting effect limited to 1 hour and increase in paradoxical sleep (15 to 20 mg/kg). This pharmacological profile suggests an effect of amineptine upon certain dopamine structures. At synapse, neurobiochemistry confirms a mechanism of inhibition of DA incorporation and inhibition of uptake and/or release of 5 HT. Amineptine is virtually devoid of peripheral activity, particularly anticholinergic Amineptine may be indicated for the treatment of depression where retardation is dominant.
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PMID:[Amineptine, a new antidepressant: pharmacological review (author's transl)]. 4 71

Significant increases of both alpha peak amplitude and power were found in the EEG after delivery as compared to those observed at the 32nd week of pregnancy. Controls failed to display the same gain in the alpha rhythm. The frequency was unaffected. Beside these quantitative changes no particular EEG pattern occurred. Neither the methodology nor habituation were considered responsible for these increases, which are also independent of the prolactin levels, because they were observable after blockage by bromocryptine, a drug which also fails to modify the EEG. Significant reduction of anxiety, tension and irritability was scored in the Hamiltonian test for depression. It is likely that both aspects depend on a common humoral process. The role of the progesterone drop is discussed.
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PMID:Alpha increase in puerperium. 8 27

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

Chronic alcoholics with secondary depression were treated with protirelin in a double-blind, placebo-controlled study. Behavioral data, collected only during the acute alcohol withdrawal state, indicated a beneficial effect of protirelin three hours after injection, but not during subsequent days. Injections caused only mild and infrequent subjective side effects and no cardiovascular effects. Endocrine data were recorded in the acute withdrawal state and after clinical remission. Findings in the acute state suggested thyroid activation and increased central dopaminergic activity, as evidenced by elevated baseline levels of growth hormone, low baseline levels of prolactin, and blunted thyroid-stimulating hormone (TSH) response to protirelin. The first two abnormalities returned to normal levels in the remission state. A blunted TSH response was observed in both the acute and the remission states. Partial persistence of this finding suggests that TSH blunting may not be solely state-dependent. In the acute withdrawal state, TSH blunting was associated with favorable behavioral responses to protirelin.
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PMID:TRH (protirelin) in depressed alcoholic men. Behavioral changes and endocrine responses. 10 8

1. In the present experiments evidence was shown which demonstrates that PGF2alpha treatment of the rat produces a rapid fall in circulating progesterone in the latter part of pseudopregnancy but not shortly after corpus luteum formation. This refractory period of at least 3 days following ovulation is similar to that which occurs in large animals, such as the cow. 2. Loss of luteal LH receptors was associated with a loss in LH-stimulated progesterone synthesis and an attenuation of LH-stimulated cyclic AMP synthesis in vitro, a finding which supports a functional loss of LH activity in such tissues exposed in vivo to PGF2alpha. Tissue levels of cyclic GMP were generally decreased by both LH, PGF2alpha, and incubation and the relevance of the latter cyclic nucleotide remains obscure in luteolysis and corpus luteum function. 3. The depression of progesterone induced by PGF2alpha precedes a marked drop in corpus luteum LH receptors but no change in reeptor affinity was seen. For example, the first significant drop in LH receptors was observed 8 hr after PGF2alpha treatment whereas serum progesterone was depressed within 2 hr. 4. Prolactin administration to animals simultaneously with PGF2alpha blocked the loss in LH receptors and serum progesterone observed with PGF2alpha treatment alone. In one experiment, but not in the other, prolactin treatment alone produced an elevation in corpus luteum LH receptors. Suppression of endogenous prolactin secretion with ergocryptine mimicked the effect of PGF2alpha on both the LH receptor and serum progesterone and this effect was also blocked with simultaneous prolactin treatment. It is concluded that the mechanism of PGF2alpha-induced luteolysis has several components. The initial event appears to be due to direct gonadotropin antagonism which occurs independently from a change in quantity of luteal LH receptors. This effect has been shown in vitro (10) as well as in vivo (3) and the mechanism appears not to be related to changes in ovarian hemodynamics and not to direct antagonism of LH binding to its receptor (23). Possibly the early effect of PGF2alpha may be due to elevation of cGMP which then antagonizes cyclic AMP action, but our studies to date have been unsuccessful in demonstrating such a response. Eight hours following PGF2alpha administration, the first measurable decrease in LH receptors was seen and this response was correlated with the first sign of functional luteolysis, elevation of serum 20alpha-ol. The latter response is correlated with a loss of prolactin action on the corpus luteum; it was therefore interesting to observe that prolactin blocked, and ergocryptine mimicked, the PGF2alpha effect on the LH receptor and serum progesterone. Thus, one is lead to the conclusion that the mechanism of luteolysis produced by PGF2alpha in the rat is closely associated with a loss in prolactin activity...
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PMID:Studies on the mechanism of PGF2alpha and gonadotropin interactions on LH receptor function in corpora lutea during luteolysis. 18 87

To investigate whether a direct influence exists between the prolactin suppressive effect of alpha-bromoergocriptine (CB 154) and the aldosterone response to a potassium stimulation, the present study was performed in 7 anephric patients and in 7 non-nephrectomized patients, all on regular haemodialysis. The increase in the plasma potassium concentration between dialysis was used as a stimulus to the adrenals, and was correlated to the increase in the plasma aldosterone concentration (PAC). Plasma samples were obtained during a control period and during a corresponding period of treatment with bromocriptine. Despite a significant fall in the prolactin levels during the bromocriptine treatment, no differences in the aldosterone response to the increasing potassium concentration in the two periods were found neither in the anephric nor in the non-nephrectomized patients. It is concluded that depression of prolactin levels by the dopamine agonist (bromocriptine) has no influence on the ability of the adrenals to react with an increase in aldosterone secretion following potassium stimulation in dialysis patients with and without preserved renin-angiotensin system.
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PMID:Lack of effect of prolactin inhibition by alpha-bromoergocriptine (CB 154) on plasma aldosterone in anephric and non-nephrectomized patients on regular haemodialysis. 19 47

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 effects of an altered content of dietary iodine and fat on the development of N-nitrosomethylurea-induced mammary tumors in rats were studied and correlated with thyroid and pituitary function studies. In three separate experiments, animals fed a semisynthetic diet containing 11.8% fat had an earlier time of tumor appearance and greater tumor burden than did controls maintained on a diet containing 4.6% fat. These diet-associated changes were markedly inhibited by ovariectomy, indicating that the tumor growth was hormone responsive. We examined the possibility that the diet with increased fat content enhanced tumor growth through alterations in prolactin metabolism but could find no consistent elevation in serum prolactin and no increase in pituitary prolactin synthesis in vitro. Our data further showed that rats on an iodine-deficient form of the high-fat diet had no greater tumor growth than did animals receiving an iodine-supplemented form of the same diet. We conclude from these results that iodine deficiency does not promote mammary tumorigenesis. An incidental finding of great interest was that ovariectomy led to a highly significant depression of thyroid-stimulating hormone production in vitro. This suggests that estrogens may directly influence thyroid-stimulating hormone synthesis in vivo and thus contribute to the sex-related differences in thyroid physiology.
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PMID:Effects of iodine deficiency and high-fat diet on N-nitrosomethylurea-induced mammary cancers in rats. 42 60

The effect of intravenous somatostatin on blood levels of metabolites and hormones has been examined in normal subjects who performed a 30-minute period of bicycle exercises at 70% maximal exercise capacity. The results have been compared with control studies in the same subjects. Measurements were made of blood levels of lactate, glucose, free fatty acids, glycerol, acetoacetate, 3-hydroxybutyrate, insulin, glucagon, growth hormone (hGH) and prolactin. Growth hormone and glucagon release were suppressed during exercise with somatostatin and there was a subsequent elevation during recovery. There was slight post-exercise depression of insulin, but no alteration of plasma prolactin secretion. Blood glucose was reduced during exercise with somatostatin and increased during recovery. The elevation of ketone bodies after exercise was greater in the investigation with somatostatin, but there were no significant changes in other metabolites. Somatostatin, although causing inhibition of hGH release, appeared to have no significant effect upon fatty acid mobilization during exercise.
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PMID:The effect of somatostatin on metabolic and hormonal changes during and after exercise. 47 77


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