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)

A protein has been isolated from the venom of the western diamondback rattlesnake (Crotalus atrox) which induces acute myocardial depression when administered to experimental animals. Purification was achieved by gel filtration on Sephadex G-100, DEAE- and CM-cellulose ion-exchange chromatography, ultra-filtration, and adsorption chromatography on hydroxyapatite. Amino acid analysis of the highly purified protein indicated N-terminal isoleucine and C-terminal tyrosine residues, and the absence of free sulfhydryl groups. Rabbits were immunized against the myocardial depressor protein (MDP) and a highly specific antiserum prepared which made it possible to study other snake venoms for the presence or absence of MDP. All of the North American Crotalid species of snakes contain MDP in varying degrees of concentration, but none of the Asiatic snake venoms tested reacted with the antiserum to the myocardial depressor protein. Intravenous administration of MDP to experimental animals (dogs, cats) produces an immediate and profound decrease in the cardiac output, the left ventricular systolic and mean pressures, the velocity of shortening of the contractile element, the systemic arterial pressure and an elevation in the left ventricular end-diastolic and pulmonary wedge pressures. These hemodynamic changes indicate that MDP administration induces an acute myocardial failure which is does dependent. The potential use of this protein for the reproducible causation of left ventricular failure, obviating the need for the more commonly used surgical ligation of the coronary arteries, warrants a full investigation into its structure, active site and its mechanism of action on the myocardial cell.
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PMID:Comparative biochemistry and pharmacology of salivary gland secretions. III. Chromatographic isolation of a myocardial depressor protein (MDP) from the venom of Crotalus atrox. 96 63

Tryptophan and 5-hydroxyindoleacetic acid (precursor and metabolite respectively of 5-hydroxytryptamine) were determined in ventricular CSF of psychiatric patients undergoing stereotactic subcaudate tractotomy. Tyrosine and homovanillic acid (precursor and metabolite respectively of dopamine) were also determined. Results suggest an association between affective state and the above precursor amino acids with lower concentrations in primary depression and higher ones when anxiety or agitation predominate. This leads to lower 5-hydroxyindoleacetic acid concentrations in depression and higher concentrations in anxiety and agitation.
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PMID:Precursors and metabolites of 5-hydroxytryptamine and dopamine in the ventricular cerebrospinal fluid of psychiatric patients. 99

The object of this study was to determine the effects of individual amino acid supplements on the development of tyrosine toxicity in growing rats fed 10% casein containing 5% tyrosine. Each amino acid was added at levels equivalent to its content in 20% casein. Supplement of methionine to the high tyrosine diet partially alleviated both growth depression and pathological lesions. Threonine and cystine had a somewhat beneficial effect, but the single addition of other amino acids was not effective. Besides, some amino acids enhanced the severity of the toxicity even more. The effects of methionine supplementation were highest at 0.66 to 1.32% levels (equivalent to the methionine content in 20 to 40% casein). By the supplement of both 0.66% methionine and 0.90% threonine to the high tyrosine diet, growth was significantly improved and toxic lesions were completely prevented. It was confirmed that the counteracting effects to the toxicity, caused by the extra addition of protein (casein) to rats fed a high tyrosine-low protein diet, were mainly attributed to the effectiveness of the methionine and threonine, i.e., first-and second-limiting amino acids, respectively, contained in it.
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PMID:Effect of individual amino acid supplements on the toxicity of excess tyrosine in rats. 101 Oct 50

Injections of D,L-5-hydroxytryptophan (D,L-5-HTP) into pigeons and rats working on approach schedules produce a period of behavioral depression that is temporally correlated to increased levels of total serotonin (5-?HT) in the telencephalon and diencephalon. Administration of alpha-methyl-meta-tyrosine (alpha-MMT) also results in depressed responding; however, the temporal correlation is with decreased levels of total 5-HT in brain. Our hypothesis to explain these two apparent opposite biochemical states which result in similar behavioral disruptions is that in both cases more 5-HT is released within certain key serotonergic synapses mediating this behavior. Evidence from subcellular studies supports this concept. tnot only are the levels of 5-HT significantly higher in preparations of nerve endings isolated from the telencephalon and diencephalon of pigeons given injections of D,L-5-HTP, but in vitro studies also show that low concentrations of L-5-HTP significantly increased the release of radioactive 5-HT from serotonergic nerve endings. On the other hand, L-5-HTP in much higher concentrations had no effect on the release of labeled dopamine or norephinephrine. A major metabolite of alpha-MMT, alpha-methyl meta tyramine, also caused a significant increase in the release of labeled 5-?HT from similar preparations of nerve endings. Whereas serotonin appears to be involved in the disruption of approach behavior, another series of studies have indicated that acetylcholine may play a role in excitation during avoidance behavior. Behavioral excitation observed following administration of tetrabenazine 18 hr after iproniazid pretreatment to rats working on shock-avoidance schedules was temporally correlated with lowered levels of acetylcholine in the telencephalon. Pretreatment with 0.8 mg/kg of atropine blocked excitation whereas one-eight of this dose increased the duration. Excitation in these rats was shortened by 50% following bilateral septal lesions, which lowered brain acetylcholine levels. Mechanisms to explain these neurochemical correlates of behavior are discussed.
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PMID:Serotonergic and cholinergic mechanisms during disruption of approach and avoidance behavior. 108 Jan 20

The antigonadotropic activity of cyclic 2,6-cis-diphenylhexamethylcyclotetrasiloxane was investigated in be male rat. The compound was administered orally and the effects were compared with those caused by the subcutaneous administration of estradiol benzoate. The cyclosiloxane lowered serum luteinizing hormone (LH) and follicle stimulating hormone (FSH) in association with sex accessory weight depression. LH declined to 50% of the control level withing 5 hours of a single dose (1 mg/kg/day) of the cylosiloxane while FSH declined more slowly. After 1 week of treatment gonadotropin levels were further decreased to 15-20% of the control level. A direct anterior pituitary block was demonstrated in LH-releasing hormone challenged animals 8 hours after a single dose of cyclosiloxane while estradiol blocked the pituitary as early as 1 hour after estrogen administration. Available releasing hormone activity was decreased at 24 hours by the cyclosiloxane. An increase in the median eminence content of dopamine synthesis form carbon 14-tyrosine was also seen. The effect of estradiol was similar but weaker. It is postulated that this nonsteroid structure exerts its effects at the level of the anterior pituitary and the hypothalamus.
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PMID:The antigonadotropic activity of an organosiloxane in the male rat: 2,6-cis-diphenylhexamethylcyc otetrasiloxane. 108 Mar 35

The effects of some drugs on apomorphine-induced stereotyped behavior were studied in male cynomolgus monkeys. Apomorphine produced the dose-dependent stereotyped behavior characterized mainly by continuous licking and biting, and repetitive movements of the hands, head and body in the monkeys. Penfluridol as well as haloperidol showed a clear antagonistic effect on the apomorphine-induced stereotyped behavior, while chlorpromazine was less antagonistic than haloperidol. The antagonistic effect of penfluridol lasted longer than that of haloperidol. Reserpine did not inhibit the apomorphine-induced stereotyped behavior though the drug elicited markedly the behavioral depression and alpha-methyl-p-tyrosine also did not block the stereotyped behavior. Nialamide did not depress the apomorphine-induced stereotyped behavior. In provoking the stereotyped behavior in monkeys, apomorphine probably acts directly on dopamine receptors in the extrapyramidal system, and penfluridol is suggested to act as a dopamine receptor blocker with a long action. The results indicate that protection against apomorphine-induced stereotyped behavior in monkeys may be a useful method for evaluating neuroleptic drugs.
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PMID:Effects of penfluridol and other drugs on apomorphine-induced stereotyped behavior in monkeys. 117 Oct 14

Biochemical human post-mortem studies on depressed patients indicate an unspecific deficiency of neurotransmitters in several brain areas. The loss of drive of these patients could be correlated with a decrease of striatal dopamine concentration. Noradrenaline was significantly diminished in red nucleus, a fact which points to the characteristic posture of depressed patients. Serotonin was diminished in all brain areas. During remission all values trended to be normal. There also exists a circadian disrhythm in depressed patients resulting in lowered VMA- and HVA-levels in urines during the morning and a remission to normal values in the evening. This agrees with the findings of lowered blood tyrosine levels in the morning. The ratio of blood tyrosine and tryptophan is disturbed during depression and recovers during remission. Central and peripheral biochemical mechanisms seems to be involved in depression syndrom.
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PMID:Biochemical post-mortem findings in depressed patients. 118 63

Effects of histidine or methionine imbalance and dietary levels (3-50%) of casein on food intake and preference of young, adult, and diabetic (2.5 month old) rats were examined. Depressions in food intake and growth caused by ingestion of the imbalanced diet were greatest in young rats and least or absent in diabetic rats. Alloxan diabetes induced hyperphagia and elevated concentrations of plasma branched-chain amino acids and decreased concentrations of tryptophan and tyrosine. The diabetic rats fed the imbalanced diet for 9 days had a higher concentration of the limiting amino acid in the plasma than the adult normal rats fed the same diet. The diabetic rats preferred the imbalanced diet over a protein-free diet when they were fed these diets concurrently. Ingestion of the imbalanced diet by normal rats caused greater changes in plasma and brain amino acid patterns than did the protein-free diet. Unlike the diabetic rats, the normal rats, especially the young rats, strongly preferred the protein-free diet over the imbalanced diet. The normal rats also preferred a 10% casein diet supplemented with L-methionine over a low or high casein diet. It seemed that young rats were able to select a protein diet that supported maximal growth when proportions of dietary amino acids were balanced. It also seemed that the susceptibility of the rats to amino acid imbalance varied directly with the status of overall protein synthesis of the animals.
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PMID:Effects of amino acid imbalance and protein content of diets on food intake and preference of young, adult, and diabetic rats. 119 6

There was a depression of transformation of noradrenaline, DOPA and thyrosine added in vitro, into catecholamines in the adrenal glands of rats after swimming for a period of 8 hours. This permitted to suppose a depression of the activity of phenylethanolamine-N-methyl-transpherase, DOPA-decarboxylase, and, possibly, of tyrosine hydroxylase under these conditions. After the end of swimming, in the presence of 1-tyrosine, there is at first an activation of noradrenaline synthesis, and then there occurs a gradual normalization (on the 7th day) of adrenaline formation. In rats trained for a period of 2 months the extent of reduction of the catecholamine synthesis in the adrenal glands in response to the 8-hour swimming was much less in comparison with the untrained aniamals.
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PMID:[Mechanisms of catecholamine synthesis disorders in the adrenals of rats subjected to physical fatigue]. 122 89

We have reported earlier that administration of 3-nitro-L-tyrosine (MNT), 8 mM in drinking water, to rats receiving a low iodine diet (LID) results in greater TSH secretion, larger goiters, and more rapid uptake and release of radioiodine than LID alone, and ultimately may produce hypothyroidism. These findings have been confirmed, and hypothyroidism documented by demonstrating depressed levels of hepatic mitochondrial alpha-glycerophosphate dehydrogenase. Also, prolonged treatment with MNT + LID produced a depression in labeled iodothyronine (ITh) synthesis, as judged by chromatographic analysis of thyroid digests from rats killed 4 or 24 hours after ip injection of radioiodine, or two weeks after adding radioiodine to drinking fluid. Low thyroidal ITh levels were accompanied by low levels of ITh in serum, despite the presence of various other labeled organic iodine compounds. Cessation of MNT treatment, or ip injection of small amounts (0.5-1.0 mug) of Na 127I together with radioiodine 4 h before sacrifice reversed the defect, and large amounts of ITh were found in both thyroid and serum. Labeled thyroprotein from MNT-treated rats showed increased susceptibility to disaggregation during freezing at pH 8.5; this abnormality was also reversed by stable iodine treatment. In glands labeled with radioiodine 24 h before sacrifice, stable iodine injection 20 h later was followed by increased thyroidal ITh. It is concluded that profound iodine deficiency, induced by MNT + LID, can lead to diminished ITh synthesis, or a "coupling defect". The results provide an explanation for the finding of low thyroidal ITh in patients with hereditary deficiency of tyrosine dehalogenase. The findings confirm an important role for iodine supply in ITh synthesis and thyroglobulin stability, and suggest that rats treated with MNT + LID provide a model for study of the effects of extreme iodine deficiency.
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PMID:Induction of a coupling defect in rats during inhibition of tyrosine dehalogenase. 124 38


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