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)

Asparagine was a superior nitrogen source for clavine-alkaloid production in Claviceps purpurea. Its transport into the cell excedded the cell's biosynthetic need for this amino acid. Asparagine entered the cell without degradation. This disturbed the relative pool sizes of various amino acids resulting in a change in the genetically determined ratio at which amino acids were utilized for protein synthesis. Overproduction of alkaloids (4500 mug.ml-1) may be associated with increased availability of tryptophan because of the enhanced assimilation of asparagine-derived ammonia via glutamine synthetase (EC 6.3.1.2). However, ammonium salts in the fermentation broth led to a depression of the alkaloid yield. Partial replacement of the ammonium salt by aspartic acid elevated alkaloid production.
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PMID:The cellular role of nitrogen in the biosynthesis of alkaloids by submerged culture of Claviceps purpurea (Fr.) Tul. 1 58

The biological mechanisms through which oral contraceptives influence the central nervous system and produce depression were examined. Oral contraceptives reduce the level of serotonin and norepinephrine available at the central adrenergic receptor sites, alter folate and B12 levels, and perhaps influence hypothalamic releasing hormone levels. The level of serotonin is influenced in the following manner. The estrogens in oral contraceptives increase tryptophan available for the brain to convert to serotonin and tryptamine. Depression is associated with lower levels of serotonin, tryptamine, and perhaps tryptophan in the brain. Estrogens in oral contraceptives may also alter pryridoxal phosphate which in turn affects the production of serotonin. Oral contraceptives possibly lower norepinephrine levels by 1) decreasing tyrosine; 2) influencing coenzymes necessary to norepinephrine production; and 3) increasing monoamine oxidase levels. Oral contraceptives apparently inhibit the metabolism of folate and B12, and lower levels of these substances are associated with depressive symptoms. Decreased norepinephrine and serotonin levels may inhibit the release of gonadotrophin-releasing hormones, and these hormones may in turn influence behavior. Recommendations to clinicians were: 1) patients should be screened for a history of depression prior to prescribing oral contraceptives; 2) pill users should be monitored for depression; and 3) 25 mg daily of pyxidoxine should be administered if a patient taking oral contraceptives is deficient in B6.
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PMID:Oral contraceptives and depressive symptomatology: biologic mechanisms. 3 42

Biological functions are regulated by feedback mechanisms. In old age disorders occur in this regulation by insufficiency of biochemical transmitters. The synthesizing enzymes of Tyrosine Hydroxylase, Tryptophan Hydroxylase, Dopa Decarboxylase and 5-Hydroxytryptophan Decarboxylase are diminished in old age. Minus symptoms as depression, or exhaustion and disorders of circulation occur. A substitution by biogenic transmitters is not possible, because these don't pass the blood-brain-barriere. Therefore a medication of psychopharmacological drugs is necessary. For instance Anxiety--tranquilizer, exhaustion--anti depressive drugs.
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PMID:[Psychological problems of incurable patients in old age (author's transl)]. 4 75

The influence of serotonergic system on the changes in locomotor activity of mice and rats brought about by morphine, fentanyl, codeine and pentazocine and on morphine induced catalepsy in rats was studied. p-Chlorophenylalanine (pCPA) did not affect the behavioral changes produced in mice by morphine, fentanyl, codeine and pentazocine but reduced the behavioral depression produced by these drugs in rats. 5-Hydroxytryptophan (5-HTP) but not tryptophan (TP) reversed the action of pCPA on the effect of morphine and fentanyl. After reserpine the depression produced in rats by morphine and fentanyl was more pronounced. TP did not change the depression produced by combination of reserpine and morphine but counteracted the depression observed after combination of reserpine and fentanyl. In mice reserpine protected against hypermotility produced by morphine or fentanyl and TP potentiated the depression produced by the combination of reserpine and morphine or reserpine and fentanyl. Serotonin precursors, 5-HTP and TP evidently potentiated the morphine induced catalepsy. pCPA counteracted only the enhancement of the catalepsy observed after TP administration. Naloxone abolished the catalepsy after combined treatment with morphine and TP. Similarly but weaker acted cyproheptadine. The results suggest that the serotonin system plays a role in the effects of morphine and fentanyl on rat locomotor activity. An increase in the cerebral serotonin level increases the morphine catalepsy in rats.
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PMID:Central action of narcotic analgesics. V. Participation of serotonin in the mechanism of action of narcotic analgesics. 4 45

Tryptophan and 5-hydroxytryptophan have now been extensively investigated in affective disorders. There is now very good evidence that tryptophan increases the antidepressant activity of monoamine oxidase inhibitors. The antidepressant activity of tryptophan and 5-hydroxytryptophan has also been the subject of numerous investigations. There is evidence that patients with decreased cerebrospinal fluid concentration of 5-hydroxyindoleacetic acid respond particularly favourably to this treatment. The therapeutic activity of tryptophan has led to the investigation of the plasma concentration of tryptophan. Free plasma tryptophan, that is tryptophan unbound to plasma protein, appears decreased. There is also evidence that tryptophan and 5-HT transported are abnormal in depression.
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PMID:[Indoleamine precursors in depression (author's transl)]. 9 9

Various mechanisms respond to intakes of amino acids in excess of those required for normal tissue function. When excessive amounts of amino acids are taken, catabolism by enzymes in the liver and elsewhere is accelerated when intake exceeds requirements. In addition, changes in the free amino acid levels in the brain signal the nervous system centers regulating food consumption, and eating patterns are affected. This central nervous system mechanism may even determine the proportions of protein and of energy--yielding nutrients chosen in the diet through a mechanism regulated by the entry of tryptophan and other neurotransmitter precursors into the brain. These observations on protective mechanisms are considered in relation to effects obtained by feeding disproportionate amounts of amino acids. Intakes of large amounts of amino acids can produce toxicities, in which plasma concentrations of the administered amino acid rise to very high levels. Antagonisms arise from feeding excess of one amino acid that can be relieved by feeding a structurally related amino acid. Finally, amino acid imbalances are produced by adding surpluses of essential amino acids other than the essential amino acid most limiting for growth; the growth depression caused by this addition can be relieved by adding more of the most limiting amino acid to the diet. In all circumstances involving feeding with disproportionate amounts of amino acids, there is evidence of changes in brain amino acid levels. It is suggested that these changes play an important role in initiating protective responses against abnormal amino acid intakes.
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PMID:Nutritional consequences of excess amino acid intake. 10 72

Some recent publications relating to the allegedly antidepressive and sedative effects of L-tryptophan the precursor of 5-HT have been reviewed. The evidence to date suggests that the amino acid is as effective as standard tricyclic drugs in alleviating the symptoms of depression, especially those cases presenting with mainly psychomotor retardation, and is synergistic with MAOIs. L-Tryptophan would also appear to be a 'physiological sedative'. This action, however, appears to be related to the time of administration and at present has only been demonstrated at night. when endogenous levels of 5-HT are at their peak. In terms of practical therapeutics L-tryptophan would appear to have greater potential as an 'antidepressant' than as a 'sedative'.
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PMID:Tryptophan antidepressant 'physiological sedative': fact or fancy? 10 27

Treatment of rats with one electroconvulsive shock (ECS) per day for 10 days enhanced the hyperactivity syndrome produced by administration of tranylcypromine (10 mg kg-1) and L-tryptophan (50 mg kg-1) given 24 h after the final shock. Similar enhancement was seen whether the shock was alternating sinusoidal or direct current (fractionated), whether it was given through unilaterally or bilaterally placed electrodes and whether or not a neuromuscular blocking agent (fazadinium) was used. Five shocks spread over 10 days or 8 shocks spread over 17 days were similarly effective, whilst 8 shocks in 1 day were ineffective. Therefore when ECS are given to rats in ways similar to those in which electroconvulsive therapy is given to patients with depression, enhancement of behavioural responses to increased 5-HT function is produced.
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PMID:Enhanced 5-hydroxytryptamine-mediated behavioural responses in rats following repeated electroconvulsive shock: relevance to the mechanism of the antidepressive effect of electroconvulsive therapy. 10 33

C-fiber reflex were recorded from an ipsilateral S1 ventral root in the acute decerebrate spinal (T10) cat after stimulation of the superficial peroneal nerve. L-Tryptophan, infused in a dose of 150 mg/kg, increased the C-fiber reflex to 210% (S.E.M. +/- 30.1%) of control. This effect was antagonized by cyproheptadine, 0.5 mg/kg. L-Tryptophan increased the C-fiber reflex to 176% (S.E.M. +/- 13.0%) of control after p-chlorophenylalanine pretreatment. Pretreatment of the cats with the decarboxylase inhibitor alpha-methyldopa, 100 mg/kg, 30 minutes before infusion, antagonized the facilitatory effects of L-Tryptophan. L-Tryptophan, 150 mg/kg, had no effect on the monosynaptic or short latency polysynaptic reflexes. 5-Hydroxytryptophan, 20 mg/kg, had erratic effects on the C-fiber reflex producing both facilitation and depression which were not statistically significant. The recovery of tryptamine from brain perfusates, after perfusion of the anterior cerebellum and pons, with a modified Gaddum push-pull cannula, decreased across time. L-Tryptophan caused a slight increase in tryptamine release which was not statistically significant, whereas in cats pretreated with p-chlorophenyl alanine, a significant increase in tryptamine release was seen.
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PMID:The effect of L-tryptophan on spinal cord C-fiber reflexes. 13 Apr 82

The free and total plasma tryptophan concentrations were measured in 41 female depressive. Fifteen patients were subsequently treated with L-tryptophan. The free and total tryptophan were normal in the drug-free depressives and in the depressives on lithium. No significant in free and total plasma tryptophan were found between unipolar and bipolar depressed subjects, or between patients who recovered from depression following L-tryptophan therapy and patients who were resistant. The results suggest that the basal free tryptophan concentration in the plasma of depressed subjects is normal. They furthermore indicate that neither free nor total plasma tryptophan concentrations are valid predictors for the course of a treatment of depressed subjects with L-tryptophan.
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PMID:Free and total plasma tryptophan in endogenous depression. 16 83


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