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)

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

Cerebrospinal fluid (CSF) levels of 5-hydroxyindoleacetic acid (5HIAA), tryptophan (TRYP), and homovanillic acid (HVA), were determined prior to electroconvulsive therapy (ECT) and after an average course of 6.7 ECT in six endogenous depressed patients. Depression rating scale (DRS) scores were also obtained by a "blind" research psychiatrist before and after ECT at the time of each lumbar puncture. ECT markedly reduced DRS scores but did not significantly alter CSF levels of 5HIAA, TRYP, or HVA. We found no correlation between ECT-induced DRS score reductions and changes in any of the CSF constituents studied, or between the absolute DRS score and the corresponding CSF concentration of any of the compounds. These data are consistent with those previously reported for ECT and do not suggest that ECT alters cerebral amine metabolism in depressed patients. Neither do they provide any evidence for direct amine mediation of the depression-relieving effects of ECT in man, nor for any relation between severity of depressive illness and CSF concentrations of 5HIAA, TRYP, or HVA.
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PMID:Concentration of 5-hydroxyindoleacetic acid, homovanillic acid, and tryptophan in the cerebrospinal fluid of depressed patients before and after ECT. 126 78

Animal data indicate that serotonin (5-HT) is a major neurotransmitter involved in the control of numerous central nervous system functions including mood, aggression, pain, anxiety, sleep, memory, eating behavior, addictive behavior, temperature control, endocrine regulation, and motor behavior. Moreover, there is evidence that abnormalities of 5-HT functions are related to the pathophysiology of diverse neurological conditions including Parkinson's disease, tardive dyskinesia, akathisia, dystonia, Huntington's disease, familial tremor, restless legs syndrome, myoclonus, Gilles de la Tourette's syndrome, multiple sclerosis, sleep disorders, and dementia. The psychiatric disorders of schizophrenia, mania, depression, aggressive and self-injurious behavior, obsessive compulsive disorder, seasonal affective disorder, substance abuse, hypersexuality, anxiety disorders, bulimia, childhood hyperactivity, and behavioral disorders in geriatric patients have been linked to impaired central 5-HT functions. Tryptophan, the natural amino acid precursor in 5-HT biosynthesis, increases 5-HT synthesis in the brain and, therefore, may stimulate 5-HT release and function. Since it is a natural constituent of the diet, tryptophan should have low toxicity and produce few side effects. Based on these advantages, dietary tryptophan supplementation has been used in the management of neuropsychiatric disorders with variable success. This review summarizes current clinical use of tryptophan supplementation in neuropsychiatric disorders.
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PMID:L-tryptophan in neuropsychiatric disorders: a review. 130 30

Drug-induced depression which is classified as DSM-III-R is difficult for clinicians to diagnose because the cause is not easily distinguishable from adjustment disorders or nonorganic mood disorders. This review summarizes the few articles published within 20 years as searched in the Index Medicus about the clinical manifestations of organic mood syndromes from oral contraceptives (OCs), beta blockers, alcohol and sedative-hypnotic drugs, and other medications. There was a noticeable lack of articles and specific clinical features which would help differentiate causes. Oral contraception may cause depression by inducing hepatic tryptophan oxidase, which may lead to a deficiency of vitamin B6. The most common reason for discontinuing OCs is depression, i.e., there are reports of a rate of 70/1000 woman years during the 1st year of OC use. However, the rate among females examined in a catchment study was similar at 6.6%. There is some indication that depression may be dose related, i.e., low dose is related to the same prevalence as in the control group. A basic requirement of DSM-III-R is severe and persistent depression; OC-related depression does not exhibit sleep or appetite disturbances. The relationship between beta blockers and depression indicates that the prevalence and the nature of the relationship are not consistently confirmed. Depressive episodes (14) reported in 8 studies showed major depression and suicidal thoughts or attempts just after initiation of propranolol and resolution when the drug was discontinued; timing of the symptoms may be the best basis upon which to make a clinical judgement. Alcohol use is usually seen as associated with depression, but the extent to which alcohol induces depression is unknown. Symptoms are transitory and appear during bouts of heavy drinking. Studies on benzodiazepine use and depression are reported to be confounded by other factors. Other depression-causing agents for which information was unavailable are identified as psychostimulants, metoclopramide, H-2 blockers, methyldopa, and steroids.
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PMID:Can drug-induced depressions be identified by their clinical features? 135 May 3

6R-L-erythro-5, 6, 7, 8-Tetrahydrobiopterin (6R-BH4) is known as a cofactor for the hydroxylases of phenylalanine, tyrosine and tryptophan and also as a cofactor for nitric oxide synthase. Recently, a novel function of 6R-BH4 has been found: that is, 6R-BH4 acts on specific membrane receptors to directly stimulate the release of monamine neurotransmitters such as dopamine and serotonin, independently of its cofactor activity. In addition, it indirectly stimulates the release of non-monoamine neurotransmitters such as acetylcholine and glutamate, through activation of monoaminergic systems. In this paper, we briefly review recent experimental data, which provide new insights into the role of 6R-BH4 as a regulator of neuronal function. We also discuss the possibility of treatment by 6R-BH4 of neuropsychiatric diseases such as Parkinson's disease, Alzheimer's disease, depression and infantile autism.
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PMID:[A novel function of tetrahydrobiopterin]. 136 Nov 76

The study concerned 72 schizophrenic and 200 depressed patients hospitalised between 1983 and 1990. The erythrocyte membrane transports (EMT) of L-tyrosine and L-tryptophan (at 37 degrees, 0 degrees and 37-0 degrees) of schizophrenics without treatment nor depression were different compared to controls and depressed patients. The schizophrenics under neuroleptic treatment and/or depressed showed same means of EMT values as depressed patients. The slopes of the correlations between EMT of tyrosine or tryptophan at 37 degrees, 0 degrees and 37-0 degrees, as well as that between plasma levels of these amino acids, were parallel. However the slopes of the correlations between EMT of tyrosine and tryptophan were different according to the subgroups of patients: the perturbations of EMT were related to the clinical characteristics. In depressed patients and in schizophrenic patients under neuroleptic treatment and/or depressed, little changes in EMT of tyrosine were related to high changes of EMT of tryptophan.
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PMID:[Erythrocyte membrane transport of amino acid precursors of monoamines in schizophrenic patients. Comparison with depressive patients]. 136 21

A 55-year-old man presented with a 5-year history of Parkinson's disease and a 6-month history of major depression. The patient's depressive symptoms responded to treatment with fluvoxamine, a selective and potent serotonin reuptake inhibitor. Tryptophan depletion testing, which acutely lowers central serotonin levels, caused a brief exacerbation of the depressive illness, which resolved upon tryptophan repletion. Serotonergic dysfunction may be an etiologic factor in depression that occurs in Parkinson's disease.
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PMID:Serotonergic dysfunction in depression associated with Parkinson's disease. 835 Oct 31

1. Experiments were performed on the brain stem-spinal cord preparation of newborn rats, in which the phrenic and hypoglossal nerves continue to show rhythmic respiratory activity in vitro, in order to compare the effects of serotonin (5-HT) on both activities and to analyse the mechanisms responsible for the depression by 5-HT of the hypoglossal activity. 2. Under control conditions, simultaneous recordings of the inspiratory discharges of hypoglossal and cervical roots showed that the two bursts did not start simultaneously and had different patterns (time-to-peak and peak values); this suggests that both pools of motoneurons did not share the same central drive(s). 3. Adding 5-HT and related agents to the bathing medium delayed and depressed the hypoglossal inspiratory discharge via activation of 5-HT2 receptors since these effects were elicited by 5-HT2 agonists (alpha-methyl-5-HT and 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane-HCl (DOI)) but not by 5-HT1 agonists (RU 24969 and (+/-)-8-hydroxy-2-(di-N-propylamino)tetralin hydrobromide (8-OH-DPAT)). The 5-HT depression of the hypoglossal discharge was prevented by applying a pretreatment with a specific 5-HT2 antagonist (ketanserin). Parallel to the hypoglossal discharge decrease, 5-HT elicited a permanent cervical root discharge along with a persistent inspiratory bursting. Adding the 5-HT precursor L-tryptophan to the bathing medium depressed the hypoglossal (XII) discharge without affecting the cervical one. 4. Local application of 5-HT within the hypoglossal motor nucleus decreased the hypoglossal output, revealing that the 5-HT depression of the hypoglossal discharge was at least partly mediated by the 5-HT effects at the level of the motoneurons. Local application of 5-HT within the cervical motor nucleus elicited a permanent firing in the cervical root with a persistent inspiratory bursting. 5. Intracellular analysis confirmed the existence of differences in central respiratory drive between cervical and hypoglossal motoneurons under control conditions, as well as differences in response to 5-HT. All the hypoglossal motoneurons became silent under 5-HT bathing, and showed no change in the input membrane resistance, a moderate depolarization, and a delayed central respiratory drive with a decreased amplitude. The cervical motoneurons became more active during inspiration, despite a decrease in the amplitude of the central respiratory drive, which was compensated for by a large depolarization and an increased input membrane resistance. Some cervical motoneurons even fired at a low rate during expiration.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Compared effects of serotonin on cervical and hypoglossal inspiratory activities: an in vitro study in the newborn rat. 140 27

The effects of depletion of the serotonin precursor, L-tryptophan, on the threshold and tolerance to cold pressor pain, and the analgesic effect of morphine (10 mg intramuscularly), were tested in a double blind trial on human volunteers. Effects on mood were also assessed using the Profile of Mood States and the Addiction Research Center Inventory (ARCI) Scales. To deplete tryptophan, subjects were fed a tryptophan-deficient amino acid mixture 4.5 h before morphine was administered. Controls received the mixture with tryptophan, which is equivalent to a nutritionally balanced protein. The tryptophan-deficient meal reduced plasma tryptophan more than 70% but had no effect on threshold or tolerance to cold pressor pain. After morphine, tolerance to cold pressor pain increased in controls. Tryptophan depletion abolished this analgesic effect. Pain threshold was not altered by morphine. In subjects with normal tryptophan, the analgesic effect of morphine was predicted by the level of plasma morphine-6-glucuronide, but not by the level of morphine. Morphine increased scores on the LSD scale of the ARCI, but had no effect on other measures of mood. Tryptophan depletion also failed to alter mood in these subjects, who had unusually low depression scores before tryptophan depletion.
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PMID:Acute tryptophan depletion blocks morphine analgesia in the cold-pressor test in humans. 141 Jan 47

Serotonergic mechanisms have been implicated in the pathophysiology of depression and in the neuropharmacology of antidepressant treatment. One measure of central serotonergic function is the prolactin (PRL) response to IV L-tryptophan (L-TRP). We used the L-TRP test to assess the role of serotonin in the mechanism of action of lithium augmentation in refractory major depression. Twenty-six patients with antidepressant-refractory major depression each received three L-TRP tests (after 2 weeks of placebo, after 4 weeks of active primary antidepressant, and after 1 week of lithium augmentation). Primary antidepressant treatment did not increase the PRL response, but lithium augmentation resulted in a statistically significant increase in PRL response as compared to both placebo pretreatment (P less than 0.04) and antidepressant treatment alone (P less than 0.025). This study supports a role for serotonergic mechanisms in the action of lithium augmentation.
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PMID:Serotonergic function during lithium augmentation of refractory depression. 141 Jan 50


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