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)

Substrate regulation of System A transport activity in rat H4 hepatoma cells is described. The uptake of several amino acids was tested in the presence of system-specific inhibitors. System A activity was increased in a RNA- and protein synthesis-dependent manner by amino acid deprivation of the cells (adaptive regulation), whereas transport by Systems ASC, N, y+, and L was unaffected. Unlike human fibroblasts, the H4 cells did not require serum to exhibit the depression of System A. At cell densities between 88 X 10(3) and 180 X 10(3) cells/cm2, the degree of adaptive regulation was inversely related to cell density. Both transport of AIB and adaptive regulation of System A were nearly abolished if either K+ or Li+ was substituted for Na+ in the medium. The presence of cycloheximide or tunicamycin blocked further increases in starvation-induced activity within 1 hr of addition, suggesting the involvement of a plasma membrane glycoprotein. In contrast, if the medium was supplemented with actinomycin after the stimulation of System A had begun, the activity continued to increase for an additional 2 hr before being slowed by the inhibitor. The contributions of trans-inhibition and repression to the amino acid-induced decay of System A activity were estimated for several representative amino acids. In general, the System A activity in normal rat hepatocytes was much less sensitive to trans-inhibition than the corresponding activity in H4 hepatoma cells. The half-life values for the amino acid-dependent decay of System A ranged from 0.5 to 2.0 hr.
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PMID:Adaptive regulation of neutral amino acid transport System A in rat H4 hepatoma cells. 257 76

Neutral amino acid transport was characterized in human synovial cells. The amino acids tested are transported by all three major neutral amino acid transport systems, that is, A, L, and ASC. The model amino acid 2-aminoisobutyric acid (AIB) was found to be a strong specific substrate for system A in synovial cells. When cells were starved of amino acids, the activity of AIB transport increased, reaching a maximum within 1 h. The stimulation of transport activity was not blocked by cycloheximide and would thus appear to be related to a release from transinhibition. Similarly, the decrease in the activity of AIB transport observed after the addition of alpha-methyl-aminoisobutyric acid (meAIB) appeared to be related to transinhibition. However, using a different approach, that is, amino acid starvation followed by incubation with 10 mM meAIB and transfer to an amino acid-free medium with or without cycloheximide supplementation, a clear increase in AIB uptake, due both to derepression and a release from transinhibition, was observed. Unlike human fibroblasts, the depression of system A in these synovial cells was not serum-dependent. The process of derepression was observed only after preloading with meAIB. Neither AIB nor alanine produced this phenomenon. Moreover, alanine preloading led to a large increase in AIB transport activity due to a release from transinhibition. These observations indicate that the process of derepression and release from transinhibition are specific to the substrates present in the culture medium prior to amino acid starvation.
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PMID:Neutral amino acid transport in human synovial cells: substrate specificity of adaptative regulation and transinhibition. 277 95

The mechanism of transport of alanine and aminoisobutyric acid into chondrocytes in rabbit articular cartilage was shown to be mediated by transport systems similar to that described for other eukaryotic cells namely the A, ASC, and L systems. Three days after the initiation of an acute inflammatory arthritis by the intra-articular injection of carrageenin into one knee joint the rate of transport of both these amino acids was decreased. Although all three transport systems were depressed, it appeared that the A and ASC systems were partially susceptible to damage by the induced inflammation. The rate of amino acid transport by the affected cartilage had recovered by 28 days after carrageenin treatment. This depression in amino acid transport is discussed in relation to a decrease in general metabolic processes in chondrocytes as a consequence of inflammation.
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PMID:Carrageenin-induced arthritis. VI. Alterations in amino acid transport by articular cartilage in acute inflammatory arthritis. 402 8

The passive avoidance learning and extinction in mice strain ASC with high predisposition to catalepsy as compared with mice of CBA and AKR strains were analyzed. Impairment of fear extinction as a major symptom of depression was revealed in ASC mice, whereas a delay of extinction in CBA mice and fast formation of new inhibitory learning in AKR mice were found. It is suggested that the long persistence of fear in ASC mice results from increased anxiety during the repeated presentation of a context in the absent of aversive stimulus. Defect of fear inhibition in ASC mice makes it possible to use this strain of mice as genetic model of depression.
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PMID:[Learning and extinction of passive avoidance in mice with high predisposition to catalepsy]. 1872 70

Recent data from several studies suggest that oxidative stress is involved in the biochemical mechanisms that underlie neuropsychiatric disorders. The present study was designed to investigate oxidative stress status in depressive patients with gastric adenocarcinoma (GA) at TNM stage III. Oxidative stress, depression and expression of specific genes were monitored during a pretreatment period. Serum total antioxidant capacity, catalase, superoxide dismutase concentrations, and antisuperoxide anion capacity (A-ASC) were significantly decreased in depressive patients compared to control subjects, whereas serum malondialdehyde (MDA) levels were significantly increased. Importantly, the formation of 8-hydroxy-deoxyguanosine (8-OHdG) accumulated. Furthermore, SYBR Green real-time PCR revealed that the expression levels of human oxoguanine glycosylase 1 and APEX nuclease 1 (APEX1) were increased in depressive patients. Pearson correlation analysis revealed that depression was positively correlated with SAS, SCL-90, MDA, 8-OHdG and APEX1, but negatively correlated with A-ASC. Thus, this study confirms oxidative imbalance in depressive patients with GA, and oxidative stress may play a role in the onset and exacerbation of depression.
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PMID:Oxidative stress in depressive patients with gastric adenocarcinoma. 1927 8

This report presents results obtained from comparative analysis of learning and the dynamics of extinction of a conditioned passive avoidance response in ASC mice, which were bred for a high level of predisposition to catalepsy, and in CBA and AKR mice. The following findings were obtained: 1) impairments to the extinction of the memory of fear represent an important symptom of depression in ASC mice; 2) extinction is delayed in CBA mice; and 3) new inhibitory learning occurs quickly in AKR mice. Prolonged retention of the fear memory in ASC mice appears to be related to increased anxiety on prolonged testing without a punishment. The deficit of inhibition of the fear reaction in ASC mice allows this strain to be regarded as a genetic model of depression.
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PMID:Learning and extinction of a passive avoidance response in mice with high levels of predisposition to catalepsy. 1943 Sep 79

We studied effects of chronic thyroxin administration (2 mg/l, for 60 days) on motor activity, anxiety and depression-like behavior in cataleptic (ASC/Icg) and non-cataleptic (AKR/J) strains of mice. No effects of thyroxin on anxiety indicators in "open field" and "light/dark" tests were revealed in mice of the strains under study. At the same time, thyroxin increased moveability in the "open field" test in AKR/J mice and produced an antidepressant effect in the "forced swimming" test in animals from ASC/Icg strain. Obtained results are indicative of the role of inherited predisposition to catalepsy in determining the sensitivity to thyroid hormones.
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PMID:Effect of thyroxin on behavior of mice with inherited difference in predisposition to catalepsy. 1951 25

Experiments on C57BL/6J mice of submissive stereotype and behavioral despair response and ASC/Icg mice with high predisposition to catalepsy, which served as depression-like state models, were used to study the influence of benzodiazepine receptor antagonist flumazenil on the restoration of a passive avoidance reaction learned under conditions of the amnesic effect of animal detention in a dark compartment. It is established, that flumazenil (10 mg/kg) reactivated retrieval of the amnesic memory trace in mice of submissive stereotype with the behavioral despair response, while being ineffective in ASC mice.
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PMID:[Flumazenil restores amnesic trace of memory in mice with depression-like state]. 1992 67

ASC (Antidepressant-Sensitive Catalepsy) mice, bred for a high predisposition to catalepsy, are characterized by depression-like behavior and decreased immune responses. Chronic administration of fluoxetine, which is a selective serotonin reuptake inhibitor antidepressant widely used in clinical practice, to mice of this strain weakened catalepsy and normalized the number of rosette-forming cells in the spleen. In mice of the parental cataleptic strain CBA/Lac, fluoxetine had no effect on the level of catalepsy or the immune response. Analysis of the effects of fluoxetine on the functional activity of 5-HT(1A) and 5-HT(2A) receptors, and the expression of 5-HT(1A) receptor genes in the frontal cortex and midbrain and 5-HT(2A) receptors in the frontal cortex, as well as the tryptophan hydroxylase-2 and the serotonin transporter genes in the midbrain showed that the antidepressant had no effect on these parameters in ASC mice, but decreased the functional activity of 5-HT(2A) receptors in CBA/Lac mice. The possibility that the actions of fluoxetine on catalepsy and the immune response in mice with depression-like states are mediated via other serotoninergic mechanisms is discussed.
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PMID:Effects of chronic fluoxetine treatment on catalepsy and the immune response in mice with a genetic predisposition to freezing reactions: the roles of types 1A and 2A serotonin receptors and the tph2 and SERT genes. 2046 12

Single administration of brain-derived neurotrophic factor (BDNF) into the lateral ventricle of ASC mice (Antidepressant Sensitive Catalepsy), a model of depression-like state, significantly decreased predisposition to cataleptic freezing in these animals. These findings indicate that BDNF can appear as a promising antidepressant of new generation and that ASC mice can be used as an adequate model for investigations of the mechanisms of behavior modification by BDNF.
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PMID:Intracerebral administration of brain-derived neurotrophic factor (BDNF) reduces severity of cataleptic freezing in mice with genetic predisposition to catalepsy. 2111 99


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