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

1. In the posterior half of the pulvinar of cats anaesthetized with halothane and nitrous oxide, the majority of neurons were fired by ACh released with small electrophoretic currents. In the anterior part of that nucleus, ACh had more variable effects: excitation, depression or none. 2. In comparison with L-glutamate, DL-homocysteic acid and DL-aspartic acid, ACh appeared to be the most potent excitant. 3. ACh-induced discharges were easily and reversibly blocked by low doses of atropine. In most cases, ACh effects could not be blocked selectively by mecamylamine or dihydro-beta-erythroidine. 4. Nicotine failed to mimic ACh, whereas carbachol was a potent excitant and was readily blocked by low doses of atropine. 5. The histochemical reaction to acetylcholinesterase was moderate in the pulvinar. 6. These observations support the view that pulvinar cells differ from other thalamic cells.
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PMID:Micro-electrophoretic studies in the cat pulvinar region: effect of acetylcholine. 2 59

A lethal protein with hemagglutinating activity but without trypsin inhibitory activity was isolated from beans of Phaseolus vulgaris, cultiva, and Kintoki and proved homogeneous by ultracentrifugation, disc polyacrylamide gel electrophoresis, sodium dodesyl sulfate polyacrylamide gel electrophoresis and isoelectric focusing. The molecular weight was estimated to be 104, 000 by ultracentrifugal analysis and gel filtration on Sephadex G-200. The molecule dissociates into three identical subunits in the presence of 8 M urea or 0.1% sodium dodesyl sulfate. The amino acid composition was characterized by the high content of aspartic acid and the complete absence of methionine and cystine. The carbohydrate content was 8.1%; 5.0% mannose and 3.1% glucosamine. The addition of the lethal protein to a basal diet (0.4%) resulted in the intensive depression of the growth and finally in the death of rats. The intraperitoneal injection of 250 microgram per g body weight of mouse brought about an acute toxicity which caused death of all the injected mice.
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PMID:The isolation and characterization of a lethal protein from Kintoki beans (Phaseolus vulgaris). 61 Nov 61

In vivo voltammetry at electrochemically pretreated carbon fibre electrodes was used to investigate the effect of intracerebroventricular (i.c.v.) administration of N-methyl-D-aspartic acid (NMDA) on neuronal activity in rat nucleus accumbens. Infusion of a low dose of NMDA (1 nmol) was followed a few minutes later by rapid changes in both Peak 1 and Peak 2 heights indicating large but short-lived increases in the extracellular concentrations of ascorbate and catecholamines, respectively. These responses did not seem to be dependent on the dose infused since infusion of NMDA for a longer time period neither changed the amplitude nor the time-course of these effects. The increase in Peak 2 height was resistant to pargyline pretreatment indicating that this response mainly reflected the release of dopamine. The administration of NMDA was followed by behavioural activation in the animals but not convulsions. Co-administration of the competitive NMDA receptor antagonist, CPP (1 nmol), completely blocked these effects while the acetylcholine receptor antagonist, atropine (1.5 nmol), and the GABA receptor antagonist, picrotoxin (1 nmol), failed in this respect. The phenomenon spreading depression is discussed as a possible explanation of these results.
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PMID:Rapid changes in ascorbate and dopamine release in rat nucleus accumbens after intracerebroventricular administration of NMDA. 152 Nov 53

We have previously shown that subcutaneous administration of aspartic acid (a dicarboxylic acidic amino acid) at a dose of 580 mg/kg causes long lasting depression of ventilation in adult intact and postpubertally castrated male rats, but not in intact female rats. The purpose of the present study was to determine if hypogonadism induced by perinatal administration of testosterone propionate (TP) will alter ventilation, oxygen consumption, and the ventilatory response to aspartic acid and to hypercapnia in adult males. TP treatment resulted in adult males who had lower body, prostate, heart, and testes weights than those of control male rats. Ventilation in air and oxygen consumption were comparable between the two groups as was the ventilatory response to aspartic acid. In contrast, TP-treated rats exhibited a significantly decreased ventilatory response to hypercapnia due predominantly to lower tidal volumes compared to control animals. Aspartic acid treatment did not affect oxygen consumption in either group. Thus, TP treatment results in the development of adult male rats who, although hypogonadal, retain a male-like ventilatory response to aspartic acid, but whose response to hypercapnia is more like that of hypogonadal men and rats.
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PMID:Control of ventilation in androgenized hypogonadal male rats. 152 34

Previously we observed that acute subcutaneous administration of aspartic acid (580 mg/kg) depressed ventilation in awake male, but not female, rats, suggesting that this agent may be used as a marker for sexual dimorphism in the control of ventilation. Moreover, males castrated postpubertally showed a response similar to that of intact male rats. Thus the hormonal milieu of male rats appear not to be necessary to elicit the masculine type of ventilatory response to aspartic acid. The purpose of this study was 1) to determine whether adult female rats androgenized by the administration of testosterone propionate (TP) 1 day after birth would alter their ventilation in response to aspartic acid to be more malelike and 2) to compare these results with those of intact (I) and ovariectomized (O) female rats. Minute ventilation and O2 consumption in air and in response to aspartic acid administration were evaluated in awake animals in all three groups. Furthermore the minute ventilation of all rats to a hypercapnic challenge was also evaluated. Ovariectomy resulted in rats increased body weights but decreased weight-corrected ventilation and O2 consumption compared with TP-treated and I animals. Minute ventilation after hypercapnic challenge in the three groups was similar. TP-treated rats responded to aspartic acid administration with a marked depression of ventilation similar to that previously noted in males, whereas neither I nor O rats showed such a response. The depression of ventilation in the TP-treated group in response to aspartic acid was not a consequence of a depression of O2 consumption.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of aspartic acid on control of ventilation in androgenized and ovariectomized female rats. 162 80

An alanine-rich, alpha-helical antifreeze polypeptide (AFP) from the winter flounder and seven analogs with variations in the arrangement of neutral, polar amino acids were synthesized. Circular dichroism studies determined that all of the peptides, except for one containing a proline residue, were essentially 100% alpha-helical. Freezing point depression data, analyzed by three methods, showed that rearrangement of polar residues resulted in moderate to complete loss of anti-freeze activity. It was observed that ice crystals grow as hexagonal bipyramids in dilute solutions, with a constant c to alpha axis ratio of about 3.3. Above a critical threshold concentration, which may depend on the AFP to ice binding constant and reflect the onset of cooperative interactions, growth ceases until the temperature is lowered to the freezing point. We conclude that a specific arrangement of both threonine and asparagine (or aspartic acid) residues is critical for maximal activity and that the AFPs probably bind to the pyramidal faces of ice with a specific orientation. These conclusions are consistent with a recent report (Knight, C. A., Cheng, C. C., and DeVries, A. L. (1991) Biophys. J. 59, 409-418) that a similar AFP adsorbs to the [2021] pyramidal planes of ice in dilute solution.
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PMID:Structure-function relationships in an antifreeze polypeptide. The role of neutral, polar amino acids. 162 10

To investigate the role of glutamic (Glu) and aspartic acid (Asp) in migraine, we measured the plasma amino acids in migraine patients with and without aura, between and during attacks, and compared the profiles with the plasma amino acid profiles of tension headache patients and healthy controls. Between attacks, migraineurs (notably with aura) had substantially higher plasma Glu and Asp levels than did controls and tension headache patients. In addition, patients with migraine without aura showed low plasma histidine levels. During migraine attacks, Glu (and to a lesser extent Asp) levels were even further increased. The results suggest a defective cellular reuptake mechanism for Glu and Asp in migraineurs, and we hypothesize a similar defect at the neuronal/glial cell level, predisposing the brain of migraineurs to develop spreading depression.
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PMID:Neuroexcitatory plasma amino acids are elevated in migraine. 197 2

The acute effects of hypoxia and/or hypoglycaemia on DC potentials recorded from CA1 pyramidal neurones of the gerbil hippocampal slice maintained in vitro were investigated. Depolarizing potential changes were recorded when the slice was superfused with the excitatory amino acid agonists: NMDA (N-methyl-D-aspartic acid; 3-30 microM), AMPA ((RS)alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate; 1-30 microM), kainate (3-100 microM) and L-glutamate (1-10 mM). In response to a 20 min period of superfusion with an hypoxic artificial CSF solution at 30 degrees C, a transient depolarization occurred followed by a marked hyperpolarization. A further hyperpolarization occurred when superfusion of the slice with an oxygenated artificial CSF recommenced. Post-hypoxia, when the neurones had repolarized, the response to NMDA (10 microM) was less than the pre-hypoxic response. The extent of the depression of the NMDA response was found to depend on three variables: a) the duration of the period of hypoxia, b) the glucose concentration of the artificial CSF, and c) the temperature of the slice. As the duration of hypoxia was increased, the depression of the NMDA response was more marked. Reduction of the glucose concentration from 11 mM to 2 mM by partial substitution with sucrose (9 mM) made the tissues more sensitive to the effects of hypoxia, whereas reduction of the temperature from 30 degrees C to 20 degrees C made them less sensitive. The depression of the response to NMDA was observed over a range of concentrations of NMDA. The concentration response curve for AMPA was also flattened, however, the depolarizations in response to kainate or GABA were preserved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of hypoxia and hypoglycaemia on DC potentials recorded from the gerbil hippocampus in vitro. 209 Sep 52

Excitatory amino acids depolarize central mammalian neurons by increasing membrane conductance. This increase in conductance can be voltage-dependent (i.e. N-methyl-D-aspartate or L-aspartic acid (L-ASP)) or voltage-independent (i.e. kainic acid (KA)) depending on whether or not the channel is blocked by Mg2+ [8,9]. Intracellular recordings were made from dissociated mouse spinal cord cells and conductance was calculated using constant current techniques. The dissociative anesthetics, ketamine and phencyclidine caused a selective depression in the change in conductance evoked by L-ASP but not that by KA. Under whole cell voltage-clamp (in the absence of extracellular Mg2+) this depression of responses to L-ASP was found to be highly voltage-dependent suggesting a blockade of the channel.
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PMID:Ketamine and phencyclidine cause a voltage-dependent block of responses to L-aspartic acid. 241 68


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