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)

L-Glutamate applied exclusively to the CA3 cell body region of the rat hippocampal slice resulted in long-term potentiation (LTP) of the CA1 population spike evoked by Schaffer collateral stimulation. The same localized glutamate application to the CA1 area caused a prolonged depression of the response. These observations are consistent with the possibility that LTP is at least partly presynaptic and that the depression is due to an effect of glutamate on the postsynaptic elements and/or the presynaptic terminals.
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PMID:Effects of localized applications of L-glutamate on the population spike in the hippocampal slice preparation. 613 98

Five experiments were conducted using crystalline amino acid and semipurified diets containing adequate levels of all indispensable amino acids, vitamins, and minerals to study the effects of dispensable amino acids on growth and the incidence of leg abnormalities of male chicks. Purified diets containing 5% L-glutamic acid as the sole source of nonspecific nitrogen resulted in poor growth and feed efficiency, high mortality, and a high incidence of leg abnormalities with many severe cases of this condition. Increasing the dietary level of L-glutamic acid to 10% of the purified diet or supplementing the 5% L-glutamic acid diet with 2.40% glycine or 1.68% L-serine improved weight gain but did not eliminate the leg conditions. Higher L-serine (3.36%) resulted in a growth depression, indicating that this level was toxic to the birds. It was necessary to increase the dietary L-glutamic acid to 12.5% to reduce the incidence of leg problems to a minimum. Plasma dispensable amino acid levels (aspartic acid, glutamic acid, and alanine) paralleled the levels of L-glutamic acid in the diets fed to the chicks. Plasma serine and glycine levels were increased by adding either serine or glycine, but the magnitude of the increase of either amino acid was greatest with the addition of that amino acid to the diet. Plasma proline concentrations increased when chick diets were supplemented with high levels of glycine (2.4%), serine (3.36%), or glutamic acid (9.7%) in relation to those supplemented with only 5% L-glutamic acid. Feeding an intact protein (isolated soybean protein) diet did not alleviate leg disorders, although it did improve weight gain.
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PMID:Effects of a nonspecific nitrogen deficiency on growth rate and leg problems in chicks. 614 10

Spreading depression (SD) in the chick retina is completely suppressed by 10 mM MgCl2 in the bathing solution (Mg-sensitive SD). However, after increasing the KCl concentration in the Mg solution to values between 10 and 20 mM the retina can again exhibit SDs (Mg-insensitive SD). It has been postulated that the Mg-sensitive SD is a glutamatergic phenomenon. This is supported by the effect of four gl(utamate)-antagonists--L-proline, glutamic acid diethyl ester (GDEE), D-alpha-aminoadipate (D-AA), and 2-amino-4-phosphonobutyrate (APB)--which all suppressed this type of SD. It was suggested that this effect is due to competitive binding of glutamate involved in the Mg-sensitive SD and the gl-antagonist to glutamate receptors. The suppression of SD could be reversed by washing the preparation in a physiologic salt solution. The gl-antagonists in relatively high concentrations had a cytotoxic effect which, when severe, suppressed SD and prevented the recovery of this phenomenon by washing the compound out of the tissue. The compounds examined had, in addition to their gl-antagonistic properties, a gl-agonistic effect, which was postulated to enhance the Na+ permeability of neural membranes resulting in a release of K+ into the extracellular space. In preparations bathed in 10 mM MgCl2 (which suppresses Mg-sensitive SDs) the four compounds investigated promoted Mg-insensitive SDs supposedly when the extracellular K+ concentration reached values between 10 and 20 mequiv.
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PMID:The nature of the chick's magnesium-sensitive retinal spreading depression. 615 68

The effects of several dietary factors on the anorexigenic response to monensin in chicks fed corn-soybean meal diets varying in crude protein (CP) were investigated. In Trial 1, crossbred chicks (New Hampshire X Columbia) were fed a 16% CP diet with or without 160 mg/kg monensin and/or .53% potassium carbonate in a 2 X 2 factorial design. Monensin supplementation caused a 24.5% growth depression, and potassium carbonate had no effect on the monensin-induced depression. Trials 2 and 3 were designed to evaluate the effects of dietary energy level on the monensin response in commercial broiler chicks fed diets containing 24, 20, or 16% CP. As CP level was decreased, the depression in performance from 121 mg/kg monensin increased. Increasing the energy concentration of the 24 and 20% CP diets to that of the 16% CP diet had no consistent effect on the response of chicks to monensin. Trial 4 was conducted to determine the influence of amino acid (AA) supplementation on the monensin response in broiler chicks fed a low-protein diet. Supplementation of a 16% CP diet with an AA mixture (3% glutamic acid plus essential AA equal to the 24% CP diet) improved growth performance markedly. Deletion of methionine, arginine, and lysine from the AA mixture yielded performance well below that of chicks fed the unsupplemented 16% CP diet, indicating a severe AA imbalance. Monensin supplementation at 121 mg/kg caused a much greater growth depression in chicks fed 16% CP or 16% CP plus the complete AA mixture than in those fed 24% CP or the AA-imbalanced 16% protein diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of dietary electrolyte balance, energy, and amino acid supplementation on the monensin response in chicks fed diets varying in protein content. 653 32

L-Proline and some of its analogs have been shown to prevent spreading depression (SD) in the chick retina at relatively low concentrations and to impair memory processing without provoking toxic or electrophysiological disturbances. Both effects are hypothesized to be caused by inhibition of the effects of glutamate released into the extracellular space. L-Proline, its D-enantiomer, six proline analogs including two homologs (L-azetidine-2-carboxylic acid and DL-pipecolic acid), and five other compounds were examined for their effects on spreading depression and their amnestic and electrophysiological effects. L-Proline, L-baikiain, DL-3,4-dehydroproline, and L-4-hydroxyproline all reduced the incidence of SD in the chick retina and proved to be amnestic. D-Proline, L-pyroglutamic acid, L-azetidine-2-carboxylic acid, DL-pipecolic acid, L-glutamic acid diethylester, L-isoleucine and L-norleucine neither depressed SD nor caused retrograde amnesia. L-Prolyl-L-proline and L-glutamine did not depress SD at low concentrations but had significant amnestic effects. None of the listed compounds induced EEG disturbances. Implications for memory mechanisms are discussed in the light of these results.
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PMID:Amnestic potency of proline analogs correlates with anti-spreading depression potency. 719 Feb 93

The chick's choline and methionine requirements are both increased by high dietary protein level. Studies were conducted to test the hypothesis that the chicks' need for preformed methyl groups is increased by high protein diets (not methionine or choline per se). Chicks fed 25% isolated soybean protein (ISP) diets responded to methionine supplementation (162 vs 110 g gained in 14 days) but not to choline (119 g vs. 110 g), while those fed 50% ISP responded to either methionine (174 g vs. 126 g) or choline (181 g vs. 126 g) supplementation. Further, neither cystine nor homocystine could replace methionine in improving the growth of chicks fed the high protein diet. In other experiments, L-methionine and betaine HCl were found to alleviate the growth depression caused by excessive levels of L-glutamic acid. Excessive levels of L-methionine had a protective effect against growth depression caused by L-glutamate and diammonium citrate, and conversely, supplementary L-serine and sodium formate were not protective against glutamic acid- or arginine-induced growth depression. The results are consistent with the hypothesis that the preformed methyl group requirement is increased by high levels of dietary protein and excessive nitrogen from a single amino acid.
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PMID:The effects of high dietary protein and nitrogen levels on the preformed methyl group requirement and methionine-induced growth depression in chicks. 726 36

Twenty dogs underwent 15 minutes of normothermic ischemic arrest and 30 minutes of reperfusion while on cardiopulmonary bypass. In 10 control dogs, the reperfusate blood was not modified. In 10 other dogs, the aorta was reclamped and the heart reperfused for 5 minutes with blood containing L-glutamate (0.026M). We measured coronary blood flow (microspheres), left ventricular (LV) metabolism [O2 content, adenosine triphosphate (ATP)], LV compliance (intraventricular balloon), and LV performance (balloon and Starling curves) before and 30 minutes after ischemia. Fifteen minutes of ischemic arrest produced significant depression in contractility and oxidative metabolism. L-Glutamate infusion resulted in higher oxygen uptakes (9.7 versus 6.9 cc/100 gm/min) and allowed more complete recovery of ATP content (80% versus 67%). Glutamate-treated hearts had more complete recovery in the rate of contraction, +dP/dt, (96% versus 68%), and relaxation, --dP/dt (99% versus 72%), the best recovery of compliance (74% versus 88%), and complete (100%) recovery of stroke work index (1.55% versus 0.87% gm - m/kg). We conclude that the addition of L-glutamate to reperfusate blood reverses ischemic damage. We suspect that l-glutamate acts by replenishing Krebs' cycle intermediates lost during ischemia, thereby stimulating oxidative metabolism and enhancing ATP production.
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PMID:Reversal of ischemic damage with amino acid substrate enhancement during reperfusion. 743 10

We have investigated the effects of administration of exogenous glutamate receptor agonists on the amplitude of field excitatory post-synaptic potentials (fEPSPs) evoked in the CA1 region of the rat hippocampal slice by stimulation of the Schaffer collateral-commissural fibres. L-Glutamate applied by iontophoresis or by bath perfusion (50 microM for 5 min) evoked a slowly rising increase in the amplitude of the fESPS which persisted for over 90 min. L-Glutamate induced potentiation was blocked by either D(-)-2-amino-5-phosphonopentanoic acid (40 microM) or by (RS)-alpha-methyl-4-carboxyphenylglycine (500 microM). In slices in which synaptic long-term potentiation had been saturated, iontophoretically applied L-glutamate did not induce further potentiation, but reset the fEPSP amplitude back to control levels. Iontophoretic administration of N-methyl-D-aspartate (NMDA) evoked a transient potentiation which decayed back to control levels within 90 min whereas bath perfusion of NMDA (50 microM) evoked a persistent depression. Bath perfusion of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA, 50 microM) evoked no persistent effects. Bath administration of (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD, 50 or 100 microM) caused a short term depression of the fEPSP and no significant persistent effects. Perfusion of 100 microM ACPD in medium containing 1 microM picrotoxin caused a much smaller short term depression of the fEPSP and this was followed by a gradually developing and persistent potentiation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Potentiation of synaptic transmission in the rat hippocampal slice by exogenous L-glutamate and selective L-glutamate receptor subtype agonists. 753 Aug 14

Aspartic acid, 5-hydroxyindoleacetic acid, glutamic acid, homovanillic acid and 3-methoxy-4-hydroxyphenylethylene glycol was determined in samples of ventricular fluid from 82 subjects. Laminar distribution of the total number (Bmax value) of serotonin 1A receptors was determined on seven neurosurgical samples of neocortex. Apart from an association in a small subgroup of subjects between homovanillate concentration and corticosteroid medication, no complicating influences of treatment preceding operation were found. The content of the serotonin metabolite alone was significantly reduced in intractable depressive illness (bipolar and major depressive disorders) compared with neurological conditions subdivided into Alzheimer's disease, other dementias and other conditions. There was no other significant difference between these groups for the compounds measured. The total number of serotonin 1A receptors was highest in the superficial layers, being considerably higher than in the rat, irrespective of cortical layer. This part of the study indicated that these receptors are important for regulating activity of human corticocortical glutamatergic neurons. The results are discussed in relation to treating depression with serotonergic agents and targeting corticocortical glutamatergic neurons as well as acetylcholine in Alzheimer's disease.
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PMID:Antemortem measurements of neurotransmission: possible implications for pharmacotherapy of Alzheimer's disease and depression. 767 42

The effect of L-glutamate to alter ethanol-induced central depression was studies in male Swiss-Webster mice. The duration loss of the righting reflex (LORR) was used as a measurement of CNS depression. Mice were injected (IP) with ethanol (4.0 g/kg), which caused them to lose the righting reflex. After mice regained the righting reflex following ethanol injection (IP), they were immediately injected (ICV) with saline or L-glutamate (1, 15, or 25 mumol/kg). L-Glutamate induced a return to the LORR within 60 s after ICV injection of drug. When L-glutamate was administered (ICV) in the absence of ethanol, no significant loss of the righting occurred. In other experiments, DL-2-amino-5-phosphonovaleric acid (APV), a competitive inhibitor of NMDA, was given ICV with L-glutamate in the presence of ethanol. APV did not significantly antagonize the interaction between ethanol and L-glutamate. When bicuculline methiodide, a GABA antagonists, was administered with L-glutamate (ICV), bicuculline methiodide reduced the effect of L-glutamate to produce a return to the LORR in the presence of ethanol. These data indicate the L-glutamate, an excitatory amino acid neurotransmitter, can enhance the central depressant action of ethanol. It appears that an interaction between the GABAergic and glutamatergic systems may be involved in ethanol intoxication.
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PMID:Interaction between L-glutamate and ethanol on the central depressant properties of ethanol in mice. 790 47


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