Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:4.1.1.15 (glutamate decarboxylase)
2,169 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pregnant rats (for prenatal exposure), 5-day-old rats, and 5-week-old rats were exposed orally to lead acetate daily for 10 weeks. Lead values in the brain of animals from all three lead-exposed groups were similar. Brain norepinephrine (NE) and GABA levels and glutamate decarboxylase (GAD) activity were decreased, and brain glutamate (glu), glutamine + asparagine (gln/asn), and tyrosine (tyr) levels, and monoamine oxidase (MAO) activities were increased in rats prenatally or 5 days postnatally exposed to lead. Brain ammonia, alanine (ala), aspartic acid (asp), and dopamine (DA) values were not affected by the prenatal or 5-day-postnatal lead treatment. Brain uptake index (BUI) values for glu were significantly elevated in rats exposed to lead prenatally or 5 days after birth. Exposure of 5-week-old rats to lead did not affect the brain catecholamine and amino acid levels. These results suggest that the brains of young rats were more sensitive to lead exposure than the brains of adult rats, although the accumulation of lead in brain was not affected by age.
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PMID:Neurotoxicity in rats sub-chronically exposed to low levels of lead. 271 3

Effects of oral administration of NC-1100 on the metabolism of neuroactive amino acids in rat brain were studied using stroke-prone spontaneously hypertensive (SHR-SP) and Wistar Kyoto rats. The repeated administration of NC-1100 induced a significant increase of gamma-aminobutyric acid (GABA) content in the cerebellum and medulla oblongata of SHR-SP. The decrease of aspartic acid contents in the cerebellum and medulla oblongata of SHR-SP was also noted following NC-1100 administration. Although the activity of L-glutamic acid decarboxylase did not change in these cerebral areas, the activity of GABA-transaminase:succinic semialdehyde dehydrogenase was found to be significantly reduced in the cerebellum of SHR-SP following the repeated administration of NC-1100. The turnover rate of GABA was also significantly reduced in the cerebellum and medulla oblongata of SHR-SP. It was also found that the spontaneous release of preloaded [3H]GABA from cerebral cortical slices was significantly retarded by the continuous oral administration of NC-1100. These results suggest that NC-1100 may be a drug inducing the increase of GABA in the cerebellum and medulla oblongata following continuous administration, especially in animals having hypertension associated cerebrovascular disorders such as SHR-SP.
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PMID:Effect of NC-1100 [1-(3,4-dimethoxyphenyl)-2-(4-diphenylmethylpiperazinyl) ethanol dihydrochloride] on gamma-aminobutyric acid (GABA) metabolism in rat brain: analysis using stroke-prone spontaneously hypertensive rat. 277 51

Mycobacillin lacks amino groups but contains two free alpha-carboxyl groups, indicating the presence of two side-chain peptide linkages. The five aspartic acid residues of mycobacillin are all in alpha-peptide linkage whereas the two glutamic acid residues are in gamma-linkage. Mycobacillin does not react with hydroxylamine to give hydroxamate, indicating the absence of anhydride, lactone and ester linkages. This is also confirmed by i.r. spectroscopy and titration of the molecule. Of the 15 peptides obtained from partial hydrolysates of mycobacillin, 12 contain aspartic acid. Results obtained by treatment of hydrolysates of aspartic acid-containing peptides with d-amino acid oxidase and l-glutamate decarboxylase (containing l-aspartate decarboxylase activity) indicate that residue 5 is l-aspartic acid and residues 2, 8, 11 and 13 are d-aspartic acid. The d- or l-peptide sequence and nature of peptide linkages in mycobacillin are proposed on the basis of these findings and the amino acid sequence reported earlier.
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PMID:Gamma-glutamyl and D- or L-peptide linkages in mycobacillin, a cyclic peptide antibiotic. 439 25

The intralaminar distributions of transmitter and nontransmitter enzyme activities and amino acid levels were determined in the midtemporal cortices from normal individuals and established cases of Alzheimer's disease. In the normal, choline acetyltransferase (CAT) and acetylcholinesterase (AChE) activities were relatively high in the outer cortical layers, particularly, for CAT, in the two granular layers (II and IV). Both activities were reduced in Alzheimer's disease at all, although generally most extensively in the outer and middle layers of the grey matter whereas activities were near normal in the white matter. Further, the enzyme distribution patterns of these cholinergic activities were also disrupted in Alzheimer's disease and the activity of CAT throughout the cortex was generally reduced to that found in the white matter. No such differences in distribution were found for two other enzymes, pseudocholinesterase and lactate dehydrogenase. Assessment of the gamma-aminobutyric acid (GABA) system in the normal revealed a much more extensive intralaminar variation in the enzyme, glutamate decarboxylase, compared with the level of GABA itself. In contrast with the cholinergic enzymes, neither the levels nor intralaminar patterns of GABA were altered in Alzheimer's disease. From an analysis of free amino acids at the different cortical levels, the cortical pattern of glutamic acid in the normal was different from that for GABA, aspartic acid, or nontransmitter amino acids such as alanine. Neither of the putative amino acids, glutamate or aspartate, was altered in Alzheimer's disease. These findings demonstrate the relatively selective nature of microchemical changes occurring in the cortex in Alzheimer's disease and suggest that a functional abnormality in cholinergic input to the outer neocortical layers (I-IV) with predominantly receptive and associative functions may be an important feature of the disease.
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PMID:Intralaminar neurochemical distributions in human midtemporal cortex: comparison between Alzheimer's disease and the normal. 614 24

Six groups of five female rats each aged 6 weeks at start were fed different diets for a period of 15 days. The protein sources of diets used were: a) 10% casein: b) wheat: c) Bengalgram: d) wheat + lysine: and e) Bengalgram + methionine + cystine + tryptophan, all containing 1.6 g nitrogen/100 g, and f) 20% casein (3.2 g nitrogen/100 g diet). The group of five rats fed a 10% casein diet served as control. It was observed that total brain RNA, protein and free alpha amino nitrogen content and protein/DNA ratio were significantly decreased on wheat and Bengalgram diets as compared to the control. The specific activities of glutamine synthetase, glutaminase I, glutaminase II and glutamate decarboxylase and concentrations of aspartic acid, glutamic acid, glutamine and gamma-aminobutyric acid (GABA) in the brain were also decreased on wheat and Bengalgram diets. The fortification of wheat with lysine and of Bengalgram with methionine, cystine and tryptophan did not alter brain weight and DNA content. While brain RNA, protein free alpha amino nitrogen (F alpha AN) and activities of enzymes of glutamic acid metabolism and related amino acid levels were restored, the activity of enzyme glutamine transferase and alanine concentration remained unaltered on various diets fed. The observations on 20% casein diet showed that levels were similar to those observed on 10% casein diet.
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PMID:Effect of wheat and Bengalgram diets on brain glutamate metabolism in postweanling rats. 615 61

The release of prelabeled [3H]-GABA and endogenous GABA evoked by KCl and excitatory amino acid analogs was compared in intact chick retina and retina previously lesioned by the neurotoxins, kainic acid and N-methyl-D,L-aspartic acid. Significant discrepancies were found in the results obtained by the two techniques; and while changes in endogenous GABA release after neurotoxin lesions correlated with retinal glutamate decarboxylase activity, a marker for GABAergic neurons, the release of [3H]-GABA did not. These results call into question the validity of the prelabeling technique for studying GABA release from retina.
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PMID:The dissociation of evoked release of [3H]-GABA and of endogenous GABA from chick retina in vitro. 638 64

The neurotoxic and convulsant properties of conformationally restricted and synthetic analogues of excitatory acidic amino acids were examined after stereotaxic injection into the striatum and the dentate gyrus of the hippocampal formation. In the striatum, neurotoxicity was quantified by the reduction in the activity of choline acetyltransferase and glutamate decarboxylase, markers for striatal intrinsic neurons. The following sequence of neurotoxic potencies was defined; kainic acid approximately equal to domoic acid much greater than alpha-keto kainic acid approximately equal to alpha-allo kainic acid greater than ibotenic acid approximately equal to cis-cyclopentyl glutamic acid greater than quisqualic acid approximately equal to N-methyl-D-aspartic acid. When normalized for neurotoxic potencies, a wide variation in the convulsant effects of the agents was observed after hippocampal injection. N-Methyl-D-aspartate produced nearly continuous electroencephalographic seizures for 2 hr after injection, where alpha-keto-kainate and kainate and quisqualate caused seizure activity for 64 and 45% respectively of this period; kainate, alpha-allo kainate and domoate caused intermittent seizure activity during approximately 30% of the recording period; ibotenate and cyclopentylglutamate had minimal convulsant effects. Seizures were associated with a significant reduction in the levels of norepinephrine and with increases in the levels of 5-hydroxyindoleacetic acid in the cortex and hippocampal formation and increases in the levels of gamma-aminobutyric acid in the hippocampal formation. Kainate, domoate, keto-kainate and alpha-allo-kainate caused extensive lesions of the hippocampal formation that also involved the pyriform cortex; ibotenate and cyclopentylglutamate caused uniform but substantial lesions limited to the dentate gyrus, whereas quisqualate and N-methyl-D-aspartate produced small and restricted lesions. The results demonstrate a poor correlation between the neurotoxic and convulsant potencies of these excitatory amino acid analogues and suggest that receptor-specific interactions may account for these disparities.
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PMID:Excitatory amino acid analogues: neurotoxicity and seizures. 706 5

6-week-old, female albino rats were fed one of three diets containing 5, 10 and 20% casein for a period of 15 days. Rats fed the low protein diet (5% casein) lost weight (6.3 +/- 0.7 g/week), whereas those on the two higher protein diets gained weight. The concentrations of protein and free amino nitrogen in the brain were significantly lower in those on the low protein diet (5% casein) compared to those on the high protein diet (20% casein). The activities of brain enzymes, glutamine synthetase, glutamine transferase, glutaminase I, glutaminase II and glutamate decarboxylase, and the concentrations of free amino acids, aspartic acid, glutamic acid, glutamine, alanine and GABA were also lower. The prospect for nutritional rehabilitation of rats fed the low protein diet appeared to be excellent and was illustrated by the reversal of the above changes after 15 days on the high protein diet. The diet containing 10% casein was sufficient for the normal production of enzymes and free amino acids related to glutamate metabolism.
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PMID:Protein deprivation and the brain: effect on enzymes and free amino acids related to glutamate metabolism in rats. 730 87

The hyperexcitability observed following ethanol withdrawal in dependent animals is thought to be related to increased sensitivity of glutamate receptors. This may predispose to 'excitotoxic' neural damage. The aim of this study was to test this hypothesis by intrahippocampal injection of N-methyl-D-aspartic acid (NMDA) in ethanol-dependent rats and to quantify brain damage using enzymic neuronal markers, viz. choline acetyltransferase (ChAT) and glutamate decarboxylase (GAD). Specific activity of GAD but not ChAT was found to be significantly decreased in hippocampi of ethanol-dependent animals following injection of NMDA, suggesting that chronic ethanol administration sensitizes GABAergic neurons to the toxic effects of excitatory amino acid transmitters.
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PMID:Chronic ethanol administration sensitizes hippocampal neurons to neurotoxicity of N-methyl-D-aspartic acid. 774 24

Chronic administration of ethanol in animals leads to CNS tolerance and physical dependence. Subsequent withdrawal of ethanol causes hyperexcitability which is thought to be related to increased sensitivity of N-methyl-D-aspartic acid (NMDA) receptors. The purpose of this study was to investigate sensitivity to NMDA in ethanol-treated animals by detecting damage after intrahippocampal injection of NMDA. Choline acetyltransferase (ChAT) and glutamate decarboxylase (GAD) specific activity was used as markers of cholinergic and gamma-aminobutyric acid neurons, respectively. Ethanol-dependent animals were more liable to die following intrahippocampal injection of either 120 or 240 nmol of NMDA. There was a significantly greater decrease in hippocampal GAD but not ChAT specific activity in the surviving animals. These data support the hypothesis that ethanol dependence is associated with increased sensitivity to NMDA which may be responsible for excitotoxic brain damage and death.
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PMID:Increased sensitivity of the hippocampus in ethanol-dependent rats to toxic effect of N-methyl-D-aspartic acid in vivo. 846 3


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