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At least 631 records · Page 35Linked to original sources
PubMed1986

Development of a micromethod to study the Na+-independent L-[3H]glutamic acid binding to rat striatal membranes. I. Biochemical and pharmacological characterization.

A micromethod was developed to measure the Na+-independent L-[3H]glutamic acid (Glu) binding to rat striatal membranes by using slightly purified membranes from very small tissue amounts, ranging from 0.2 to 0.5 mg wet tissue. The specific binding reached equilibrium in about 30 min incubation at 37 degrees C and was shown to be partly reversible. Scatchard's analysis of saturation data suggest the presence on striatal membranes of an apparent single homogeneous population of Na+-independent binding sites with Kd value 1.75 microM and Bmax 3.89 nmol/g protein. Hill's plot of these data was linear with slope not significantly different from unity, indicating the absence of cooperative interactions. Cl- and Ca2+ ions were shown to severely influence the L-[3H]Glu binding to striatal tissue. Maximal activating effects were obtained in the presence of both ions, although Cl- alone was shown to have a powerful stimulating action on the binding. Pharmacological studies suggested, however, the presence of at least two subpopulations of binding sites which bound quisqualic acid as well as ibotenic acid with differential affinities. L-aspartic acid and L-serine-O-sulfate were shown to be potent inhibitors of the L-[3H]Glu binding while DL-2-amino-4-phosphonobutyric acid (DL-APB) and glutamic acid diethylester (GDEE) competed with the binding but only at high concentrations. N-methyl-D-aspartic acid (NMDA), DL-2-amino-5-phosphonovaleric acid (DL-APV), D-alpha-aminoadipate (D-alpha AA) and kainic acid were shown not to significantly influence the binding of Glu to striatal membranes.

Amino Acids↗
PubMed1985

Inhibition of crayfish glutamic acid decarboxylase by structural analogs of the substrate and product.

Crayfish glutamic acid decarboxylase (GAD) is inhibited by some aliphatic carboxylic acid analogs of glutamate and gamma-amino-n-butyric acid (GABA). Variations in the length of the carbon skeleton, substitution of a keto for a methylene group, replacement of the carboxyl group or attachment of a bulky basic moiety to the amino terminus of GABA all lead to a drastic reduction in its inhibitory activity. Substitution of a methyl group for the amino group of GABA is a permissible alteration which does not reduce the inhibitory potency. Some structural analogs of glutamate are inhibitory also, particularly if they possess a comparable carbon skeleton and a keto group in the alpha position or a sulfhydryl group. Most of the sulfhydryl analogs are significantly more potent as inhibitors than the corresponding compounds in which the SH group is replaced by an H atom.

Animals↗
PubMed1994

Identification of autoantibody epitopes of glutamic acid decarboxylase in stiff-man syndrome patients.

Stiff-man syndrome is a neurologic disorder characterized by progressive rigidity of skeletal muscles. Deficiency of the neurotransmitter gamma-aminobutyric acid and autoantibodies to glutamic acid decarboxylase (GAD), the enzyme synthesizing gamma-aminobutyric acid, are closely associated with the disorder, although the relevant antigenic epitopes have not been identified. In the present study, sera from two patients with SMS was used in an immunoblotting assay with recombinant GAD67 (M(r) 67,000) and GAD65 (M(r) 65,000) isoforms to test whether SMS sera can recognize specific epitopes. We found that both SMS sera recognized the GAD65, but not the GAD67, isoform. Using 13 different synthetic GAD peptides to block the autoantibodies, two GAD65 epitopes were identified. One epitope recognized by both patients' sera, was blocked by the peptide representing amino acid residues 354-368. In one patient only, blocking was also observed by a peptide representing residues 390-402, which includes the binding site of the GAD cofactor, pyridoxal 5'-phosphate. A single amino acid substitution in GAD65 at position 401 (leucine to proline) and representing the analogous GAD67 sequence in this region significantly reduced the peptide's inhibitory effect. These findings suggest that SMS GAD autoantibodies share distinct GAD65 linear epitopes and that some SMS patients' autoantibodies may block the active site, explaining SMS GABA deficiency.

Adult↗
PubMed1986

Escape behavior produced by the blockade of glutamic acid decarboxylase (GAD) in mesencephalic central gray or medial hypothalamus.

Microinjections into the mesencephalic central gray (CG) or the medial hypothalamus (MH) of three drugs (L-allylglycine, Semicarbazide or 4,5 dihydroxy-isophtalic acid) known to block glutamic acid decarboxylase (GAD) produced a dose-dependent behavioral activation accompanied by jumps. These effects are qualitatively similar to those produced by microinjections of SR 95103 (a GABA-A receptor antagonist) at the same site. These findings suggest that, at both the level of the CG and the MH, gamma-aminobutyric acid (GABA) tonically inhibits a neuronal substrate involved in the generation of flight reactions.

Allylglycine↗
PubMed1976

[Relationship between the changes of spontaneous activity and responses of cortical neurons under microiontophoretic administration of glutamic acid].

In neurons of the gyrus sigmoideus posterior of cats, the influence of microiontophoretic application of varying doses of glutamic acid upon the reaction of those neurons to stimulations of the ischiadic nerve and clicks, and the changes of spontaneous activity were studied. The application of glutamic acid led, in 97% of the 90 neurons studied, to a dose-dependent increase in the mean firing rate; in 34% of neurons, to effectuation of click responses, and affected the reaction to stimulation of the ischiadic nerve to a varying extent. With increasing doses of glutamic acid, there was a linear correlation between the logarithm of spontaneous activity and the activity of excitatory responses with considerable differences in the steepness of the resulting straight lines for the individual neurons.

Action Potentials↗
PubMed1989

Usefulness of trehalose fermentation and L-glutamic acid decarboxylation for identification of biochemically aberrant Providencia stuartii strains.

A total of 849 Providencia isolates were collected during a 4-year period when an increased incidence of nosocomial Providencia stuartii infection was noted in urologic wards. Of these isolates, 630 were identified as P. stuartii, 206 were identified as Providencia rettgeri, and 1 was identified as Providencia alcalifaciens. Twelve inositol-positive isolates from 10 patients (10 strains) resembled P. stuartii in fermenting trehalose but resembled P. rettgeri in fermenting D-arabitol or meso-erythritol or both. The latter traits, however, were not stable in all cases. These aberrant strains were identified as P. stuartii on the basis of their O antigens and DNA hybridization experiments. All isolates were tested for L-glutamic acid decarboxylase activity by a qualitative thin-layer chromatography method. All P. stuartii isolates, including the aberrant ones, were trehalose positive and L-glutamic acid decarboxylase negative. None of the P. rettgeri isolates fermented trehalose, while 99.0% of them and the single P. alcalifaciens strain were L-glutamic acid decarboxylase positive. Thus, trehalose fermentation and L-glutamic acid decarboxylation are more useful for separating P. stuartii from P. rettgeri than are D-arabitol and meso-erythritol fermentation.

DNA, Bacterial↗
PubMed1998

Synthesis and proteinase inhibitory properties of diphenyl phosphonate analogues of aspartic and glutamic acids.

The synthesis of diphenyl phosphonate analogues of aspartic and glutamic acid, and their inhibitory activity against S. aureus V8 protease and granzyme B, is described. The study has revealed difficulties with protecting group compatibility in the synthesis of these analogues. Two analogues, Acetyl. AspP (OPh)2 and Acetyl.GluP (OPh)2 were found to function as irreversible inactivators of V8 proteinase, yet exhibit no activity against granzyme B.

Aspartic Acid↗
PubMed1981

Huntington disease and Tourette syndrome. II. Uptake of glutamic acid and other amino acids by fibroblasts.

Injection of kainic acid, a rigid analog of the excitatory neurotransmitter glutamic acid (glu), into the neostriatum of rats produces a condition that mimics Huntington disease (HD) in at least 12 different morphological and biochemical parameters. These results suggested that one of the possible basic mechanisms in HD is a defect in the presynaptic of glial uptake of glu, resulting in chronic hyperstimulation and death of a specific set of neurons. To test this hypothesis, the uptake of glu was studied in 12 carefully matched sets of control-HD pairs and two lines of Tourette syndrome fibroblasts. Although the first six sets suggested a glutamate transport defect in HD cells, examination of 12 sets indicated that there were no significant differences between control and HD cells. The fibroblasts showed both a high and low affinity uptake of glutamic acid. Sodium dependent uptake of L-glutamate (L-glu) minus D-glutamate (D-glu) at 100, 1,000, and 10,000 Micrometers glutamate was normal in HD and Tourette syndrome cells.

Adolescent↗
PubMed1972

Specific immune response genes of the guinea pig. V. Influence of the GA and GT immune response genes on the specificity of cellular and humoral immune responses to a terpolymer of L-glutamic acid, L-alanine, and L-tyrosine.

The ability of guinea pigs to make immune responses to the random linear copolymer of L-glutamic acid and L-alanine, GA, and to L-glutamic acid and L-tyrosine, GT, is each controlled by a different immune response gene. On the other hand, the random linear terpolymer of L-glutamic acid, L-alanine, and L-tyrosine, GAT, which contains both GA and GT antigenic determinants, is immunogenic in all guinea pigs. After GAT immunization, all animals develop delayed hvpersensitivity and serum antibody specific for GAT. However, only those guinea pigs possessing the GA immune response gene demonstrate cross-reactive delayed hypersensitivity when challenged with GA. In addition, the anti-GAT antisera produced by those animals having the GA gene contain cross-reacting anti-GA antibodies. The sera from guinea pigs lacking the GA gene have no anti-GA antibody activity. Thus, we have demonstrated that a specific immune response gene controlling responsiveness to a "simple" antigen can determine the specificity of both cellular and humoral immune responses to a more complex antigen.

Alanine↗
PubMed2001

H+-ATPase defect in Corynebacterium glutamicum abolishes glutamic acid production with enhancement of glucose consumption rate.

A mutant of Corynebacterim glutamicum ('Brevibacterium flayum') ATCC14067 with a reduced H+-ATPase activity, F172-8, was obtained as a spontaneous neomycin-resistant mutant. The ATPase activity of strain F172-8 was reduced to about 25% of that of the parental strain. Strain F172-8 was cultured in a glutamic-acid fermentation medium containing 100 g/l of glucose using ajar fermentor. It was found that glucose consumption per cell during the exponential phase was higher by 70% in the mutant than in the parent. The respiration rate per cell of the mutant also increased to twice as much as that of the parent. However, the growth rate of the mutant was lower than that of the parent. Under those conditions, the parent produced more than 40 g/l glutamic acid, while the mutant hardly produced any glutamic acid. Instead the mutant produced 24.6 g/l lactic acid as the main metabolite of glucose. Remarkably, the accumulation of pyruvate and pyruvate-family amino acids, i.e., alanine and valine, was detected in the mutant. On the other hand, the parent accumulated alpha-ketoglutaric acid and a glutamate-family amino acid, proline, as major by-products. It was concluded that the decrease in the H+-ATPase activity caused the above-mentioned metabolic changes in strain F172-8, because a revertant of strain F172-8, R2-1, with a H+-ATPase activity of 70% of that of strain ATCC14067, showed a fermentation profile similar to that of the parent. Sequence analyses of the atp operon genes of these strains identified one point mutation in the gamma subunit in strain F172-8.

Corynebacterium↗
PubMed1984

Evidence that L-glutamic acid mediates baroreceptor function in the cat.

The possible role of L-glutamic acid (L-glu) as a neurotransmitter of baroreceptor afferent neurons was investigated in the cat by monitoring the changes in three indices of baroreceptor function seen with the L-glu antagonists L-glutamic acid diethyl ester (GDEE) and 1-hydroxy-3-amino-pyrrolidone-2-(HA-966). Baroreceptor function was determined from a) the computer summed inhibition of sympathetic nerve discharge (SND) evoked by electrical stimulation of vagal baroreceptor afferent pathways, b) the locking of SND to the cardiac cycle, and c) the sympathoinhibitory response to i.v. pressor doses of phenylephrine. Direct bilateral microinjections of GDEE (20 micrograms) and HA-966 (4 micrograms) into the region of the nucleus tractus solitarii (NTS) resulted in immediate, marked reductions in the SND inhibitory response to vagal stimulation, a loss in SND locking to the cardiac cycle, a shift in the arterial pulse/SND phase relation, and a diminished sympathoinhibitory response to phenylephrine. Control microinjections of isotonic saline (1 mu 1/NTS) were devoid of these effects. The vagal induced sympathoinhibitory response was restored after NTS microinjections of GDEE by increasing the intensity of the vagal stimulus, or by directly stimulating the NTS injection site, suggesting that the impairment in baroreceptor function seen with this L-glu antagonist was independent of mechanical or local anesthetic effects. These data strongly suggest that L-glu may act as a neurotransmitter of baroreceptor afferent neurons in the NTS of the cat.

Afferent Pathways↗