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PubMed1996

Fluorimetric method of analysis for D-norpseudoephedrine hydrochloride, glycine and L-glutamic acid by reversed-phase high-performance liquid chromatography.

The determination of D-norpseudoephedrine HCl, an appetite suppressant, and glycine and L-glutamic acid, both dietary supplements, in pharmaceutical formulations and dissolution media using reversed-phase high-performance liquid chromatography (HPLC) combined with fluorimetric detection is reported. A reagent solution containing omicron-phthalaldehyde and a reducing agent, mercaptoethanol, appeared to be the most favourable reagent for derivatising the three compounds. The use of this HPLC method allowed for selective and quantitatively accurate analysis and was sufficiently specific, precise and sensitive for analytical characterisation.

Appetite Depressants↗
PubMed1996

4(R)- and 4(S)-(5-phenylpentyl)-glutamic acids attenuate excitatory postsynaptic potential on hippocampus without inhibiting postsynaptic NMDA and AMPA receptors.

The electrophysiological effects of 4(R)- and 4(S)-(5-phenylpentyl)-glutamic acids (C5R and C5S analogues) were investigated. In the presence of 5 microM C5R or C5S, excitatory postsynaptic potentials (EPSPs), elicited by stimulating the Schaffer collateral-commissural pathway, recorded in the hippocampal CA1 region on rat brain slices were reduced by more than 50% of the control. Both the NMDA receptor- and the non-MNDA receptor-mediated components of the EPSP were attenuated to the similar extent. The blockade of the presynaptic input, by 0.5 microM tetrodotoxin (TTX), resulted in that C5 analogues no longer inhibited the depolarization induced by AMPA or NMDA on brain slices. On the other hand, the AMPA- and NMDA-induced whole cell inward current of the dissociated hippocampal neurons was not affected by the presence of C5 analogues, investigated with the whole cell patch-clamping technique. These results suggest that the site of the inhibitory action of C5R and C5S may be at the presynaptic termini and that the release of the excitatory neurotransmitter, most likely the glutamate, may be tampered.

Animals↗
PubMed1980

Plasma glutamic acid levels in premature newborn.

24 premature, newborn infants were investigated for plasma glutamic acid (GA) levels before and after a normal milk feed, to ascertain if the ingestion of GA present in the milk could result in an increase of its plasma level. No increases were detected in plasma between 5 and 90 min after the feed. These results may be important in respect to the problem of the possible toxicity of monosodium glutamate (MSG) added to baby foods.

Animals↗
PubMed1997

Critical glutamic acid residues affecting the mechanism and nucleotide specificity of Vibrio harveyi aldehyde dehydrogenase.

Fatty aldehyde dehydrogenase (ALDH) from the luminescent marine bacterium, Vibrio harveyi, differs from other ALDHs in its unique specificity and high affinity for NADP+. Two glutamic acid residues, Glu253 and Glu377, which are highly conserved in ALDHs, were investigated in the present study. Mutation of Glu253 to Ala decreased the kcat for ALDH activity by over four orders of magnitude without a significant change in the K(m) values for substrates or the ability to interact with nucleotides. Both thioesterase activity and a pre-steady-state burst of NAD(P)H were also eliminated, implicating Glu253 in promoting the nucleophilicity of the cysteine residue(Cys289) involved in forming the thiohemiacetal intermediate in the enzyme mechanism. Mutation of Glu377 to Gln (E377Q mutant) selectively decreased the kcat for NAD(+)-dependent ALDH activity (> 10(2)-fold) compared to only a 6-fold loss in NADP(+)-dependent activity without comparable changes to the K(m) values for substrates. Consequently, the E377Q mutant had a very high specificity for NADP+(kcat/K(m) > 10(3) of that for NAD+) which was over 20 times higher than that of the wild-type ALDH. Although a pre-steady-state burst of NAD(P)H was eliminated by this mutation, thioesterase activity was completely retained. Using [1-2H]acetaldehyde as a substrate, a significant deuterium isotope effect was observed, implicating Glu377 in the hydride transfer step and not in acylation or release of the acyl group from the cysteine nucleophile. The increase in specificity of the E377Q mutant for NADP+ is consistent with a change in the rate-limiting step determining kcat from nucleotide-dependent NAD(P)H dissociation to hydride transfer. The results provide biochemical evidence that the two highly conserved Glu residues are involved in different functions in the active site of V. harveyi ALDH.

Aldehyde Dehydrogenase↗
PubMed1994

[Effects of L-glutamic acid and its antagonist on spontaneous discharge of nucleus paragigantocellularis lateralis neurons in brainstem slice in rat].

We studied the effects of iontophoretic application of L-glutamic acid (L-Glu) and its antagonist DL-2-amino-5-phosphonovaleric acid (AP5) on the spontaneous discharge of the nucleus paragiganto-cellularis lateralis (PGCL) neurons and the influence of AP5 on L-Glu effect in brainstem slice in rat with the multibarrel microelectrode techniques. One hundred and thirty six units with stable spontaneous discharge were recorded in 51 rat brain slices, their discharge pattern being primarily a repetitive one. Both L-Glu and AP5 showed three kinds of effect on the PGCL neuronal spontaneous discharge: excitatory, inhibitory and no-effect, with the percentage of 80.65%, 8.06%, 11.29% for L-Glu and 28.00%, 8.00%, 64.00% for AP5 of the neurons tested, respectively. The excitatory effect showed a dose-response relationship. AP5 could block partially the excitatory effect of L-Glu on most neurons tested (71.87%). The results indicated that the neurons in PGCL in rat brain slice in vitro principally showed a spontaneous discharge with a repetitive firing pattern, and suggested that at cellular level there existed endogenous excitatory amino acid as neurotransmitter in PGCL and the neurons there possessed EAA receptors of both N-methyl-D-aspartate (NMDA) and non-NMDA subtypes.

2-Amino-5-phosphonovalerate↗
PubMed2001

Regulatory and effector CD4 T cells in nonobese diabetic mice recognize overlapping determinants on glutamic acid decarboxylase and use distinct V beta genes.

The 524--543 region of glutamic acid decarboxylase (GAD65), GAD65(524--543), is one of the first fragments of this islet Ag to induce proliferative T cell responses in the nonobese diabetic (NOD) mouse model of spontaneous autoimmune diabetes. Furthermore, NOD mice given tolerogenic doses of GAD65(524--543) are protected from spontaneous and cyclophosphamide-induced diabetes. In this study, we report that there are at least two I-A(g7)-restricted determinants present in the GAD65(524--543) sequence, each capable of recruiting unique T cell repertoires characterized by distinct TCR V beta gene use. CD4(+) T cells arise spontaneously in young NOD mice to an apparently dominant determinant found within the GAD65 peptide 530--543 (p530); however, T cells to the overlapping determinant 524-538 (p524) dominate the response only after immunization with GAD65(524--543). All p530-responsive T cells used the V beta 4 gene, whereas the V beta 12 gene is preferentially used to encode the TCR of p524-responsive T cell populations. T cell clones and hybridomas from both of these T cell groups were responsive to APC pulsed with GAD65(524--543) or whole rGAD65. p524-reactive cells appeared to be regulatory upon adoptive transfer into young NOD mice and could inhibit insulin-dependent diabetes mellitus development, although they were unable to produce IL-4, IL-10, or TGF beta upon antigenic challenge. Furthermore, we found that i.p. injection with p524/IFA was very effective in providing protection from cyclophosphamide-induced insulin-dependent diabetes mellitus. These data demonstrate that the regulatory T cells elicited by immunizing with GAD65(524--543) are unique and distinct from those that arise from spontaneous endogenous priming, and that T cells to this limited region of GAD65 may be either regulatory or pathogenic.

Adoptive Transfer↗
PubMed1993

GABA interneurons in the rat medial frontal cortex: characterization by quantitative in situ hybridization of the glutamic acid decarboxylase (GAD67) mRNA.

In situ hybridization of mRNA encoding one isoform of glutamic acid decarboxylase (GAD67) was performed in the rat medial frontal cortex (MFC) to characterize GABA interneurons. Qualitatively, the labelling obtained with a [35S]cDNA probe was in register with neurons and was never associated with glial cells. No obvious differences in the density of labelled cells were observed between the different areas of the MFC examined (infralimbic, prelimbic, anterior cingulate and precentral medial) and between the various cortical layers. Grain counting was performed on single cells in the various layers of the prelimbic and the anterior cingulate area, two main areas of the MFC. According to their grain density, neurons were arbitrarily classified as low, high and very high GAD67 mRNA content. The neurons with the high GAD67 mRNA content corresponded to around 50% of the labelled cells in all the layers and in both areas. In the prelimbic area, the neuronal population with a low GAD67 mRNA content varied from 50% in layers I and II-III to 40% in layers V-VI whereas the very high GAD67 mRNA content neurons corresponded to around 5% of the labelled neurons in all layers. In the anterior cingulate area the neuronal population showing low GAD67 mRNA content varied from 35% in layers I and II-III to 20% in layers V-VI. In this area, neurons with a very high GAD67 mRNA content were more numerous than in the prelimbic area: they varied from 15% in layers I and II-III to 30% in layers V-VI. Parallel to the presence of very highly labelled cells, GAD enzymatic activity measured both in the presence and in the absence of pyridoxal 5'-phosphate was higher in the anterior cingulate area than in the prelimbic area. The heterogeneity of GAD67 mRNA content at the cellular level might underlie the existence of subpopulations of GABA interneurons in the MFC and suggests a higher GABAergic inhibitory control in the anterior cingulate area than in the prelimbic area.

Animals↗
PubMed1994

Localization of mRNAs encoding two forms of glutamic acid decarboxylase in the rat hippocampal formation.

The mRNAs for two forms of glutamic acid decarboxylase (GAD65 and GAD67) were localized in the rat hippocampal formation by nonradioactive in situ hybridization methods with digoxigenin-labeled cRNA probes. Some neurons in all layers of the hippocampus and dentate gyrus were readily labeled for each GAD mRNA, and the patterns of labeling for GAD65 and GAD67 mRNAs were very similar. All major groups of previously described GAD- and GABA-containing neurons appeared to be labeled for each GAD mRNA. Such findings suggest that most GABA neurons in the hippocampal formation contain both GAD mRNAs. When the labeling of neurons in the hippocampal formation and cerebral cortex was compared in the same sections, the intensity of neuronal labeling for GAD67 mRNA was generally similar in the two regions. However, the intensity of labeling for GAD65 mRNA was generally stronger for many neurons in the hippocampal formation than for most neurons in the cerebral cortex. Neurons in the hilus of the dentate gyrus were particularly well labeled for GAD65. The nonradioactive labeling for the GAD mRNAs was confined to the cytoplasm of neuronal cell bodies, and this allowed a clear visualization of the relative number and location of labeled neurons. Several distinct patterns of GAD mRNA-containing neurons were observed among different regions of the hippocampal formation. In the hilus of the dentate gyrus, GAD mRNA-containing neurons were numerous in the regions deep to the granule cell layer as well as in more central parts of the hilus. Within CA3, the densities (quantities) of labeled neurons varied among the regions. In the inner or hilar segment of CA3, the density of labeled neurons was often lower than that in the outer part of CA3 where numerous labeled neurons were distributed throughout all layers. In CA1, GAD mRNA-labeled neurons were distributed in a relatively laminar pattern with the highest density in stratum pyramidale and moderate densities in stratum oriens and at the interface between strata radiatum and lacunosum-moleculare. Lower densities were found within the latter two layers. The prominent localization of the two GAD mRNAs in the hippocampal formation suggests that a dual system for GABA synthesis is necessary for normal GABAergic function in this brain region. Most putative GABA neurons contain relatively high levels of GAD67 mRNA as might be expected if this GAD form is responsible for the synthesis of GABA for metabolic and baseline synaptic function.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2003

Dual impairment of GABAA- and GABAB-receptor-mediated synaptic responses by autoantibodies to glutamic acid decarboxylase.

Anti-glutamate decarboxylase autoantibodies (GAD-A) are associated with a group of patients with progressive cerebellar ataxia. We reported previously that cerebellar GABA(A)-mediated synaptic transmission was presynaptically depressed by GAD-A in the cerebrospinal fluid (CSF). Using whole-cell recording of rat cerebellar slices, we found in the present study that CSF immunoglobulins from ataxic patients reduced gamma-aminobutyric acid (GABA) release from cerebellar interneurons, thereby attenuating presynaptic inhibition on neighboring excitatory synapses through GABA(B) receptors (GABA(B)Rs). Our results suggest that in in vitro slices, GAD-A elicited the pathophysiological action of reduction in GABA release, which subsequently resulted in dual synaptic impairment in the cerebellar circuit, by depression of GABA(A) receptor (GABA(A)R)-mediated inhibitory synaptic transmissions, and attenuation of GABA(B) receptor-mediated inhibition of excitatory transmissions.

Action Potentials↗
PubMed1985

GABA and benzodiazepine-induced modification of [14C]L-glutamic acid release from rat spinal cord slices.

The spontaneous and potassium-evoked release of [14C]-label from rat spinal cord slices preloaded with [14C]L-glutamic acid and its modification by GABA and related drugs, such as flurazepam, was studied as a possible indirect measure of presynaptic inhibition and of the ability of benzodiazepines to augment it. GABA (100 microM) reduced the spontaneous release of [14C]-label (glutamate) provided that GABA metabolism was blocked by amino-oxyacetic acid (AOAA), but failed to reduce the potassium-evoked release of glutamate, although muscimol (10 microM) had some effect. In contrast, flurazepam (1-100 microM) did not affect spontaneous release but produced some inhibition of the evoked release (through a system insensitive to 10 microM bicuculline). This inhibition became more marked in the presence of both GABA and AOAA, and was then overcome by bicuculline. It is concluded that either some benzodiazepine receptors must be occupied for GABA to produce an effect on evoked release and/or, that the benzodiazepines can only augment GABA function once a certain amount has been released. Studies of the rapid distribution of [14C]-label from glutamate, to GABA, glutamine and other amino acids, using high voltage electrophoresis, showed the importance of blocking metabolic pathways in studies of this kind.

Aminooxyacetic Acid↗
PubMed2005

Sodium chloride enhanced oligomerization of L-glutamic acid in aqueous solution.

The presence of NaCl was found to significantly enhance the formation of longer peptides in N,N'-carbonyldiimidazole induced oligomerization of L-glutamic acid in homogeneous aqueous solution. The enhancement was detected in the presence of as low as 0.01-M NaCl and the highest yield of longer oligomers was achieved in the presence of 1-M NaCl. The possible prebiotic relevance is discussed.

Chromatography, High Pressure Liquid↗
PubMed2000

Double labeling immunoelectron microscopic study on the synaptic connections between glutamic acid neurons and GABA neurons in the hippocampus of rats.

In order to explore the roles of different neurotransmitters in epileptic pathogenesis, the synaptic connections between glutamic acid (Glu) neurons and GABA neurons in normal rat hippocampus were studied by pre-embedding double labeling immunoelectron microscopy. The GABA immunoreaction was first demonstrated by chromogen DAB, then the Glu immunoreaction was demonstrated by molybdic acid-TMB method. After being stabilized by DAB-cobalt chloride, the sections were processed for electron microscopic embedding. Under electron microscope, there were many Glu immunoreaction-positive neurons in the pyramidal layer of hippocampal CA1 area and some GABA immunoreaction-positive neurons with pyramidal or polygonal perikarya in the pyramidal, polymorphic and radiant layer of CA1 area. There were also symmetric dendro-axonic synapses formed by GABA-positive dendrites and Glu-positive axons in the polymorphic layer and symmetric axo-dendrites synapses formed by GABA-positive axons and Glu-positive dendritic in the radiant layer. In addition, there were symmetric autoregulatory axo-dendritic synapses between Glu-positive axons and dendrites and autoregulatory axo-axonic synapses (both symmetric and asymmetric) between GABA-positive axons. Above mentioned results, for the first time, showed that there were complex synaptic regulatory relationships between excitatory Glu neurons and inhibitory GABA neurons in the hippocampal CA1 area, thereby, providing ultrastructural evidence for different neurotransmitters participating in epileptic pathogenesis.

Animals↗
PubMed1981

Effect of high dietary glutamic acid on the excretion of 35S-thiamin in kittens.

Six kittens individually housed in stainless steel metabolism cages were fed a control diet containing 3% glutamic acid (Glu) for 2 weeks and then subsequently for 12 weeks were fed a 12% Glu diet. All diets contained 4.4 mg thiamin/kg diet. The 12% Glu diet significantly depressed weight gain during the first 6 weeks and food intake during the 3rd and 4th weeks of dietary regimen as compared to the control period. Plasma levels of Glu increased with the duration of the 12% dietary regimen. On days 0, 14, 28 and 42, the kittens were given a 4 g meal containing 10 microCi of 35S-thiamin. Although the mean excretion of isotope in the feces, calculated as a percentage of the ingested dose, was about 25% greater in the first 2 weeks of the 12% Glu dietary regimen than the control period, the difference was not significant. Urinary excretory rate of 35S-thiamin was depressed during the first 4 weeks of the 12% dietary regimen. When exponential relationships were fitted to the excretion data, the coefficients for the first and second 2-week intervals of the 12% Glu dietary regimen were -0.177 and -0.167, respectively, compared to -0.199 and -0.212 obtained for the control period and the third 2-week interval of the high Glu dietary regimen, respectively.

Animals↗