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PubMedDate not supplied

Convulsant properties of L-glutamic acid di-tert butyl ester.

Glutamic acid di-tert butyl ester (GTBE) was found to have a pronounced convulsant effect in mice and rats, producing recurrent clonic convulsions combined with postural and respiratory disturbances in a dosage of 0.5 mmol/kg (148 mg/kg). Tert-butyl ester derivatives of aspartic acid and alanine, and glutamic acid gamma-benzyl ester did not produce seizures. Various other glutamate esters, such as glutamic acid diethyl ester and glutamic acid dimethyl ester, have previously been found to have anticonvulsant effects, and also do not induce seizures. It is suggested that glutamic acid di-tert butyl ester may have specific pharmacological properties which differ from those of other known convulsant drugs.

Animals↗
PubMed1989

Specificity of aspartate aminotransferases from leguminous plants for 4-substituted glutamic acids.

Aspartate aminotransferase (glutamate-oxalacetate transaminase) was partially purified from extracts of germinating seeds of peanut (Arachis hypogaea), honey locust (Gleditsia triacanthos), soybean (Glycine max), and Sophora japonica. The ability of these enzyme preparations, as well as aspartate aminotransferase purified from pig heart cytosol, to use 4-substituted glutamic acids as amino group donors and their corresponding 2-oxo acids as amino group acceptors in the aminotransferase reaction was measured. All 4-substituted glutamic acid analogs tested were poorer substrates than was glutamate or 2-oxoglutarate. 2-Oxo-4-methyleneglutarate was least effective (lowest relative V(m)/K(m)) as a substrate for the enzyme from peanuts and honey locust, which are the two species studied that accumulate 4-methyleneglutamic acid and 4-methyleneglutamine. Of the different aminotransferases tested, the enzyme from honey locust was the least active with 2-oxo-4-hydroxy-4-methylglutarate, the corresponding amino acid of which also accumulates in that species. These results suggest that transamination of 2-oxo-4-substituted glutaric acids is not involved in the biosynthesis of the corresponding 4-substituted glutamic acids in these species. Rather, accumulation of certain 4-substituted glutamic acids in these instances may be, in part, the result of the inefficacy of their transamination by aspartate aminotransferase.

Journal Article↗
PubMed2004

Synthesis of peptide ribonucleic acid consisting of D- and L-gamma-glutamic acid as a backbone structure.

A novel nucleic acid model using peptide ribonucleic acid (PRNA), which contains 5-amino-5-deoxyribonucleoside as a recognition site for nucleic acids and consists D-glutamic acid (D-PRNA) instead of L-glutamic acid (L-PRNA) as a backbone structure, has been designed and synthesized. Difference between D-PRNA and L-PRNA oligomers was elucidated on the basis of the effects of chirality of gamma-glutamic acid backbone upon structure elucidated by CD spectra.

Buffers↗
PubMed1993

Effects of neurotensin on the release of glutamic acid in the prefrontal cortex and striatum of the rat.

The effects of neurotensin (NT) on the extracellular concentrations of excitatory amino acids (EAA) glutamic acid (GLU) and aspartic acid (ASP) in the medial prefrontal cortex (MPC) and striatum (ST) of the conscious rat have been studied. NT was infused directly into these two structures for 10 min at doses of 10, 100 and 1000 nM. In the MPC, NT produced a dose-related increase of GLU. Also, NT produced a delayed increase of ASP at the highest dose. In ST, NT at doses of 10, 100 and 1000 nM produced no effect on GLU and ASP. It is suggested that the increase of GLU and ASP in the MPC could be due to a direct effect of NT on pyramidal cortical neurones. On the contrary, it is suggested that a direct interaction NT-GLU does not exist in the ST of the rat.

Animals↗
PubMed1989

Regulation of the mesocorticolimbic dopamine system by glutamic acid receptor subtypes.

Glutamic acid and excitatory amino acids specific for the glutamate receptor subtypes were microinjected into the A10 region of the rat. Glutamate produced an increase in motor behavior that was antagonized by pretreatment with the dopamine D2 receptor antagonist, haloperidol. This motor stimulant effect was produced by kainate, but not by N-methyl-D-aspartate (NMDA) or quisqualic acid. By using in vivo dialysis it was found that dopamine release in the nucleus accumbens and locomotor activity were enhanced by glutamate injection into the A10 region. Whereas glutamate was found to increase the postmortem concentration of dopamine metabolites in the medial prefrontal cortex, nucleus accumbens and A10 region, NMDA selectively increased dopamine metabolism in the prefrontal cortex, and kainate produced increases in the nucleus accumbens and A10 region. When glutamate and the NMDA receptor antagonist, 3-[(+/-)-2-carboxypiperazine-4-yl)propyl-1-phosphonic acid (CPP) were coadministered, CPP selectively abolished the effect of glutamate on medial prefrontal cortical dopamine metabolites. A physiological role for the NMDA receptor modulation of A10 dopamine neurons was shown by intra-A10 pretreatment with CPP antagonism of mild footshock-induced increase in dopamine metabolites in the prefrontal cortex. These data argue that glutamate is a regulatory transmitter of A10 dopamine neurons, and that the NMDA receptor subtype modulates neurons projecting to the prefrontal cortex whereas the kainate subtype modulates mesoaccumbens neurons.

Amino Acids↗
PubMed1985

[Correction of contractile function and metabolism in canine ischemic myocardium due to exogenous glutamic acid].

The effect of intravenous glutamic acid infusion (3 mg/kg/min) was studied during myocardial ischemia and reperfusion in anesthetized dogs. Left ventricular ischemia was induced by underperfusion of the anterior descending and circumflex coronary arteries. Glutamic acid reduced the ischemic contractile depression 2 min after a 60%-reduction of the coronary blood flow. The left ventricular systolic pressure was decreased by 9% versus 22%, dP/dt by 16% versus 29%, left ventricular systolic pressure heart rate product by 16% versus 31%. Reperfusion with glutamic acid improved the recovery of cardiac performance without any increase in myocardial oxygen consumption. Glutamic acid infusion resulted in a 2-fold augmentation of glutamate uptake by the ischemic myocardium. It led to cessation of ammonia release by the heart due to activation of glutamine synthesis, enhancement of alanine formation coupled with pyruvate utilization and did not change lactate production. The mechanisms of the protective action of glutamic acid are discussed.

Alanine↗
PubMed1999

Requirements of protein kinase cdelta for catalytic function. Role of glutamic acid 500 and autophosphorylation on serine 643.

Recently, we reported that, in contrast to protein kinase C (PKC)alpha and betaII, PKCdelta does not require phosphorylation of a specific threonine (Thr505) in the activation loop for catalytic competence (Stempka et al. (1997) J. Biol. Chem. 272, 6805-6811). Here, we show that the acidic residue glutamic acid 500 (Glu500) in the activation loop is important for the catalytic function of PKCdelta. A Glu500 to valine mutant shows 76 and 73% reduced kinase activity toward autophosphorylation and substrate phosphorylation, respectively. With regard to thermal stability and inhibition by the inhibitors Gö6976 and Gö6983 the mutant does not differ from the wild type, indicating that the general conformation of the molecule is not altered by the site-directed mutagenesis. Thus, Glu500 in the activation loop of PKCdelta might take over at least part of the role of the phosphate groups on Thr497 and Thr500 of PKCalpha and betaII, respectively. Accordingly, PKCdelta exhibits kinase activity and is able to autophosphorylate probably without posttranslational modification. Autophosphorylation of PKCdelta in vitro occurs on Ser643, as demonstrated by matrix-assisted laser desorption ionization mass spectrometry of tryptic peptides of autophosphorylated PKCdelta wild type and mutants. A peptide containing this site is phosphorylated also in vivo, i.e. in recombinant PKCdelta purified from baculovirus-infected insect cells. A Ser643 to alanine mutation indicates that autophosphorylation of Ser643 is not essential for the kinase activity of PKCdelta. Probably additional (auto)phosphorylation site(s) exist that have not yet been identified.

Animals↗
PubMed1992

Familial increase in plasma glutamic acid in epilepsy.

Plasma levels of glutamic acid and leukocyte glutamate dehydrogenase (GDH) activity were determined in patients with primary generalized epilepsy, patients with partial epilepsy and in the first-degree relatives of these subjects. The results show a significant increase in plasma glutamic acid in both groups of patients and their relatives compared to non-epileptic controls. The leukocyte GDH activity in the patients and the relatives was not different from controls. The data support a genetic basis for plasma glutamic acid increase in both primary generalized and partial epilepsy and are compatible with the multifactorial mode of inheritance of these disorders. This is the first study showing a familial plasma glutamic acid increase in epilepsy in a Japanese population.

Adolescent↗
PubMed1976

Is L-glutamic acid nutritionally a dispensable amino acid for the young chick?

The importance of dispensable amino acids for the chick was reinvestigated. Two-week chick weights were 75.7 g. and 143.7 g. when dietary nitrogen was provided solely by indispensable amino acids and by indispensable amino acids and 10% L-glutamic acid, respectively. Weight gain increased four-fold when L-glutamic acid was added to the mixture of indispensable amino acids. Plasma free amino acid concentrations were considerably decreased and total indispensable amino acid concentration (including cystine and tyrosine) was reduced to approximately a half or less with L-glutamic acid supplementation. Increments of L-glutamic acid as the sole nitrogen source for dispensable amino acids in the diet increased two-week weight gain proportionately over a range from 0 to 10%. When 10% of L-glutamic acid was included in the amino acid diet, growth rate was equivalent to that with a practical diet up to two weeks of age. The mixture of leucine, isoleucine, valine, lysine and arginine produced little growth promotion as a nitrogen source for dispensable amino acids. L-aspartic acid, L-alanine and the mixture of dispensable amino acids devoid of L-glutamic acid were found not as effective as L-glutamic acid. The estimate of effectiveness of L-aspartic acid, L-alanine and the mixture was approximately 80%, 60%, and 80%, respectively, of that of L-glutamic acid during first two weeks. Utilization of diammonium citrate for growth promotion varied with the amount used and the age of chicks. A combination of dispensable amino acids plus nominal levels of DAC was not as effective as glutamic acid during the first week but shortly after that, produced good gains. Even during the 3rd week or 4th week high levels of DAC alone did not produce normal gains of chicks. The activities and the subcellular distribution of glutamic pyruvic transaminase (GPT) and glutamic oxaloacetic transaminase (GOT) in the liver of young chicks were measured. GOT activity was considerably higher than GPT activity. Initially, GOT activity was found primarily in cytosol, but the mitochondrial activity increased to 57% of total activity by day 10, whereas GPT activity was exclusively in mitochondria regardless of the age.

Alanine↗
PubMed1998

Aminobicyclo[2.2.1.]heptane dicarboxylic acids (ABHD), rigid analogs of ACPD and glutamic acid: synthesis and pharmacological activity on metabotropic receptors mGluR1 and mGluR2.

Isomeric norbornane-derived rigid analogs mimicking different potential conformations of ACPD (1-aminocyclopentane-1,3-dicarboxylic acid) and glutamic acid have been synthesized, via the hydantoin route, to be used as conformational probes for bioactive conformations at the glutamatergic receptors of the central nervous system. Activities on metabotropic receptors mGluR1 and mGluR2 are reported and discussed.

Chromatography, High Pressure Liquid↗
PubMed2006

C-terminal amino acid residue loss for deprotonated peptide ions containing glutamic acid, aspartic acid, or serine residues at the C-terminus.

Deprotonated peptides containing C-terminal glutamic acid, aspartic acid, or serine residues were studied by sustained off-resonance irradiation collision-induced dissociation (SORI-CID) in a Fourier transform ion cyclotron resonance (FT-ICR) mass spectrometer with ion production by electrospray ionization (ESI). Additional studies were performed by post source decay (PSD) in a matrix-assisted laser desorption ionization/time-of-flight (MALDI/TOF) mass spectrometer. This work included both model peptides synthesized in our laboratory and bioactive peptides with more complex sequences. During SORI-CID and PSD, [M - H]- and [M - 2H]2- underwent an unusual cleavage corresponding to the elimination of the C-terminal residue. Two mechanisms are proposed to occur. They involve nucleophilic attack on the carbonyl carbon of the adjacent residue by either the carboxylate group of the C-terminus or the side chain carboxylate group of C-terminal glutamic acid and aspartic acid residues. To confirm the proposed mechanisms, AAAAAD was labelled by 18O specifically on the side chain of the aspartic acid residue. For peptides that contain multiple C-terminal glutamic acid residues, each of these residues can be sequentially eliminated from the deprotonated ions; a driving force may be the formation of a very stable pyroglutamatic acid neutral. For peptides with multiple aspartic acid residues at the C-terminus, aspartic acid residue loss is not sequential. For peptides with multiple serine residues at the C-terminus, C-terminal residue loss is sequential; however, abundant loss of other neutral molecules also occurs. In addition, the presence of basic residues (arginine or lysine) in the sequence has no effect on C-terminal residue elimination in the negative ion mode.

Amino Acid Sequence↗
PubMed1999

Cyclobutane quisqualic acid analogues as selective mGluR5a metabotropic glutamic acid receptor ligands.

The conformationally constrained cyclobutane analogues of quisqualic acid (Z)- and (E)-1-amino-3-[2'-(3',5'-dioxo-1',2', 4'-oxadiazolidinyl)]cyclobutane-1-carboxylic acid, compounds 2 and 3, respectively, were synthesized. Both 2 and 3 stimulated phosphoinositide (PI) hydrolysis in the hippocampus with EC50 values of 18 +/- 6 and 53 +/- 19 microM, respectively. Neither analogue stimulated PI hydrolysis in the cerebellum. The effects of 2 and 3 were also examined in BHK cells which expressed either mGluR1a or mGluR5a receptors. Compounds 2 and 3 stimulated PI hydrolysis in cells expressing mGluR5a but not in those cells expressing mGluR1a. The EC50 value for 2 was 11 +/- 4 microM, while that for 3 was 49 +/- 25 microM. Both 2 and 3 did not show any significant effect on cells expressing the mGluR2 and mGluR4a receptors. In addition, neither compound blocked [3H]glutamic acid uptake into synaptosomal membranes, and neither compound was able to produce the QUIS effect as does quisqualic acid. This pharmacological profile indicates that 2 and 3 are selective ligands for the mGluR5a metabotropic glutamic acid receptor.

Animals↗
PubMed1991

Glutamic acid and gamma-aminobutyric acid neurotransmitters in central control of breathing.

We review recent cross-disciplinary experimental and theoretical investigations on metabolism of the amino acid neurotransmitters glutamic acid and gamma-aminobutyric acid (GABA) in the brain during hypoxia and hypercapnia and their possible role in central control of breathing. The roles of classical modifiers of central chemical drive to breathing (H+ and cholinergic mechanisms) are summarized. A brief perspective on the current widespread interest in GABA and glutamate in central control is given. The basic biochemistry of these amino acids and their roles in ammonia and bicarbonate metabolism are discussed. This review further addresses recent work on central respiratory effects of inhibitory GABA and excitatory glutamate. Current understanding of the sites and mechanisms of action of these amino acids on or near the ventral surface of the medulla is reviewed. We focus particularly on tracer kinetic investigations of glutamatergic and GABAergic mechanisms in hypoxia and hypercapnia and their possible role in the ventilatory response to hypoxia. We conclude with some speculative remarks on the critical importance of these investigations and suggest specific directions of research in central mechanisms of respiratory control.

Animals↗