Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: CAS:6893-26-1 (glutamate)
 73,096 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Imidazole propionic acid (ipa), a gratuitous inducer of the histidine-utilization (hut) system in Salmonella typhimurium, inhibits the organism's growth on succinate minimal medium. Induction of the hut system is necessary, but not sufficient, to cause inhibition. A study of the ability of single amino acids to relieve ipa-restricted growth suggests that insufficient glutamate is the cause of slow growth. The inhibition of growth by imidazolone propionic acid (iopa), an intermediate in the catabolism of histidine to glutamate, is similar to that by ipa. Studies using 2, 3, 5-triphenyl tetrazolium chloride plates to examine amino acid catabolism suggest that accumulation of ipa or iopa leads to inactivation of aspartate amino-transferase (AAT). This interpretation is supported by studies of an Escherichia coli mutant lacking AAT. The mutant grows poorly on succinate minimal medium, and the poor growth is relieved by the same amino acids that relieve ipa- and iopa-restricted growth. These and other findings are discussed in terms of coordination of the histidine-utilization system with enzymatic activities involved in the catabolism of other amino acids.
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PMID:Inhibition of growth by imidazol(on)e propionic acid: evidence in vivo for coordination of histidine catabolism with the catabolism of other amino acids. 37 43

19 The effect of pent-4-enoic acid, propionic acid and several other short-chain fatty acids on citrulline synthesis in rat liver mitochondria was studied. 2.Pent-4-enoate at 1 mM inhibited mitochondrial citulline synthesis by about 80-90%. It is concluded that pent-4-enoate inhibits citrulline synthesis by interfering with some aspect of mitochondrial energy metabolism. This results in impairment of mitochondrial ornithine uptake or depletion of mitochondrial ATP, which, in turn, impairs carbamoyl phosphate synthesis or both. Evidence in support of this conclusion includes: pent-4-enoate has no effect on citrulline synthesis supported by succinate or exogenous ATP; pent-4-enoate lowers the medium plus mitochondrial ATP concentration; finally, when glutamate is the oxidizable substrate, pent-4-enoate decreases the carbamoyl phosphate concentration in mitochondria incubated without ornithine to minimize citrulline synthesis and impairs the mitochondrial uptake of ornithine, but it has neither effect when succinate is the oxidizable substrate. 4. Propionate, butyrate and crotonate also inhibit mitochondrial citrulline synthesis, but much less than pent-4-enoate. 5. Acetate, pentanoate, pent-2-enoate, hexanoate, octanoate, isovalerate, tiglylate and alpha-methylbutyrate have little or no effect on mitochondrial citrulline synthesis.
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PMID:Effect of pent-4-enoic acid, propionic acid and other short-chain fatty acids on citrulline synthesis in rat liver mitochondria. 94 11

The formation of alanine, glutamate, and aspartate from muscle was studied in the isolated perfused hindquarter of rats fasted for 48 h. Tracer doses of (14C) compounds with high specific activity were tested as precursors for the amino acids. Total amounts and radioactivities of the tested amino acids were determined. Alanine was produced more efficiently than glutamate and aspartate even if no exogenous substrate was offered. (14C) Pyruvate was most efficient as precursor of labeled alanine. However, labeled leucine, propionic acid, valine and fumaric acid also produced labeled alanine efficiently. The efficiency as precursor for labeled alanine seemed to be related to the ability to label intermediates in the citric acid cycle in the perfused muscle. From the relation between the ability to label alanine in the perfusion medium and lactate and succinate in the muscle it is suggested that pyruvate may be produced intramitochondrially and is efficiently transaminated to alanine in this compartment.
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PMID:Sources of carbon skeleton of alanine released from skeletal muscle. 96 39

Fast application of L-glutamate, AMPA (alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) or kainate to cultured rat thalamic neurons revealed properties of non-NMDA (N-methyl-D-aspartate) receptors similar to those described in hippocampal neurons. The kinetics of non-NMDA receptor-mediated currents were altered by the addition of the dye Evans Blue (EB). Macroscopic desensitization was reduced and activation and deactivation kinetics were slowed. Delayed addition of EB, after desensitization of non-NMDA receptors, resulted in reactivation of desensitized receptors. Thus, both ion channel gating and entry into the desensitized state were affected. Evans blue also slowed the activation and the decay of glutamatergic miniature EPSCs (excitatory postsynaptic currents), demonstrating that receptor kinetics determine the time course of the synaptic response.
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PMID:Evans blue reduces macroscopic desensitization of non-NMDA receptor mediated currents and prolongs excitatory postsynaptic currents in cultured rat thalamic neurons. 128 26

1. Intracellular recordings were obtained from 112 supraoptic nucleus magnocellular neurosecretory cells (MNCs) in superfused explants of rat hypothalamus maintained in vitro. The effects of glutamate receptor agonists and antagonists were examined at 32-34 degrees C. 2. In control solutions, spontaneously active (> 5 Hz) phasic or continuous neurones showed interspike interval distributions slightly skewed toward short intervals, but did not feature pauses in the 0.4-2 s range. Current injection to alter the rate of cell discharge shifted the histograms according to the mean firing rate, but failed to induce intermittent pauses in the 0.4-2 s range. 3. Application of N-methyl-D-aspartate (NMDA) induced a mode of firing in which bimodal interspike interval distributions reflected a high incidence of clusters of short interspike intervals (0.5-1.5 s) recurring every 1-3 s. In contrast, firing evoked by application of D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxalone propionic acid (AMPA) was not associated with a clustering of impulse discharge. 4. The putative endogenous excitatory amino acid transmitters L-glutamate, L-aspartate and quinolinate all mimicked the effects of NMDA. Clustered spiking responses to these agents were reversibly blocked by D,L-2-amino-5-phosphono-valerate (APV), but not by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). In contrast, the non-NMDA receptor ligands kainate and quisqualate caused CNQX-sensitive increases in firing rate, but these responses were not associated with the appearance of clustered activity. 5. When applied to cells showing negative resting potentials (< -70 mV), or to neurones hyperpolarized by current injection, responses to NMDA consisted of rhythmic (approximately 1 Hz) voltage oscillations associated with bursts of spike discharge. In the presence of TTX, NMDA could induce subthreshold voltage oscillations in the absence of action potentials. 6. Application of a voltage clamp to potentials between -75 and -55 mV during rhythmic bursting responses failed to reveal any rhythmic oscillation of the membrane current. In all cases, rhythmic bursting activity resumed upon returning to the current-clamp mode. 7. Rhythmic bursting responses to NMDA application were abolished in Mg(2+)-free solutions, suggesting that the voltage dependence of NMDA channels served to promote regenerative voltage changes throughout the cycle. The NMDA-induced current itself, however, did not appear to decrease with time, suggesting that a distinct, outward current, was necessary to initiate the repolarizing phase of each cycle.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:NMDA receptor-mediated rhythmic bursting activity in rat supraoptic nucleus neurones in vitro. 130 82

A full-length cDNA clone encoding a glutamate receptor was isolated from a human brain cDNA library, and the gene product was characterized after expression in Xenopus oocytes. Degenerate PCR primers to conserved regions of published rat brain glutamate receptor sequences amplified a 1-kilobase fragment from a human brain cDNA library. This fragment was used as a probe for subsequent hybridization screening. Two clones were isolated that, based on sequence information, code for different receptors: a 3-kilobase clone, HBGR1, contains a full-length glutamate receptor cDNA highly homologous to the rat brain clone GluR1, and a second clone, HBGR2, contains approximately two-thirds of the coding region of a receptor homologous to rat brain clone GluR2. Southern and PCR analysis of a somatic cell-hybrid panel mapped HBGR1 to human chromosome 5q31.3-33.3 and mapped HBGR2 to chromosome 4q25-34.3. Xenopus oocytes injected with in vitro-synthesized HBGR1 cRNA expressed currents activated by glutamate receptor agonists with the following specificity sequence: domoate greater than kainate much greater than quisqualate greater than or equal to alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid greater than or equal to L-glutamate much greater than N-methyl-D-aspartate. The kainate-elicited currents were specifically blocked by 6-cyano-7-nitroquinoxaline-2,3-dione but were insensitive to 2-amino-5-phosphonovalerate and kynurenic acid. These results indicate that clone HBGR1 codes for a glutamate receptor of the kainate subtype cognate to members of the glutamate receptor family from rodent brain.
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PMID:Molecular cloning, chromosomal mapping, and functional expression of human brain glutamate receptors. 131 Nov

We used methylazoxymethanol-acetate (MAM), a potent alkylating agent, to produce microencephaly in offspring by injecting it into pregnant rats on day 15 of gestation. Binding activities of central excitatory amino acid receptors were examined in Triton-treated membranes prepared from brains of adult offspring with MAM-induced microencephaly (MAM rats). MAM rats exhibited approximately 40-50% reductions of the wet weights of the cerebral cortex, hippocampus and striatum compared to those in controls. In the cortex and hippocampus of MAM-rats, total bindings of [3H]glutamate (Glu) (which is sensitive to N-methyl-D-aspartate (NMDA) receptor), and strychnine-insensitive [3H]glycine (Gly) and (+)-5-[3H]methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imi ne (MK-801; a noncompetitive antagonist of NMDA receptor), were reduced to approximately 40% of those in controls. Similarly, in both regions of MAM rats, total bindings of [3H]kainate and DL-alpha-amino-3-[3H]hydroxy-5-methylisoxazole-4-propionic acid (an agonist of quisqualate receptors), were reduced to approximately 35-50% of those in controls. However, total bindings of these radioligands in the striatum of MAM rats were more than 65% of those in controls, despite the significant loss of striatum mass. However, specific bindings of radioligands in the striatum of MAM rats were elevated by more than 60% of those in controls, and Scatchard analysis revealed that elevations of [3H]Glu, [3H]Gly and [3H]MK-801 bindings were due to a significant increase in the densities of binding sites, with their affinities remaining unaltered. Spatial recognition ability examined by an 8-armed radial maze task was markedly impaired compared to those in controls. These results suggest that the proliferation of neurons bearing excitatory amino acid receptors (EAA) in the striatum is less affected by MAM treatment on day 15 of gestation than that in the cortex and hippocampus in spite of drastic weight loss in these brain regions. The significant reduction of EAA receptors in the cortex and hippocampus may be involved in the impairment of spatial memory observed in MAM-treated rats.
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PMID:Excitatory amino acid receptors in brains of rats with methylazoxymethanol-induced microencephaly. 132 53

Two glutamate antagonists were tested in a rat model of complete, transient cerebral ischemia. Six days after 10 min ischemia the mean loss of hippocampal CA1 pyramidal neurones was 73%. Administration of the AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) antagonist NBQX (2,3-dihydro-6-nitro-7-sulfamoyl-benzo(F)quinoxaline) reduced the pyramidal neurone loss to 1%, 11% and 15%, when given before, immediately after or 1 h after ischemia, respectively. MK-801 (dizocilpine), a competitive NMDA antagonist gave no protection in this model. We suggest that the AMPA receptor transduction mechanisms are sensitized by ischemia and that the postischemic blockade of the main glutamatergic input to the CA1 cells with NBQX impairs the deleterious effect of "normal" postischemic excitatory transmission.
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PMID:Protection against ischemic hippocampal CA1 damage in the rat with a new non-NMDA antagonist, NBQX. 132 29

A study was performed to examine the specific binding of excitatory amino acid (EAA) receptor subtypes in 5 brain regions of rats kindled from the amygdala or hippocampus, using extensively washed and Triton X-100-treated membranes. Seven days after the last amygdala kindled seizure, [3H](+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10- imine maleate ([3H]MK-801) binding, which labels N-methyl-D-aspartate (NMDA)-sensitive receptor-linked cation channels, decreased significantly only in the amygdala of kindled rats compared to that of controls under equilibrium assay conditions. There was no significant change in [3H]MK-801 binding in the amygdala or hippocampus 7 days after the last hippocampal kindled seizure, or 28 days after the last amygdala kindled seizure. Nor was there a significant change in NMDA-sensitive [3H]glutamate, strychnine-insensitive [3H]glycine, [3H]spermidine, [3H]kainate or [3H]alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid ([3H]AMPA) binding in any brain region 7 days after the last amygdala kindled seizure, or in the hippocampus 28 days after the last amygdala kindled seizure. These results indicate that [3H]MK-801 binding sites labeling NMDA-sensitive receptor-linked cation channels in the amygdala undergo downregulation only transiently, but that none of the subcomponents of the NMDA receptor macromolecular complex exhibit enduring changes at steady state following the completion of amygdala kindling.
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PMID:Ionotropic excitatory amino acid receptors in discrete brain regions of kindled rats. 132 75

The contribution of excitatory amino acids (EAAs) to the development of central sensitization and persistent nociception in response to tissue injury in rats was examined following the subcutaneous injection of formalin into the hindpaw. Formalin-induced nociceptive behaviors were enhanced by intrathecal pretreatment with the EAAs L-glutamate and L-aspartate. An enhancement of the formalin nociceptive response was also produced by intrathecal pretreatment with the receptor-selective EAA agonists NMDA and trans-(+/- )-1-amino-1,3-cyclopentane dicarboxylic acid (ACPD), but not (R,S)-alpha-amino-3-hydroxy-5-methylisozazole-4-propionic acid hydrobromide (AMPA). The effect of NMDA was enhanced by a combined administration with AMPA or APCD. Formalin nociceptive responses were dose-dependently reduced by intrathecal pretreatment with the NMDA receptor antagonists 2-amino-5-phosphonovaleric acid (APV) and (+)-MK-801 hydrogen maleate, but not the selective AMPA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione or the selective metabotropic EAA receptor antagonist 2-amino-3-phosphonopropionic acid. The results suggest that EAAs acting at the NMDA receptor contribute to central sensitization and persistent nociception following subcutaneous formalin injection.
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PMID:The contribution of excitatory amino acids to central sensitization and persistent nociception after formalin-induced tissue injury. 132 10


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