High impact information on glutamate

• Dorsal periaqueductal gray (dPAG) neurons express NMDA/GLY(B) receptors suggesting a GLU physiological role in mediating the responses elicited by stimulation of this area [1].
• The intracellular pool of Glu and Asp was also reduced in kainate-lesioned striata [2].
• Our data thus suggest that neither SNAT1 nor SNAT2 meet the criteria for their postulated role in the "glutamate-glutamine" cycle, and indicate that other Gln transporters (either orphan or yet to be identified) must be expressed at axon terminals and sustain the Glu (and gamma-aminobutyric acid) neurotransmitter pool (s) [3].
• This study explored functional interactions between DA and glutamate (Glu) systems using the NMDA receptor antagonist MK-801 and the DA receptor agonists 7-OH-DPAT and apomorphine [4].
• Double-labeling studies revealed that of the c-Fos-positive neurons responsive to hypertonic NaCl, 52%, 41%, and 3% exhibited immunoreactivity for Glu, SP, and CGRP, respectively [5].

Biological context of glutamate

• We previously showed that Gln potently inhibited apoptosis in cytokine-treated human colonic HT-29 cells; this effect was specific to Gln, unaffected by Glu, and unrelated to intracellular GSH [6].
• We have used site-directed in vitro mutagenesis to replace the His codon of the esterase 6 gene with either Gln or Glu codons [7].

Anatomical context of glutamate

• These results suggest that in the nucleus accumbens, ASP and GLU may increase dopamine release through distinct mechanisms and that their stimulatory action is dependent on axonal impulse flow [8].
• However, His significantly decreased to almost the preincubation level the content of Glu in mitochondria incubated with Gln, without affecting the content of Gln [9].
• We also measured the ex vivo tissue level of glutamate (Glu), dopamine (DA) and serotonin (5-HT) as well as the DA metabolites DOPAC and the major 5-HT metabolite HIAA to determine the neurochemical effects of ketamine (12 mg/kg) and LY379268 (1 mg/kg) in the dentate gyrus (DG) [10].
• Glu released from neurons is taken up by astrocytes, and reconverted to Gln, closing the so called "glutamate-glutamine" cycle [11].
• Methionine S-sulfoximine, an inhibitor of Gln synthetase, did not reverse the inhibitory effect of Glu of PEP formation from malate in chicken liver mitochondria [12].

Associations of glutamate with other chemical compounds

• Microinjection of sodium glutamate (Glu, 0.25 M, 30 nl) or Gly (1.0 M, 30 nl) into the DM or RVLM increased SAP and VNA in similar magnitude [13].
• Cells treated with Glu, glucosamine, arginine, or nucleotide monophosphate mixture showed a decrease in proliferation compared with cells treated with Gln across all treatment doses (P < 0.03) [14].
• METHODS: Glu with added ammonia acetate, glucosamine, arginine, and nucleotide monophosphates were tested at concentrations that were isonitrogenous with respect to Gln [14].
• Glutamate + malate (glu/mal) supported respiration was diminished only in mitochondria isolated from brain stem of 2,5-HD treated rats [15].
• While Gln and Glu required 24 h for maximal stimulation of prolidase activity, P5C induced it after 6-12 h [16].

Gene context of glutamate

• Gln but not Glu decreased plasma CINC peptide (P < 0.05) [17].
• Intestinal and plasma TNF-alpha were increased in GF, LPS-treated pups (P < 0.01), and Gln and Glu both blunted this increase (P < 0.05) in the intestine but not in the plasma [17].
• Substitution of Gln for His at position 187 has little effect on the biochemical properties of esterase 6, but the presence of Glu at this position is associated with three major differences [7].
• This demand is met by intracerebral Gln synthesis from glutamate (Glu), a reaction carried out by glutamine synthetase (GS), an enzyme residing in astrocytes [11].

Analytical, diagnostic and therapeutic context of glutamate

• Perfusion of tetrodotoxin before application of either GLU or ASP blocked the excitatory effect of these amino acids on dopamine overflow [8].
• Subsequently, the mitochondrial contents of Glu and Gln were determined by HPLC [9].

References