Asp Concentration Research Articles

Effect of Zhongfeng Naodeping granule on hippocampal excitatory amino acid and neuron of stroke-prone spontaneously hypertensive rats with hemorrhagic apoplexy

To observe the effects of Zhongfeng Naodeping Granule (ZFNDPG) on hemorrhagic apoplexy. The stroke-prone spontaneously hypertensive rats (SHRsp) were used to study effects of ZFNDPG on hemorrhage apoplexy. Excitatory amino acid (EAA) concentration in hippocampus sector, neuronal density and ultrastructural changes in hippocampal CA1 sector were measured. In pathological model group glutamate (Glu) and aspartate (Asp) concentration elevated obviously. With the ZFNDPG treating SHRsp of hemorrhagic apoplexy, Glu and Asp concentration in hippocampal sector could be markedly inhibited, compared with model group, P < 0.05-0.01. Neuronal morphology was observed: neurone injury was mild and neuronal density increased in hippocampal CA1 sector of treatment group, compared with model group, P < 0.01. Electron microscopy showed: edema, degeneration and necrosis caused by hemorrhagic apoplexy were improved after the ZFNDPG treatment. Effects of protecting neurone for SHRsp on hemorrhagic apoplexy might be associated with that ZFNDPG inhibited concentration of EAA.

Comparison of glutamate metabolism in low K (LK), high K and high glutathione (HK/HG) and high K and low glutathione (HK/LG) dog red blood cells

The reasons for the high accumulation of glutamate (Glu), aspartate (Asp) and glutamine (Gin) in high K and high glutathione (HK/HG) dog red blood cells (DRBCs) have been explained as due to enhanced Glu/Asp influxes. However, in our study, Glu/Asp influxes in high K and low glutathione (HK/LG) DRBCs were low, whereas their cellular Asp and Gin contents were high. In low K (LK) DRBCs, there were also other variant cells with high Asp accumulation, but extremely low Glu/Asp influxes. So, the high amino acid accumulation in DRBCs of these new variants might not be due to Glu/Asp influxes. To examine the high accumulation of these amino acids in these variant DRBCs, first, LK and HK/LG DRBCs were classified into two subgroups with their Na-dependent Glu/Asp influxes; one had clear Na-dependent Glu/Asp transport (GAT+), and the other failed to have any transport (GAT−). The influxes of both Glu and Asp in HK/HG DRBCs were the highest, and the order was HK/HG>LK/GAT+>HK/LG/GAT+>>LK/GAT−=HK/LG/GAT−. LK/GAT+ cells represented normal DRBCs. Glu/Asp influxes were only trace in both LK/GAT− and HK/LG/GAT− cells, but Glu and Asp concentration was high in HK/LG/GAT− cells whereas Asp concentration was high in LK/GAT− cells. In HK/HG cells, the conversion of Glu into Gin in whole cells was several fold higher than in the other cell groups due to the differing amount of the substrate of glutamine synthetase, Glu, but glutamine synthetase activity itself was not different among these cell groups. Furthermore, glutamine synthetase and glutaminase activities were not different among the cell groups. Therefore, these enzymes were not involved in the high amino acid accumulation.

Evidence for neuronal origin and metabotropic receptor-mediated regulation of extracellular glutamate and aspartate in rat striatum in vivo following electrical stimulation of the prefrontal cortex.

Extracellular levels of glutamate (Glu) and aspartate (Asp) were measured at 5-s intervals in the striatum of chloral hydrate-anesthetized rats by using microdialysis coupled to an automated assay system based on capillary electrophoresis with laser-induced fluorescence. Application of a single 10-s train of depolarizing pulses to the prefrontal cortex caused a rapid increase in Glu and Asp concentrations (200-300% of basal value), which returned to basal level within 60 s. The stimulated rise in Glu and Asp concentrations was blocked completely by 2 microM tetrodotoxin or depletion of extracellular Ca2+, suggesting a neuronal origin of the Glu and Asp. Infusion of the Glu transport inhibitor L-trans-pyrrolidine-2,4-dicarboxylic acid (200 microM) increased resting Glu and Asp levels by 300-500% without altering electrically stimulated changes in Glu and Asp concentration. Stimulated Glu and Asp concentration changes were suppressed by 91 and 73%, respectively, by the metabotropic Glu receptor agonist (1S,3R)-1-aminocyclopentane-trans-1,3-dicarboxylate (200 microM). This effect was blocked by the metabotropic Glu receptor antagonist (RS)-alpha-methylcarboxyphenylglycine (MCPG; 200 microM). MCPG alone produced no effect on electrically stimulated changes in Glu and Asp levels; however, in the presence of L-trans-pyrrolidine-2,4-dicarboxylic acid, MCPG produced a five- to sixfold increase in stimulated overflow. Based on these results, it is concluded that release of Glu and Asp from corticostriatal neurons can be inhibited by activation of metabotropic Glu autoreceptors, which may be an important determinant of excitatory transmission at striatal synapses.

Conversion of Ascorbyl-2-Phosphate to Ascorbic Acid in Rainbow Trout.

Conversion of L-ascorbyl-2-phosphate (ASP) to L-ascorbic acid (AsA) was investigated in vivo in rainbow trout Oncorhynchus mykiss administered with AsP orally and intraperitoneally. AsP magnesium salt or AsA (each 200μmol in 2g of casein basal diet) was orally administered to each rainbow trout once. The fish were sacrificed at varying intervals during the experimental period, and the plasma AsA concentrations and the amounts of AsP and AsA in the contents of the alimentary canal were measured by high-performance liquid chromatography. There was no statistical difference in the plasma AsA concentration between the AsP-administered group and the AsA-administered group (control). The AsP concentration in the plasma was below detectable levels throughout the experimental period. Most of the AsP administered was hydrolyzed to AsA in the pyloric caeca and intestine but not in the stomach. AsP magnesium salt (10μmol) was also administered to rainbow trout (40-70g) intraperi-toneally. AsA concentrations in the plasma, liver, and kidney increased rapidly after the AsP injection. A little AsP was detected in the plasma, liver, and kidney 1h after the injection; the AsP concentration decreased below detectable levels after 3h. These findings indicate the ready conversion of AsP to AsA in the rainbow trout body.

Extracellular amino acid concentrations in the dorsal spinal cord of freely moving rats following veratridine and nociceptive stimulation.

In vivo microdialysis was used to sample extracellular concentrations of amino acids in the dorsal lumbar spinal cord of freely moving rats. Changes in the extracellular concentrations of amino acids were measured in response to infusion of veratridine (180 microM), a sodium channel activator, as well as during acute noxious stimulation by an injection of 5% formalin into the metatarsal region of the hindleg. Veratridine produced a tetrodotoxin (TTX)-sensitive increase in the extracellular concentration of Glu. Concentrations of Asp, taurine, Ala, Asn, and Gly were not significantly elevated following veratridine stimulation. Intradermal injection of formalin produced a TTX-sensitive increase in Asp concentration and a non-TTX-sensitive increase in Glu concentration. These data support the hypothesis that Glu and Asp are dorsal horn neurotransmitters involved in nociception.