Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.4.1.2 (glutamate dehydrogenase)
 4,380 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microfluorometry was used to investigate distribution of hypoxia-induced release of glutamate. Mongolian gerbil hippocampal slice was perfused in a medium containing glutamate dehydrogenase and NAD+. Release of glutamate into extracellular space caused an increase in fluorescence due to the formation of NADH. The hypoxia-induced release of glutamate was gradually increased throughout the slice: no significant difference was detected among CA1 region, CA3 region and the dentate gyrus.
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PMID:Visualization of hypoxia-induced glutamate release in gerbil hippocampal slice. 202 17

Transmitter glutamate/aspartate synthesis is known to proceed along different metabolic pathways. In this light, the functional relevance of glutamate dehydrogenase in postnatally maturing glutamatergic/aspartatergic structures was studied by means of quantitative enzyme histochemistry. The basic requirements concerning the kinetics and calibration of the histochemical glutamate dehydrogenase reaction used were proved to be met in order to obtain valid quantitative data. The histochemically demonstrable activity of glutamate dehydrogenase (EC 1.4.1.3) in the hippocampal formation of the rat increased markedly during postnatal development. On day 30, the distribution pattern observed was similar to that in adult animals. While the enzyme activity rose within cell body layers from day 0 to day 30 by 240-285%, the increase in neuropil layers was found to be up to 830%. Maximum values were seen in the stratum lacunosum-moleculare of CA1 and CA3 and the stratum moleculare of the dentate fascia on day 30. Since the hippocampal neuropil is supposed to be copiously provided with glutamatergic (and aspartatergic?) structures which become functional in rats during the first weeks of postnatal life, the increase in enzyme activity is discussed to be primarily a consequence of maturing synaptic systems using glutamate and/or aspartate as transmitters.
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PMID:Histophotometric evaluation of glutamate dehydrogenase activity of the rat hippocampal formation during postnatal development, with special reference to the glutamate transmitter metabolism. 287 62

The aim of this work was the comparative cytochemical study of some parameters of neurotransmitter and protein metabolism in the hippocampus (CA3 field) of August and Wistar rats, which were used as genetic-functional models demonstrating different brain organization, in particular, in respect to an emotional stress. Using quantitative cytochemical methods it was demonstrated that the activities of aminopeptidase, monoaminooxidase (substrates--tryptamine and serotonin), and glutamate dehydrogenase, were lower in the hippocampus of August rats (predisposed to emotional stress) as compared to that one in Wistar rats (resistant to emotional stress). August rats were also characterized by smaller sizes of neuronal cytoplasm and nuclei and by their lower protein content and concentration. The analysis of the data obtained has shown the existence of neurons with different modalities within the limits of CA3 hippocampal field, and these characteristics are thought to define the morphochemical differences in the hippocampus (CA3 field) of genetically different rats.
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PMID:[Morphochemical analysis of hippocampus of rats predisposed (August) or resistant (Wistar) to emotional stress]. 1523 64

It has been suggested that astrocytic glutamate release or perturbed glutamate metabolism contributes to the proneness to epileptic seizures. Here we investigated whether astrocytic contents of the major glutamate degrading enzymes glutamine synthetase (GS) and glutamate dehydrogenase (GDH) decreases on moving from the latent phase (prior to seizures) to the chronic phase (after onset of seizures) in the kainate (KA) model of temporal lobe epilepsy. Western blotting and immunogold analysis of hippocampal formation indicated similar levels of GDH in the latent and chronic phases of KA injected rats and in corresponding controls. In contrast, the level of GS was increased in the latent phase compared with controls, as assessed by Western blots of whole hippocampal formation and subregions. The increase in GS paralleled that of glial fibrillary acidic protein (GFAP). Compared with the latent phase, the chronic phase revealed a lower level of GS (approaching control levels) but an unchanged GFAP content. The decrease in GS from latent to chronic phase was significant in whole hippocampal formation, dentate gyrus and CA3. It is concluded that kainate treated rats show an initial increase in GS, pari passu with the increase in GFAP, and a secondary decrease in GS that is not accompanied by a similar loss of GFAP. In a situation where glutamate catabolism is in high demand the secondary reduction in GS level may be sufficient to contribute to the seizure proneness that develops between the latent and chronic phases.
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PMID:Expression of glutamine synthetase and glutamate dehydrogenase in the latent phase and chronic phase in the kainate model of temporal lobe epilepsy. 1838 50