Alteration of amino acid metabolism in neuronal aggregate cultures exposed to hypoglycaemic conditions.

Détails

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Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_92DA4F5C8FC8
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Alteration of amino acid metabolism in neuronal aggregate cultures exposed to hypoglycaemic conditions.
Périodique
Journal of Neurochemistry
Auteur(s)
Honegger P., Braissant O., Henry H., Boulat O., Bachmann C., Zurich M.G., Pardo B.
ISSN
0022-3042 (Print)
ISSN-L
0022-3042
Statut éditorial
Publié
Date de publication
06/2002
Volume
81
Numéro
6
Pages
1141-1151
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
The neuronal effects of glucose deficiency on amino acid metabolism was studied on three-dimensional cultures of rat telencephalon neurones. Transient (6 h) exposure of differentiated cultures to low glucose (0.25 mm instead of 25 mm) caused irreversible damage, as judged by the marked decrease in the activities of two neurone-specific enzymes and lactate dehydrogenase, 1 week after the hypoglycemic insult. Quantification of amino acids and ammonia in the culture media supernatants indicated increased amino acid utilization and ammonia production during glucose-deficiency. Measurement of intracellular amino acids showed decreased levels of alanine, glutamine, glutamate and GABA, while aspartate was increased. Added lactate (11 mm) during glucose deficiency largely prevented the changes in amino acid metabolism and ammonia production, and attenuated irreversible damage. Higher media levels of glutamine (4 mm instead of 0.25 mm) during glucose deprivation prevented the decrease of intracellular glutamate and GABA, while it further increased intracellular aspartate, ammonia production and neuronal damage. Both lactate and glutamine were readily oxidized in these neuronal cultures. The present results suggest that in neurones, glucose deficiency enhances amino acid deamination at the expense of transamination reactions. This results in increased ammonia production and neuronal damage.
Mots-clé
Amino Acids/metabolism, Animals, Cell Aggregation, Cells, Cultured, Dose-Response Relationship, Drug, Energy Metabolism, Extracellular Space/metabolism, Glucose/administration & dosage, Glucose/deficiency, Glutamine/administration & dosage, Glutamine/pharmacology, Intracellular Fluid/metabolism, Lactic Acid/pharmacology, Neurons/drug effects, Neurons/physiology, Oxidation-Reduction, Quaternary Ammonium Compounds/metabolism, Rats, Rats, Sprague-Dawley, Telencephalon/cytology
Pubmed
Web of science
Open Access
Oui
Création de la notice
24/01/2008 14:12
Dernière modification de la notice
20/08/2019 15:55
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