title: Glial-neuronal interactions following kainate injection in rats.
abstract: Limbic seizures were induced in rats by intraperitoneal injection of the glutamate receptor agonist kainic acid, followed, 24h later by injection of [1-13C]glucose and [1,2-13C]acetate. Analyses of forebrain extracts were performed using 13C magnetic resonance spectroscopy and HPLC. A significant increase in label derived from [1,2-13C]acetate was observed in glutamine and glutamate. Label in most metabolites derived from [1-13C]glucose was unchanged, however, a decrease was observed in [2-13C]GABA, possibly due to reduced GABA release, 24h after kainic acid injection. It should be noted that only astrocytes are able to utilize acetate as a substrate efficiently, whereas acetyl CoA derived from glucose is metabolized predominantly in the neuronal tricarboxylic acid cycle. No significant differences were found in total amounts of amino acids between the two groups. Thus, these results indicate that turnover of metabolites was increased predominantly in astrocytes whereas glutamatergic neurons were not affected. Previous results obtained using the same model [Neurosci. Lett. 279 (2000) 169] showed an increased turnover in both glutamatergic and GABAergic neurons 2 weeks after kainic acid injection. Combining the results from the two studies, it can be suggested that increased astrocytic activity 1 day after epileptic seizures results, subsequently, in an increased amino acid turnover in neurons.
authors.affiliation: Department of Clinical Neurosciences, Faculty of Medicine, NTNU, MTFS, Norwegian University of Science and Technology, Olav Kyrresgt. 3, N-7489 Trondheim, Norway.
authors.forename: Hong
authors.initials: H
authors.lastname: Qu
authors.forename: Haytham
authors.initials: H
authors.lastname: Eloqayli
authors.forename: Bernd
authors.initials: B
authors.lastname: Müller
authors.forename: Jan
authors.initials: J
authors.lastname: Aasly
authors.forename: Ursula
authors.initials: U
authors.lastname: Sonnewald
mesh_terms: D000085:Acetates / Q000378:metabolism; D000105:Acetyl Coenzyme A / Q000378:metabolism; D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D001253:Astrocytes / Q000378:metabolism* / Q000473:pathology; D002247:Carbon Isotopes / Q000032:analysis / Q000493:pharmacokinetics; D002851:Chromatography, High Pressure Liquid; D002952:Citric Acid Cycle; D003292:Convulsants / Q000494:pharmacology / Q000633:toxicity*; D005947:Glucose / Q000378:metabolism; D007608:Kainic Acid / Q000494:pharmacology / Q000633:toxicity*; D008032:Limbic System / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D008297:Male; D009457:Neuroglia / Q000378:metabolism* / Q000473:pathology; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D019906:Nuclear Magnetic Resonance, Biomolecular; D062907:Oxaloacetic Acid / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012640:Seizures / Q000378:metabolism / Q000473:pathology*
chemical_list: D000085:Acetates; D000596:Amino Acids; D002247:Carbon Isotopes; D003292:Convulsants; D062907:Oxaloacetic Acid; D000105:Acetyl Coenzyme A; D005947:Glucose; D007608:Kainic Acid