title: Specific alteration in the expression of glial fibrillary acidic protein, glutamate dehydrogenase, and glutamine synthetase in rats with genetic absence epilepsy.
abstract: Astrocytes play a predominant role in energy metabolism and in the catabolism of gamma-aminobutyric acid (GABA) and glutamate, neurotransmitters critically involved in epileptic processes. We show specific astrocytic alterations in the genetic absence epilepsy rats from Strasbourg (GAERS). Spontaneous absence seizures appear in this strain in the cortex and thalamus after the age of 1 month. In these brain structures, we demonstrate increased GFAP expression in both adult and young GAERS, suggesting that reactive astrocytes are already present before the onset of seizures. Glutamate dehydrogenase (GDH) and glutamine synthetase (GS), which are localized mainly in astrocytes and involved in glutamate catabolism, are shown to be differentially altered. GDH expression was increased in the thalamus of both young and adult GAERS and in the cortex of young GAERS. GS expression was slightly decreased in the thalamus of young GAERS. These astrocytic modifications are not adaptive responses to seizures, as the modifications appear before the development of absence seizures. Thus, astrocytes might be involved in the neuronal processes giving rise to epileptic seizures in this strain.
authors.affiliation: INSERM U433, Neurobiologie Expérimentale et Physiopathologie, Faculté de Médecine Laënnec, Lyon, France.
authors.forename: M
authors.initials: M
authors.lastname: Dutuit
authors.forename: M
authors.initials: M
authors.lastname: Didier-Bazès
authors.forename: M
authors.initials: M
authors.lastname: Vergnes
authors.forename: M
authors.initials: M
authors.lastname: Mutin
authors.forename: A
authors.initials: A
authors.lastname: Conjard
authors.forename: H
authors.initials: H
authors.lastname: Akaoka
authors.forename: M F
authors.initials: MF
authors.lastname: Belin
authors.forename: M
authors.initials: M
authors.lastname: Touret
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000201:enzymology*; D002540:Cerebral Cortex / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D004832:Epilepsy, Absence / Q000201:enzymology* / Q000235:genetics / Q000503:physiopathology*; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics / Q000378:metabolism*; D005969:Glutamate Dehydrogenase / Q000235:genetics / Q000378:metabolism*; D005974:Glutamate-Ammonia Ligase / Q000235:genetics / Q000378:metabolism*; D006624:Hippocampus / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D009435:Synaptic Transmission / Q000502:physiology; D013788:Thalamus / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology; D014746:Vimentin / Q000235:genetics / Q000378:metabolism
chemical_list: D005904:Glial Fibrillary Acidic Protein; D012333:RNA, Messenger; D014746:Vimentin; D005969:Glutamate Dehydrogenase; D005974:Glutamate-Ammonia Ligase