title: Astrocyte-neuronal interactions in epileptogenesis.
abstract: Pentylenetetrazol, kainic acid, or pilocarpine can be used to induce seizures in animal models of epilepsy. The present Review describes disturbances in astrocyte-neuron interactions in the acute, latent, and chronic phases analyzed by magnetic resonance spectroscopy of brain tissue extracts from rats injected with [1-(13)C]glucose and [1,2-(13)C]acetate. The most consistent change after onset of seizures was the decrease in (13)C labeling of glutamate (GLU) from [1-(13) C]glucose regardless of brain area, severity, or duration of the period with seizures and toxin used. In most cases this decrease was accompanied by a reduction in glutamine (GLN) labeling from [1-(13)C]glucose, presumably as a direct consequence of the reduction in labeling of GLU and the GLU-GLN cycle. Amounts of GLN were never changed. Reduction in the content of N-acetyl aspartate (NAA) was first detectable some time after status epilepticus but before the occurrence of spontaneous seizures. This decrease can be an indication of neuronal death and/or mitochondrial impairment and might indicate beginning gliosis. It is known that gliosis occurs in the chronic phase of temporal lobe epilepsy in hippocampus, but astrocyte metabolism appears normal in this phase, indicating that the gliotic astrocytes have a somewhat reduced metabolism per volume. A decrease in (13)C labeling of GLU from [1-(13)C]glucose is a very sensitive measure for the onset of epileptogenesis, whereas reduction of NAA is first detectable later. In the chronic phases of the hippocampal formation, astrocyte metabolism is upregulated given that the number of neurons is reduced.
authors.affiliation: Department of Neuroscience, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
authors.forename: Mussie Ghezu
authors.initials: MG
authors.lastname: Hadera
authors.affiliation: Department of Neuroscience, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan.
authors.forename: Haytham
authors.initials: H
authors.lastname: Eloqayli
authors.affiliation: Princess Haya Biotechnology Center, Jordan University of Science and Technology, Irbid, Jordan.
authors.forename: Saied
authors.initials: S
authors.lastname: Jaradat
authors.affiliation: INSERM U1129 "Infantile Epilepsies and Brain Plasticity", Paris, France; Paris Descartes University-Sorbonne Paris Cité, Paris, France.|CEA, Gif sur Yvette, France.
authors.forename: Astrid
authors.initials: A
authors.lastname: Nehlig
authors.affiliation: Department of Neuroscience, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
authors.forename: Ursula
authors.initials: U
authors.lastname: Sonnewald
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000502:physiology*; D002450:Cell Communication / Q000502:physiology*; D003292:Convulsants / Q000633:toxicity; D004195:Disease Models, Animal; D004827:Epilepsy / Q000139:chemically induced / Q000209:etiology*; D006801:Humans; D009474:Neurons / Q000187:drug effects / Q000502:physiology*
chemical_list: D003292:Convulsants
keywords: epilepsy; glucose; metabolism; neurons