Astrocytes may play a role in the etiology of absence epilepsy: a comparison between immature GAERS not yet expressing seizures and adults.

Neuronal-astrocytic interactions in 1-month-old Genetic Absence Epilepsy Rats from Strasbourg (GAERS) before the occurrence of seizures are compared to those in non-epileptic rats (NERs) and in adult GAERS expressing epilepsy. Animals received [1-13C]glucose and [1,2-13C]acetate, preferential substrates of neurons and astrocytes, respectively, and extracts from cerebral cortex, subcortex and cerebellum were analyzed by NMR spectroscopy. Increased mitochondrial metabolism took place in the cortical neurons of immature and adult GAERS and therefore does not seem to be a consequence of the occurrence of absence seizures. Glutamine supply to GABAergic neurons was reduced in cortex and subcortex in young GAERS, as reflected by increased glutamine content and decreased 13C-labeling of GABA. In the brain of immature GAERS, interactions between glutamatergic neurons and astrocytes appeared normal whereas increased astrocytic metabolism took place in adult GAERS, suggesting that astrocytic alterations could possibly be the cause of seizures.