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L'administration d'acide ascorbique (AA) a été associée à une neuroprotection contre le stress oxydatif, bien qu'à doses élevées, elle puisse faciliter l'oxydation et se comporter comme un médicament proconvulsant. Le modèle d'épilepsie induite par la pilocarpine a été largement étudié. Cependant, on en sait moins sur les effets de doses subconvulsives de pilocarpine sur l'activité cérébrale chez des animaux immatures dans des conditions nutritionnelles normales ou déficientes. Ici, nous avons étudié les effets de l'administration chronique de pilocarpine à une dose sub convulsive, avec ou sans AA, sur le phénomène lié à l'excitabilité dénommé dépression corticale (CSD) et niveaux de malondialdéhyde induit par la peroxydation lipidique chez des sujets bien nourris et mal nourris. les rats. Aux jours postnatals 7 à 28, les rats n'ont reçu aucun traitement par gavage (groupe naïf), solution saline (groupe véhicule), 45 mg / kg / j de pilocarpine et / ou 120 mg / kg / j de AA. La propagation de CSD et les taux de malondialdéhyde ont été analysés à 34-40 jours. Le groupe pilocarpine présentait des vitesses de CSD plus faibles, tandis que les groupes AA présentaient des vitesses de CSD plus élevées et des niveaux de malondialdéhyde augmentés par rapport aux témoins. L'administration concomitante d'AA a partiellement neutralisé les effets de la pilocarpine CSD, mais ne l'a pas rétablie à des niveaux de contrôle. La malnutrition a augmenté l'amplitude et la vitesse de la CDD par rapport à l'état bien nourri. L'amplitude de l'électrocorticogramme (ECoG) a augmenté après la CSD (potentialisation de l'ECoG) par rapport à l'amplitude de base avant la CSD. Cependant, aucune différence intergroupe n'a été observée dans cette potentialisation ECoG liée à la CSD. Les résultats supportent l'hypothèse d'une interaction pilocarpine / acide ascorbique dans le cerveau immature du rat et pourraient aider à mieux comprendre cette interaction sur l'activité électrique neuronale et le stress oxydatif.
Source: https://www.ncbi.nlm.nih.gov/pubmed/30232044