Acute, but reversible, kainic acid-induced DNA damage in hippocampal CA1 pyramidal cells of p53-deficient mice

摘要: Summary p53 plays an essential role in mediating apoptotic responses to cellular stress, especially DNA damage. In a kainic acid (KA)–induced seizure model mice, hippocampal CA1 pyramidal cells undergo delayed neuronal death at day 3–4 following systemic KA administration. We previously demonstrated that neurons p53−/− animals are protected from such loss. However, extensive morphological damage associated with strand breaks was found fraction of earlier time points (8 h 2 days). No comparable acute observed wild-type animals. Stereological counting confirmed there no significant loss 7 days post-KA injection. These results suggest seizure-induced accumulated greater extent but do not lead apoptosis the absence p53. animals, therefore, p53 appears stimulate repair and also mediate this excitotoxicity model. reflect remarkable plasticity recovery injury.