Sequential expression of surface antigens and transcription factor NFκB by hippocampal cells in excitotoxicity and experimental epilepsy

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• 作者：Lerner-Natoli ; Mireille ; Montpied ; Pascale ; Rousset ; Marie-Claude ; Bockaert ; Joë ; l ; Rondouin ; G&eacute ; rard
• 关键词：Kainic acid ; Neurotoxicity ; Inflammation ; Histocompatibility antigens ; Transcription factor
• 刊名：Epilepsy Research
• 出版年：2000
• 期刊代码：87_09201211
• 类别：med
• 出版时间：August, 2000
• 卷：41
• 期：2
• 页码：141-154
• 文件大小：1.86 M

摘要

Neurodegeneration and gliosis have been extensively described after long-lasting seizures; evidence for cytokine involvement in neuron-glia interactions does exist. We have therefore studied the hippocampal expression of molecules responsible for immune and inflammatory reactions, at different time-points following either experimental status epilepticus (SE) or direct excitotoxic damage. Experiments consisting of immunohistochemical labeling of glial markers, major histocompatibility complex (MHC) and nuclear factor κB (NFκB), were performed. NFκB nuclear translocation was controlled and measured using the electrophoretic mobility shift assay. One day after SE, neurodegeneration was obvious in CA3 pyramidal layers; NFκB staining in neurons and its translocation to the nucleus enhanced. From day 4 to at least day 8 post-SE, MHC-positive microglia, NFκB over-expression in thickened astrocytes, and increased levels of its activated form could be observed. The excitotoxic model caused more severe lesions, but NFκB and MHC expression were similar in both models. These results suggest that during long-lasting seizures: (i) neuronal firing activates NFκB expression and translocation; (ii) microglia expresses MHC; (iii) astrocytes, probably stimulated by microglial cytokines, over-express NFκB, the activation of which induces a cascade of reactions, particularly the transcription of cytokines and/or neuroprotective molecules. Further clarification of the toxic or protective consequences of delayed inflammatory responses may be interesting in therapy of epilepsy.