作者: M. Banerjee , V.A. Sasse , Y. Wang , M. Maulik , S. Kar
DOI: 10.1016/J.NEUROSCIENCE.2014.10.003
关键词: Kainic acid 、 Gliosis 、 Kainate receptor 、 Hippocampus 、 Biology 、 Internal medicine 、 Neurodegeneration 、 Receptor 、 Cathepsin B 、 Endocrinology 、 Microglia
摘要: Administration of kainic acid induces acute seizures that result in the loss neurons, gliosis and reorganization mossy fiber pathways hippocampus resembling those observed human temporal lobe epilepsy. Although these structural changes have been well characterized, mechanisms underlying degeneration neurons following administration remain unclear. Since lysosomal enzymes, cathepsins B D, are known to be involved clearance degenerative materials a variety experimental conditions, we evaluated their potential roles acid-treated rats. In parallel, also measured levels expression insulin-like growth factor-II/mannose 6-phosphate (IGF-II/M6P) receptors, which mediate intracellular trafficking Our results showed systemic evoked severe along with hypertrophy astrocytes microglia adult rat brain. The activity D increased time rats compared saline-injected control animals. both as evident by immunolabeling studies, was markedly activated Additionally, cytosolic were enhanced cytochrome c some extent Bax These accompanied appearance cleaved caspase-3-positive IGF-II/M6P on other hand, not significantly altered, but receptors found present subset reactive acid. results, taken together, suggest levels/expression enzymes may role and/or