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      Time-course of neuronal death in the mouse pilocarpine model of chronic epilepsy using Fluoro-Jade C staining.

      Brain Research

      Animals, Apoptosis, physiology, Apoptosis Regulatory Proteins, metabolism, Brain, pathology, physiopathology, Cerebral Cortex, Chronic Disease, Convulsants, Disease Models, Animal, Epilepsy, Fluoresceins, chemistry, Fluorescent Dyes, Glutamate Decarboxylase, Hippocampus, Immunohistochemistry, Male, Mice, Nerve Degeneration, Neural Inhibition, Neurons, Organic Chemicals, Pilocarpine, Staining and Labeling, Time Factors, gamma-Aminobutyric Acid

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          Abstract

          Epilepsy is a serious neurological disorder in human beings and the long-term pathological events remain largely obscure. We are interested in elucidating long-term brain injury that may occur in the temporal lobe epilepsy, and time-course of neuronal death was examined in a mouse pilocarpine model of chronic epilepsy by Fluoro-Jade C (FJC) dye that can specifically stain the degenerative neurons in the central nervous system. The FJC stain combined with immunohistochemistry to neuronal nuclear specific protein revealed that pilocarpine-induced status epilepticus (SE) resulted in massive degenerative death of neuronal cells in brains with their dense distribution in the cerebral cortex and hippocampus. The FJC-positive degenerating neurons, most of them also expressed apoptosis signaling molecules such as caspase-9 and activated caspase-3, occurred at 4h, increased into peak levels at 12h-3d, and then gradually went down at 7d-14d after onset of SE. More interestingly, a large percentage (about 88%) of FJC-positive degenerative neurons were GABAergic as indicated with their immunoreactivity to glutamic acid decarboxylase-67, implying that inhibitory function of GABAergic neural system might by seriously damaged in brains subject to SE attack in this mouse pilocarpine model. Taken together with previous studies, time-course of degenerative neurons in the mouse pilocarpine model by Fluoro-Jade C staining further benefits understanding of long-term brain pathological changes and recurrent seizure mechanism, and may also result in finding the most suitable time-window in therapeutic manipulation of the chronic epilepsy in human beings.

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          Journal
          18708038
          10.1016/j.brainres.2008.07.097

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