Excitotoxicity induced by kainic acid provokes glycogen synthase kinase-3 truncation in the hippocampus.

摘要: In neuronal cultures, glycogen synthase kinase 3(GSK3) is truncated at the N-terminal end by calpain downstream of activated glutamate receptors. However, in vivo biological significance that truncation has not been explored. an attempt to elucidate if GSK3 a pathophysiological relevance, we have used intraperitoneal injections kainic acid (KA) rats and intra-amygdala KA microinjections mice as models excitotoxicity. Spectrin cleavage analyzed immunohistochemistry was observed CA1 hippocampal field KA-intraperitoneal treated while CA3 region area affected after microinjections. GSK3β immunofluorescence did colocalize with spectrin both treatments using antibody recognize GSK3β. Thus, those neurons which are spectrin-positive do show immunolabelling. To study vitro, exposed organotypic slices cultured cortical leading found blocked inhibitor calpeptin. These data suggest relationship between Overall, our reinforces important receptors their role neurodegenerative processes excitotoxicity involved.