Abstract
Excitotoxic damage induced by excitatory amino acid has been implicated in the pathogenesis of a variety of neurodegenerative diseases. Recently, we have shown that cathepsin E (CE), a non-lysosomal aspartic proteinase, was markedly increased in the pathological process of ischemia and normal aging. Thus it is of special interest whether CE is involved in the process of excitotoxic neuronal death. By kainate treatment, the increased level of CE was found in the rat hippocampus by both immunohistochemistry and enzyme immunoassay (EIA). Increased CE immunoreactivity was observed especially in the neurons of the hippocampal CA3 subfield, and the content measured by EIA was 30-fold higher than the control level. Western blot analysis revealed that CE was expressed as an enzymatically inactive form with unusually high molecular weight. The results indicate that kainate induces the increased accumulation of the unusual form of CE in the neurons of CA3 hippocampal subfield, which is likely to lead to the neuronal death.
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Nakanishi, H., Tominaga, K. & Yamamoto, K. Unusual Molecular Form of Cathepsin E Expressed at Early Stage of Excitotoxic Damage in Hippocampal Neurons of Rats. Neuropsychopharmacol 11, 278 (1994). https://doi.org/10.1038/sj.npp.1380184
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DOI: https://doi.org/10.1038/sj.npp.1380184