β-amyloid peptide fragment 31–35 induces apoptosis in cultured cortical neurons

• Published in: Neuroscience 1999-01, Vol.92 (1), p.177-184
• Main Authors: Yan, X.-Z, Qiao, J.-T, Dou, Y, Qiao, Z.-D
• Format: Article
• Language: English
• Subjects: Ageing, cell death; Amyloid beta-Peptides - pharmacology; Animals; Animals, Newborn - physiology; apoptosis; Apoptosis - drug effects; Apoptosis - physiology; Aurintricarboxylic Acid - pharmacology; Biological and medical sciences; Cell physiology; Cell Survival - drug effects; Cells, Cultured; Cerebral Cortex - cytology; Cerebral Cortex - drug effects; Cerebral Cortex - physiology; cultured neurons; Dactinomycin - pharmacology; DNA fragmentation; DNA Fragmentation - physiology; Flow Cytometry; Fundamental and applied biological sciences. Psychology; Mice; Molecular and cellular biology; neurodegeneration; Neurons - drug effects; Neurons - physiology; Neurons - ultrastructure; Peptide Fragments - pharmacology; β-amyloid peptide fragment 31–35
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/S0306-4522(98)00727-1

A synthetic fragment 31–35 of β-amyloid peptide was used in cultured cortical neurons to examine whether this smaller sequence could trigger apoptotic degeneration in vitro by using morphological, biochemical and flow-cytometric examinations. The results showed that: (i) neurons treated with fragment 31–35 of β-amyloid peptide exhibited membrane blebbing, compaction of nuclear chromatin, nuclear shrinkage and nuclear fragmentation; (ii) a typical DNA ladder was revealed by agarose gel electrophoresis following fragment 31–35 of β-amyloid peptide exposure; (iii) the internucleosome DNA fragmentation was also detected by flow-cytometric examination following fragment 31–35 of β-amyloid peptide exposure; and (iv) the DNA fragmentation induced by fragment 31–35 of β-amyloid peptide in the above two examinations could be blocked by co-treatment with aurintricarboxylic acid or actinomycin D. It is suggested that fragment 31–35 of the β-amyloid peptide may be a shorter sequence of β-amyloid peptide responsible for triggering an apoptotic process in cultured neurons.