Cytotoxic Effect of β‐Amyloid on a Human Differentiated Neuron Is Not Mediated by Cytoplasmic Ca2+ Accumulation

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Abstract
The effects of synthetic β‐amyloid (Aβ1–42) on cell viability and cellular Ca2+ homeostasis have been studied in the human neuron‐like NT2N cell, which differentiates from a teratocarcinoma cell line, NTera2/C1.D1, by retinoic acid treatment. NT2N viability was measured using morphological criteria and fluorescent live/dead staining and quantified using 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide metabolism. Aβ1–42 dose‐dependently caused NT2N cell death when it was present in the cell culture for 14 days but had no effect on viability when it was present for 4 days. The lowest effective concentration was 4 µM, and the strongest effect was produced by 40 µM. Control NT2N cells produced spontaneous cytosolic Ca2+ oscillations under basal conditions. These oscillations were inhibited dose‐dependently (0.4–40 µM) by Aβ1–42 that was present in the cell culture for 1 or 4 days. Ca2+ wave frequency was decreased from 0.21 ± 0.02 to 0.05 ± 0.02/min, amplitude from 88 ± 8 to 13 ± 4 nM, and average Ca2+ level from 130 ± 8 to 58 ± 3 nM. The Ca2+ responses to 30 mM K+ and 100 µM glutamate were not different between control and Aβ‐treated cells. Thus, the results do not support the hypothesis that cytosolic early Ca2+ accumulation mediates Aβ‐induced NT2N cell death.

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