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Figure 7. Cell viability assay and Immunofluorescence imaging of cells treated with AßP1–42. AßP-induced cellular toxicity was blocked by Zn2+ and by the removal of extracellular calcium, but not by tachykinin or NMDA antagonist. Fluorescence images of neuronal cells treated with calcein (live cells: left panels A, C, E, G, I, K) and ethidium homodimer 1 (dead cells: right panels B, D, F, H, J, L) after treatment are shown. A, B) Control cells not treated with AßP1–42. C, D) Cells after treatment with 10 µM AßP1–42. E, F) Cells after treatment with AßP1–42 in the absence of extracellular calcium. G, H) Cells after treatment with AßP1–42 in the presence of 50 µM ZnCl2. Zn2+ protected cells from AßP-induced toxicity. I, J) Cells after treatment with AßP1–42 in the in the presence of 20 µM tachykinin (physalemin). K, L) Cells after treatment with AßP1–42 in the presence of 20 µM MK-801. No protection from AßP-induced cellular toxicity was observed for the cells treated with tachykinin or NMDA receptor antagonist. Immunofluorescence labeling: neurons were incubated with 5 µM AßP1–42 for 3 h and immunolabeled with either M) a monoclonal anti-AßP antibody (3D6) or N) normal mouse IgG as a negative control, followed by cy-3-conjugated secondary antibody. O) Neurons not treated with AßP1–42 exhibited none to little auto AßP immunofluorescence.
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were duplicated. The corrected figure appears below (panel K is the same; panel I is new). The authors apologize for the error and extend appreciation to the reader who brought it to light. The authors emphasize that this unintentional mistake does not alter the findings or the conclusions drawn in the original published study. 
