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. Author manuscript; available in PMC: 2014 Jul 30.
Published in final edited form as: J Alzheimers Dis. 2014;38(1):49–62. doi: 10.3233/JAD-130740

Fig. 3.

Fig. 3

Picomolar Aβ42 peptides enhance spontaneous astrocyte calcium transients. A) Frequency of spontaneous calcium transients. 200 pM Aβ42 (freshly prepared or aged oligomerized) were applied at the beginning of the second (20 min) imaging block (indicated by arrow). Vehicle n = 16 (4554 cells), fresh Aβ42 200 pM n = 18 (5241 cells), aged Aβ42 200 pM n = 17 (4798 cells). B) Amplitude of spontaneous calcium transients corresponding to A. C) Frequency of spontaneous calcium transients. 200 pM Aβ peptides (freshly prepared, Aβ42, or Aβ40) were applied at the beginning of the second (20 min) imaging block (arrow). Vehicle n = 16 (4554 cells), Aβ42 200 pM n = 18 (5241 cells), Aβ40 200 pM n = 6 (1723 cells). D) Amplitude of spontaneous calcium transients corresponding to C. E) Frequency of spontaneous calcium transients. 200 pM Aβ42 (freshly prepared) and/or 6E10 antibodies were applied at the beginning of the second (20 min) imaging block (arrow). Vehicle n = 16 (4554 cells), Aβ42 200 pM n = 18 (5241 cells), 6E10 n = 4 (1209 cells), Aβ42 200 pM + 6E10 n = 8 (2395 cells). F) Amplitude of spontaneous calcium transients corresponding to E. G) Summary of frequency data at the 30 and 40 min imaging blocks. H) Summary of amplitude data at the 30 and 40 min imaging blocks. Data presented as means ± SEM, normalized as fold changes from the baseline control block. *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001 compared to vehicle control by ANOVA.