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. 2012 Sep;167(2):383–392. doi: 10.1111/j.1476-5381.2012.01973.x

Figure 2.

Figure 2

Inhibition of Aβ aggregation and fibrillogenesis by SEN1269 protects against synthetic Aβ1–42 and 7PA2 CM-induced deficits in LTP in vitro. (A) Scatter plot showing the effect of co-administration of SEN1269 (3 µM) + synthetic Aβ1–42 (n= 4), Aβ1–42 alone (n= 7), vehicle control (n= 4) on the enhancement of fEPSP amplitude evoked by HFS on hippocampal slices. (B) Histograms showing the level of LTP recorded 80–90 min post-HFS. **P < 0.01 compared to control, ††P < 0.01 compared to Aβ1–42, †P < 0.05 compared to Aβ1–42. (C) Typical fEPSPs before and 80 min after HFS for the three treatment groups. Traces shown are the average of 10 sweeps. (D) Scatter plot showing the effect of co-administration of SEN1269 (3 µM) + 7PA2 CM (n= 4), 7PA2 CM alone (n= 4) CHO CM alone (n= 4) on the enhancement of fEPSP amplitude evoked by HFS on hippocampal slices. (E) Histograms showing the level of LTP recorded 80 min post HFS. **P < 0.01 compared to CHO CM, ††P < 0.01 compared to 7PA2 CM, †P < 0.05 compared to 7PA2 CM. (F) Typical fEPSPs before and 80 min after HFS for the three treatment groups. Traces shown are the average of 10 sweeps.