Skip to main content
. 2015 Jul 21;5:10256. doi: 10.1038/srep10256

Figure 2. Blockage of α7nAChR could not abolish the prevention of Aβ1-42 oligomers-induced inhibition of LTP by bis(heptyl)-cognitin.

Figure 2

(A-D) MLA and KT5720 block the enhancement of HFS-induced LTP, but not the prevention of Aβ1-42 oligomers-induced inhibition of LTP by bis(heptyl)-cognitin. Bis(heptyl)-cognitin, tacrine and kinase inhibitors were perfused over the slices for 60 min prior to HFS. After 15 min, Aβ1-42 oligomers were perfused. (E) α7nAChR mediates the enhancement of HFS-induced LTP caused by either bis(heptyl)-cognitin or tacrine. (F) Blockage of α7nAChR could not abolish the prevention of Aβ1-42 oligomers-induced inhibition of LTP by bis(heptyl)-cognitin. Data represent means ± SEM (n = 5). *p < 0.05 vs. vehicle; ##p < 0.01 or &&p < 0.01 vs. bis(heptyl)-cognitin or tacrine group, respectively in (E); **p < 0.01 vs. Aβ1-42 oligomers group; &&p < 0.01 vs. tacrine plus Aβ1-42 oligomers groups in (F) (ANOVA and Tukey’s test).