Fig. 5.
Inhibition of PKR restores Aβ1–42–induced LTP impairment in hippocampus. a PKRi treatment rescued the LTP deficit in Aβ1–42-treated slices. Aβ1–42 (500 nM) was treated for 2 h before recording and PKRi (1 μM) was applied for 1 h (30 min before/after LTP induction). Representative traces were shown above. Black, baseline; Green, average between 40 and 50 min after HFS. Vertical bar, 1.0 mV; horizontal bar, 5 ms. b Cumulative data showing the average field excitatory synaptic potential (fEPSP) slope of 50–60 min after LTP induction (2X HFS) (Vehicle, 143.52 ± 5.22%, n = 7 slices from 6 mice; PKRi, 144.48 ± 9.73%, n = 7 slices from 5 mice; Aβ1–42, 118.00 ± 2.99%, n = 12 slices from 8 mice; Aβ1–42 and PKRi, 146.28 ± 9.45%, n = 7 slices from 7 mice; Two-way ANOVA, interaction between Aβ1–42 and PKRi, *p < 0.05, Two-way ANOVA, Bonferroni post-tests, *p < 0.05, **p < 0.01). Bars represent as mean ± SEM