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. Author manuscript; available in PMC: 2014 Mar 1.
Published in final edited form as: Nat Neurosci. 2013 Aug 11;16(9):1299–1305. doi: 10.1038/nn.3486

Figure 5. LTP impairments in APP/PS1 mice are rescued by decreasing PERK/eIF2α signaling.

Figure 5

(a) LTP was inhibited in APP/PS1 mice (n=6) compared to LTP in WT mice (n=9). LTP was sustained in APP/PS1/PERK cKO mice (n=4) and PERK cKO mice (n=8). (b) Cumulative data showing mean fEPSP slopes 80 min post-HFS from the LTP experiments in panel a. Data were presented as mean +SEM. (c) LTP in APP/PS1/PERK cKO mice (n=7) was inhibited by anisomycin (40 μM). n=8 for WT, n=5 for anisomycin/WT, and n=7 for anisomycin/APP/PS1. Anisomycin was applied into recording chamber 30 min before HFS and present throughout the experiments. (d) Brain Aβ levels were decreased in APP/PS1/PERK cKO mice compared to APP/PS1 mice. n=6 for each group. Levels of full-length APP were not changed. n=9 for APP/PS1/PERK cKO group and n=6 for each of other three groups. (e) β-CTF, but not α-CTF was reduced in the hippocampus of APP/PS1/PERK cKO mice, compared with APP/PS1 mice. n=6. (f) Neprilysin expression was reduced in APP/PS1 mice and was corrected in APP/PS1/PERK cKO mice. n=7 for each group. (g, h) Representative blots (g) and cumulative data of densitometric analysis (h) showing that levels of activity-regulated cytoskeleton-associated protein (Arc, n=5), protein kinase M zeta (PKMζ, n=11), and synaptophysin (n=5) were reduced in hippocampal area CA1 of APP/PS1 mice and was corrected in APP/PS1/PERK cKO mice. Levels of calcium/calmodulin-dependent protein kinase II (CaMKII, n=5) and AMPA receptor subunit GluA1 (n=4) were not significantly altered. *p<0.05; **p<0.01. Full-length blots/gels are presented in Supplementary Figure 7.