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. 2020 Feb 3;10(6):2832–2848. doi: 10.7150/thno.37119

Figure 2.

Figure 2

PGC-1α protects against the cognitive impairment caused by chronic cerebral hypoperfusion. (A) Top, Western blots for PGC-1α expressions in the hippocampus from WT, PGC-1αf/fand nPGC-1α mice. Bottom, a representative image for the coronal brain section prepared from nPGC-1α mice showed the neuronal expression of IRES-eGFP. (B) The typical swimming paths of sham-operated, WT+BCAS, PGC-1αf/f +BCAS, and nPGC-1α+BCAS mice in the MWM during learning (top) and memory probe tests (bottom). (C) Escape latencies were much longer in WT+BCAS and PGC-1αf/f +BCAS mice than those in the sham mice or nPGC-1α+BCAS mice. *p<0.05 for the comparison between PGC-1αf/f +BCAS and nPGC-1α+BCAS groups; #p<0.05, ##p<0.01 for the comparison between the sham and PGC-1αf/f +BCAS groups; △p<0.05 for the comparison between WT+BCAS and nPGC-1α+BCAS groups, as determined by two-way ANOVA. (D) Mean swimming speed of these 4 groups of mice during spatial training was similar, showing that swim speed may not contribute to the differences in escape latencies. Mean percentage of time spent in target training quadrant (E), and mean number of platform crossings (F) during the probe test. (G) fEPSPs slopes were continuously recorded. (H) Mean fEPSP slope of LTP between 40 min and 60 min after TBS. *p<0.05, **p<0.01, ***p<0.001 as determined by one-way ANOVA. (A, G-H) n = 5 in each group, (B-F) n = 8 in each group.