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. 2017 Dec 7;32(2):174–190. doi: 10.1177/0269881117743484

Figure 5.

Figure 5.

Phosphorylation of glycogen synthase kinase-3β (GSK-3β) in the cortex and hippocampus of Tc1 mice injected with amyloid-β [25-35] (Aβ25-35) peptide. Wildtype (WT) or Tc1 mice were administered intracerebroventricular (i.c.v.) injections with scrambled peptide (Sc.Aβ) or Aβ25-35 peptide (9 nmol) and sacrificed 10 days after injection. The levels of GSK-3β phosphorylated at tyrosine, 216 ((a) and (b)) and serine-9 ((c) and (d)) total and GSK-3β ((e) and (f)) were assessed by Western blot in the cortical ((a), (c), (e)) and hippocampal ((b), (d), (f)) protein lysates. Typical blots are shown for the cortex (g) and the hippocampus (h). The number of animals per group is indicated below the columns. Two-way analysis of variance (ANOVA): F(1,33)=6.04, p<0.05 for the genotype, F(1,33)=1.88, p>0.05 for the treatment, F(1,33)=2.69, p>0.05 for the interaction in (a); F(1,36)=1.61, p>0.05 for the genotype, F(1,36)=4.61, p<0.05 for the treatment, F(1,36)=2.50, p>0.05 for the interaction in (b); F(1,30)=20.0, p<0.0001 for the treatment, F(1,30)=0.323, p>0.05 for the genotype, F(1,30)=0.566, p>0.05 for the interaction in (c); F(1,36)=0.800, p>0.05 for the genotype F(1,36)=0.414, p>0.05 for the treatment, F(1,36)=1.01, p>0.05 for the interaction in (d); F(1,37)=5.12, p<0.05 for the genotype, F(1,37)=0.622, p>0.05 for the treatment, F(1,37)=0.374, p>0.05 for the interaction in (e); F(1,37)=0.011, p>0.05 for the genotype, F(1,37)=0.679, p>0.05 for the treatment, F(1,37)=0.223, p>0.05 for the interaction in (f); *p<0.05; **p<0.01 vs same genotype Sc.Aβ-treated mice; #p<0.05 vs same treatment WT mice; Bonferroni’s test.