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. 2014 Jun 18;34(9):1531–1539. doi: 10.1038/jcbfm.2014.113

Figure 7.

Figure 7

Effect of necrostatin-1 and Akt (protein kinase B)/mammalian target of rapamycin (mTOR) inhibitor treatment on cognitive outcome after closed head injury (CHI). (A) In sham-injured mice (n=8/group), all groups demonstrated improvement over time (P<0.001 for time); however, there was no effect of group (necrostatin-1 (Nec-1, 4 mM), Nec-1 plus rapamycin (Rapa, 12.5 μmol/L), Nec-1 plus Akt viii, or vehicle (VEH)) on performance in hidden (P=0.9 repeated-measures ANOVA (RM ANOVA)) or visible platform (P=0.7 RM ANOVA) or (B) probe trials (P=0.97 ANOVA). (C) In closed head injury (CHI) mice (n=8–13/group), all groups improved their performance (P<0.001 for time), but no differences were observed among groups in hidden (P=0.17 for group, RM ANOVA) or visible (P=0.88 for group, RM ANOVA) platform trials. (D) Regarding probe trials, ANOVA revealed a highly significant difference among the four groups (P<0.0001). In post hoc analyses, probe trial latencies were significantly lower in vehicle-treated, Nec-1/Akt viii, and Nec-1/Rapamycin co-treatment groups compared with Nec-1 treatment (*P<0.001 for each comparison with Nec-1, Sidak's multiple comparison test). No differences were observed between Veh, Nec-1/Akt, and Nec-1/Rap groups.