Fig. 5

Effects of IPA-3 (a PAK1 inhibitor) on neuronal PAK1 S204 and NF-κB p65 S276 phosphorylations in WT and PLPP/CIN^Tg mice 2 h after KA injection. Under physiological condition, PLPP/CIN overexpression enhances PAK1 S204 and NF-κB p65 S276 phosphorylation levels. As compared to control animals, KA augments PAK1 S204 and p65 S276 phosphorylations in CA3 neurons in WT mice. PLPP/CIN overexpression further increases them. IPA-3 pretreatment ameliorates KA-induced PAK1 S204 and p65 S276 phosphorylations in both strains. a Representative photos for PAK1 S204 and p65 S276 phosphorylations in CA3 neurons. b, c Quantification of PAK1 S204 and p65 S276 phosphorylations based on immunofluorescent data (*p < 0.05 vs. WT mice, ^#p < 0.05 vs. control animals and ^$p < 0.05 vs. KA-treated animals with Newman-Keuls post-hoc test, n = 7, respectively, n = 7, respectively). d Representative Western blot data of phosphorylations of PAK1 and p65 in the whole hippocampus. (e–f) Quantifications of PAK1 S204 and p65 S276 phosphorylations based on Western blot data (*p < 0.05 vs. WT mice, ^#p < 0.05 vs. control animals and ^$p < 0.05 vs. KA-treated animals with Newman-Keuls post-hoc test, n = 7, respectively). g–h Linear regression analyses between PAK1 S204 and p65 S276 phosphorylation in WT and PLPP/CIN^Tg mice. i Linear regression analysis between PAK1 S204 phosphorylation and the latency of seizure on-set following KA injection. j Linear regression analysis between p65 S276 phosphorylation and the latency of seizure on-set following KA injection