Figure 4

ILK participated in EE-increased neurogenesis by regulating GSK3β activity.

a–c. ILK knockdown decreased the levels of p-s9-GSK3β which could not be rescued by EE exposure. Representative immunoblots are shown in a (full-length blots are presented in Supplementary Figure 5) and the relative densitometric analysis is shown in b,c (n = 4–5 per group, &: significant vector effect; £: significant housing effect; §: significant interaction effect). d,e. Inhibiting GSK3β activity rescued the hippocampal newborn neuron survival impairment induced by ILK knockdown. (d) Representative images showed BrdU⁺NeuN⁺ cells (scale bar, 20 μm). (e) Quantification of BrdU⁺NeuN⁺ cells in DG (n = 5 mice per group, &: significant vector effect; £: significant treatment effect; §: significant interaction effect). f, g. Inhibiting GSK3β activity rescued the newborn neuron survival defect induced by ILK knockdown upon EE stimuli. (f) Representative images showed BrdU⁺NeuN⁺ cells (scale bar, 20 μm). (g) Quantification of BrdU⁺NeuN⁺ cells in DG (n = 4–6 mice per group, **p < 0.01 vs Scramble-EE⁺ veh group; ^##p < 0.01). All values are presented as the mean ± SEM.