Figure 5:

Early life HFrD exposure decreases offspring BLA AMPK expression and upregulation of its activity partially rescues diet induced behavior impairment. Normalized mRNA level (mean ± SD) of AMPK subunits from BLA principal neurons (n = 12 litter per group (3 male/litter) *** p < 0.001 vs control) (a) and AMPK kinase activity as measured by the ratio of phospho-Acetyl-CoA Carboxylase (ACC) determined by immunoblotting (top panel, b) and representative blot (bottom panel, b) (n = 8 litters/group (3 male/litter) *** p < 0.001 vs control). Student t-tests indicate that HFrD decreased both the mRNA expression and the activity of AMPK. Kaplan-Meier survival curves showing the cumulative probability of not reaching criterion of adolescent HFrD adolescent males treated with eGFP or AMPKα_1–312 encoding AAV (HFrD eGFP, ● and HFrD AMPKα_1–312, ● respectively) and control counterparts (control eGFP ●; control AMPKα_1–312 ●) for phase 1 (left panel) and phase 2 (right panel) (c). Multiple comparisons indicate that HFrD AMPKα_1–312 reached criterion in phase 2 significantly faster than HFrD eGFP. The corresponding accuracy data are shown for phase 1 and phase 2 in (d) left and right panels respectively. The error rate during phase 2 training revealed a significant improvement in HFrD AMPKα_1–312 compared with HFrD eGFP (e). Performances in phase 3 as measured by the accuracy of the responses on Go and No-Go trials (f). Multiple comparisons revealed that AMPKα_1–312 encoding AAV does not improved phase 3 performances in No Go trials for the HFrD fed males. Single dots represent individual litters and bars are average mean ± SD of n = 6 litters/group.