Figure 5

The role of Dnmt1 in fetal alocohol exposure (FAE)-induced deficits. (a) Hippocampal Dnmt1 expression was affected by FAE and alleviated by neonatal treatments (N=7–20 per prenatal diet/neonatal treatment, sex combined). (b) Treatment-specific changes in adult hippocampal Ctcf expression (sex combined T4: N=9–10 per prenatal diet/neonatal treatment; metformin: N=7–13 per prenatal diet/neonatal treatment). Data are normalized to vehicle control animals. (c–h) Administration of Dnmt1 inhibitor 5-aza-2′-deoxycytidine (5-Aza, 1 μg g−1 per day, from postnatal day 1 to 10) to control neonates mimicked the effects of FAE in fear memory deficit and hippocampal gene expression changes in the adult offspring. N=13–14 per neonatal treatment, sex combined, except (f) N=4–5 males per neonatal treatment. Details are as described in Figure 1. **P<0.01 between treatment groups.