variable maternal stress, offspring showed increased Bdnf exon IV methylation in the medial prefrontal cortex of males and reduced length of telomeres in both sexes in adulthood (Blaze et al., 2017). Another report found deficits in spatial memory and reduced H3 acetylation in both males and females with a history of prenatal chronic, variable stress (Benoit et al., 2015). However, only stress-exposed females had higher Dnmt1 levels and increased basal corticosterone (Benoit et al., 2015). Mice exposed to predator odor, an ethologically relevant stressor for mice, during the second half of gestation demonstrated an increased corticosterone response and increased avoidance behavior to predator odor exposures in adulthood. This corresponded with increased expression of corticotrophin-releasing factor receptor 1 (Crfr1) in the amygdala and reduced Bdnf expression and methylation in the hippocampus of adult female animals (St-Cyr and McGowan, 2015). It is unclear why these studies have found divergent outcomes regarding sex-specificity while other reports have not found sex differences in the outcomes of stress exposure (Mychasiuk et al., 2011). While the reason underlying the impact of sex on early-life stress is unknown, there are baseline differences in the expression of epigenetic regulators between the sexes (Auger et al., 2011; Nugent et
