2009b; Roth and Sweatt, 2011; Silberman et al., 2016; Tsankova et al., 2007). Common targets of the effects of early-life stress include the prefrontal cortex (Kolb et al., 2017), hippocampus (Fenoglio et al., 2006), amygdala (Cohen et al., 2013), and HPA axis (Essex et al., 2011) (Figure 2). These brain regions are also implicated in cognitive deficits and psychiatric disorders associated with developmental stress (Aihara et al., 2007; Blair, 2008; Drevets et al., 1997; Zierhut et al., 2010). The implications of stress exposure vary as a result of developmental time period during which the stress was incurred (Gee and Casey, 2015; Lupien et al., 2009). Moreover, different forms of early-life stress can elicit different outcomes (Dong et al., 2015; Mychasiuk et al., 2011; Schmidt et al., 2011; St-Cyr and McGowan, 2015). Consequently, the following sections discuss the implications of developmental stress exposure organized by the various models used to study early stress. The same modifications discussed above regarding the effects of developmental alcohol exposure (DNA methylation, histone modifications, and ncRNAs) are described together for each model where appropriate.
