Early life stress (ELS), in interaction with the genetic make-up, can alter programming of the brain during development [10]. ELS is suggested to interfere with the HPA axis development [11], having been associated with reduced GR expression, negative feedback regulation, and disrupted stress responsivity [12]. ELS, likely through malprogramming of the reward dopaminergic system [13], contributes to vulnerability to alcohol misuse [12, 14, 15]. The interplay between the hypothalamic-pituitary-adrenal (HPA) axis and the mesocorticolimbic and striatal systems is in fact critical for the stress response, emotion processing as well as alcohol seeking and intake [16, 17].
