Experimental animal studies can provide insight into the molecular mechanisms underlying the impact of ELS on brain function and behavior [11, 22]; translational approaches can corroborate them. Similarly, to the human population-based sample, outbred rats were investigated. Episodic voluntary drinking was used to simulate human habitual drinking [29], therefore possessing high face validity. A consumption pattern with repeated drinking days and non-drinking days in-between is also known to associate with neurobiological changes similar to those seen in the transition from habitual to compulsive drinking [72]. Construct validity, as underlying biology, and predictive validity, as response to alcohol, are also likely to replicate human phenotypic endpoints. Despite differences in the environment (e.g., social stimuli), these characteristics support the translational interpretation of molecular underpinnings of individual variations in vulnerability to alcohol misuse.
