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Sleep disturbances can lead to, or exacerbate, a multitude of psychological disorders involving impulse control, behavioral inhibition, and addiction. Even modest sleep deprivation can alter reward-seeking behaviors, and chronic insomnia is linked to an increased risk of alcohol and substance use disorders (Marmorstein 2017; Stein and Friedmann 2006) and obesity (Katsunuma et al. 2017). The causal, mechanistic relationship between sleep and addictive disorders is difficult to study in human clinical populations. This is because a history of drug or alcohol consumption results in long-term alterations in sleep during active use, during withdrawal, and even after years of abstinence (Knapp et al. 2007; Knapp et al. 2014). Therefore, it is difficult to determine whether underlying sleep-related traits contribute to the initial development of substance use disorders, or whether sleep disturbances are the result of past exposure to drugs or alcohol. There are two important questions that are essential for understanding how sleep loss can lead to altered reward processing. First, are there underlying pre-existing differences in sleep characteristics that can predispose some individuals to either the initial development of addictive tendencies or to relapse? Second, are there individual differences in how the consumption of addictive substances, or a state of physical dependence, interacts with neural architecture to cause distinct post-addiction sleep patterns across individuals? The development of an animal model that can address these questions would be a major step toward understanding the impact of sleep quality on reward processing and addiction-related disorders.