MAIN TEXT
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.