2. Studies of sleep deprivation (SD) in rodents
Sleep deprivation has a major impact on the mesolimbic circuitry responsible for reinforcement learning, often resulting in hypersensitivity to reward and cue-induced motivation. SD has been shown to enhance the sensitizing effects of amphetamine (Kameda et al. 2014), increase the drug-primed reinstatement of conditioned place preference for methamphetamine (Karimi-Haghighi and Haghparast 2018), and enhances the acquisition of cocaine self-administration and the rate of responding on a progressive ratio schedule (Puhl et al. 2013). Drug exposure can alter sleep architecture in ways that exacerbate the likelihood of relapse. For example, the fragmentation of REM sleep that is caused by cocaine withdrawal expedites the development of the incubation of cocaine craving (Chen et al. 2015). SD also enhances motivation for food reward, and selectively increase the consumption of sucrose and highly palatable food, but not regular lab chow (Liu et al. 2016; McEown et al. 2016).
Sleep loss is known to cause major impairments in hippocampal-dependent memory, with several studies showing that SD prior to learning prevents the formation of new memories, and SD after learning impair the consolidation of newly formed memories (Kreutzmann et al. 2015). Impairment in the hippocampus and prefrontal cortex may also contribute to reward sensitivity, since SD impairs the type of complex cognitive processes that are mediated by these areas, such as spatial and contextual learning (Hagewoud et al. 2010a; Kreutzmann et al. 2015; McDermott et al. 2003). For example, the ability to withhold an operant response in order to receive a reward is reduced after SD, indicating reduced prefrontal inhibition and an increase in impulsive responding (Kamphuis et al. 2017). In some cases, even when sleep deprivation does not directly impair performance, it can influence the type of learning strategy recruited to perform a task, with the enhanced activity in striatal circuits acting as a compensatory mechanism to preserve performance on reward-related tasks that would normally engage hippocampal learning processes (Hagewoud et al. 2010b; Watts et al. 2012).