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).