• 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • Although prior research has linked sleep and


    Although prior research has linked sleep and impulsivity in adolescence, little of this work has sought to explain adolescent behavior in terms of naturalistic differences in sleep quality. Instead, the bulk of prior sleep research focuses on experimental sleep restriction or sleep disorders (Beebe, 2011), failing to extrapolate to the realistic patterns of adolescent sleep and the relation to buy EPZ005687 development. A major innovation of this study is the use of naturalistic sleep differences in healthy adolescents, which tells us far more about the individual sleep-related differences in adolescent behavior than experimental manipulations of sleep. Additionally, even less is known about sleep-related differences in neural network functioning. The few neuroimaging studies instead focus on exacerbated mesolimbic-prefrontal developmental imbalances (Telzer et al., 2013), leaving network functioning unexplored. The present study provides a novel perspective regarding the question of adolescent impulsivity and identified intrinsic processes of sleep quality and DMN connectivity as biomarkers of individual differences in behavior. Importantly, DMN connectivity was not affected by sleep duration, which dominates scientific and public health attention (NSF, 2014; Owens et al., 2014). Our data suggest that duration may not be the most informative metric by which to investigate neural development or impulsivity during adolescence. The current study calls for additional research investigating the influence of sleep quality on adolescent neural development as well as the need for more nuanced measures of sleep that better approximate actual sleep experiences of developing youth. The sleep quality component in the present study included micro-awakenings that went undetected by the participants. These disruptions are not captured in self-report measures or measures of duration, but, as these data suggest, they have important implications for neural and behavioral functioning. As research expands to consider sleep quality, micro-awakenings should be explored further. Although we assessed impulsivity in different domains, including trait and state measures, the sleep and connectivity interaction was driven by the Negative Urgency subscale of the UPPS-P impulsivity measure. This subscale is considered to be a representation of affect-driven impulsivity because it is defined as the tendency to act impulsively when distressed or under negative affect. Negative Urgency has been linked to risky sexual behavior (Deckman and DeWall, 2011), smoking in preadolescents, and drug use, drinking, and conduct disorder in young adults (Settles et al., 2012). These are all behaviors that increase during adolescence (Kann et al., 2016). Further, sleep-deprivation research suggests that poor sleep has a strong association with emotional responsivity and as such may be more acutely detectable when evaluating affect-related impulsivity. Although we cannot delineate directionality of our results and it is possible that negative urgency may be leading to poorer sleep quality rather than poor sleep quality leading to altered brain connectivity and behavior, this is a normative and healthy sample of adolescents with no diagnoses of psychopathology or clinical sleep issues. Thus, we interpret our findings to demonstrate that PFC-DMN connectivity may down-regulate affect-related impulsive behavioral proclivities in sleep disrupted teens. Prior work has identified alterations in PFC activation after sleep deprivation in adults (Drummond et al., 2000), such that the PFC exhibited greater activation to cognitive demands after a single night of sleep deprivation compared to normal sleep. These results suggest the brain can dynamically respond to sleep loss with increased cerebral activation to better meet cognitive demands. This type of cortical compensation has been investigated in direct relation to neural activation during cognitive activity. Our results suggest that these mechanisms also act on broader network circuitry and, as such, may provide a more flexible buffer to ongoing environmental stressors like disrupted sleep. Flexible hubs are brain regions such as the DLPFC that quickly shift their functional connectivity patterns to implement cognitive control (Cole et al., 2013). Flexible hubs implement cognitive control by redirecting information flow across large-scale functional networks (Miller and Cohen, 2001). We extended this framework to demonstrate that lateralized prefrontal regions like the DLPFC flexibly modulate DMN activity. Our results indicate that this modulation relates to real-world behavior.