Paul Whitney

Throughout its modern history, sleep research has been concerned with both the benefits of sleep and the deleterious impact of sleep disruption for cognition, behavior, and performance. When more specifically examining the impact of sleep on memory and learning, however, research has overwhelmingly focused on how sleep following learning facilitates memory, with less attention paid to how lack of sleep prior to learning can disrupt subsequent memory. Although this imbalance in research emphasis is being more frequently addressed by current investigators, there is a need for a more organized approach to examining the effect of sleep deprivation before learning. The present review briefly describes the generally accepted approach to analyzing effects of sleep deprivation on subsequent memory and learning by means of its effects on encoding. Then, we suggest an alternative framework with which to understand sleep loss and memory in terms of temporary amnesia from sleep loss (TASL). The review covers the well-characterized properties of amnesia arising from medial temporal lobe lesions and shows how the pattern of preserved and impaired aspects of memory in amnesia may also be appearing during sleep loss. The view of the TASL framework is that amnesia and the amnesia-like deficits observed during sleep deprivation not only affect memory processes but will also be apparent in cognitive processes that rely on those memory processes, such as decision-making. Adoption of the TASL framework encourages movement away from traditional explanations based on narrowly defined domains of memory functioning, such as encoding, and taking instead a more expansive view of how brain structures that support memory, such as the hippocampus, interact with higher structures, such as the prefrontal cortex, to produce complex cognition and behavioral performance, and how this interaction may be compromised by sleep disruption.

Binding information to its context in long-term memory is critical for many tasks, including memory tasks and decision making. Failure to associate information to its context could be an important aspect of sleep deprivation effects on cognition, but little is known about binding problems from being sleep-deprived at the time of encoding. We studied how sleep deprivation affects binding using a well-established paradigm testing the ability to remember auditorily presented words (items) and their speakers (source context). In a laboratory study, 68 healthy young adults were randomly assigned to total sleep deprivation or a well-rested control condition. Participants completed an affective item and source memory task twice: once after 7-hour awake during baseline and again 24 hours later, after nearly 31 hours awake in the total sleep deprivation condition or 7 hours awake in the control condition. Participants listened to negative, positive, and neutral words presented by a male or female speaker and were immediately tested for recognition of the words and their respective speakers. Recognition of items declined during sleep deprivation, but even when items were recognized accurately, recognition of their associated sources also declined. Negative items were less bound with their sources than positive or neutral items, but sleep deprivation did not significantly affect this pattern. Our findings indicate that learning while sleep-deprived disrupts the binding of information to its context independent of item valence. Such binding failures may contribute to sleep deprivation effects on tasks requiring the ability to bind new information together in memory.

Besides degrading vigilant attention, total sleep deprivation (TSD) impairs reversal learning performance and blunts affective reactions to feedback. Whether these effects are downstream consequences of information acquisition failures from degraded vigilant attention, or distinct from degraded vigilant attention, is unclear. In well-rested individuals we simulated information acquisition failures by masking a portion of trial information in a go/no-go reversal learning task with four conditions: stimulus masking, feedback masking, alternating stimulus/feedback masking, and no-masking control. No condition reproduced the previously documented pattern of TSD effects, suggesting that information acquisition failures cannot fully account for impaired reversal learning and blunted affective reactions during TSD.

Total sleep deprivation (TSD) is known to impair sustained attention. However, previously reported effects of TSD on response inhibition are mixed. We administered a "stop-signal" variation of the psychomotor vigilance test, which included 25% of trials requiring withholding of a response to assess response inhibition alongside sustained attention. Participants completed the task at baseline and after 34.5 h of wakefulness. Accuracy was not reduced during TSD. However, response times were significantly slower. A speed/accuracy trade-off allowed participants to effectively withhold responses on inhibition trials and conferred resilience of inhibitory control during TSD under conditions of relatively low time pressure.

Prospective memory pervades our daily lives and failures can have detrimental consequences. This ability to execute delayed intentions may be impacted by stress, yet few studies have examined these effects. Moreover, as many cannabis users report using cannabis to cope with stress, it is important to understand how stress impacts memory in cannabis users.

Sleep deprivation impairs performance on cognitive tasks, but it is unclear which cognitive processes it degrades. We administered a semantic matching task with variable stimulus onset asynchrony (SOA) and both speeded and self-paced trial blocks. The task was administered at the baseline and 24 hours later after 30.8 hours of total sleep deprivation (TSD) or matching well-rested control. After sleep deprivation, the 20% slowest response times (RTs) were significantly increased. However, the semantic encoding time component of the RTs remained at baseline level. Thus, the performance impairment induced by sleep deprivation on this task occurred in cognitive processes downstream of semantic encoding.

Positive mood often facilitates cognitive functions. Facilitation is hypothesized to be due to an increase in dopamine occurring in positive mood states. However, facilitation has not been consistently found in studies of cognitive flexibility. This inconsistent relationship may reflect the numerous ways cognitive flexibility is measured. Moreover, there is evidence that the role of dopamine in cognitive flexibility performance depends on the type of measure used. In the current study, we employed a probabilistic two-card reversal learning task (n = 129) and a Stroop-like task switching procedure (n = 188) in a college student population. We used a standardized set of mood videos to induce a positive, negative, or neutral mood state. Negative mood states were included to account for possible effects of arousal on performance, which is seen in both positive and negative mood inductions. Based on current theories of positive mood and cognition, we hypothesized that there would be differences in the effects of a positive mood induction on cognitive flexibility as assessed by task switching and reversal learning tasks. The mood induction successfully induced high levels of amusement and increased valence in the positive mood group and high levels of repulsion and decreased valence in the negative mood group. However, there were no differences in cognitive flexibility across any of the mood groups, as assessed by switch costs in task switching and correct choices after the reversal in reversal learning. Overall, these findings do not support the hypothesis that positive mood improves cognitive flexibility.