Memories reach the cortex rapidly: How fast do learning-induced anatomical changes occur in the brain? The traditional view postulates that neocortical memory representations reflect reinstatement processes initiated by the hippocampus and that a genuine physical trace develops only through reactivation over extended periods. Brodt et al. combined functional magnetic resonance imaging (MRI) with diffusion-weighted MRI during an associative declarative learning task to examine experience-dependent structural brain plasticity in human subjects (see the Perspective by Assaf). This plasticity was rapidly induced after learning, persisted for more than 12 hours, drove behavior, and was localized in areas displaying memory-related functional brain activity. These plastic changes in the posterior parietal cortex, and their fast temporal dynamics, challenge traditional views of systems memory consolidation. Science , this issue p. 1045 ; see also p. 994

The anticipation of a future stressor can increase worry and cognitive arousal and has a detrimental effect on sleep. Similarly, experiencing a stressful event directly before sleep increases physiological and cognitive arousal and impairs subsequent sleep. However, the effects of post- vs. pre-sleep stress on sleep and their temporal dynamics have never been directly compared. Here, we examined the effect of an anticipated psychosocial stressor on sleep and arousal in a 90-min daytime nap, in 33 healthy female participants compared to an anticipated within-subject relaxation task. We compared the results to an additional group (n = 34) performing the same tasks directly before sleep. Anticipating stress after sleep reduced slow-wave activity/beta power ratio, slow-wave sleep, sleep spindles, and slow-wave parameters, in particular during late sleep, without a concomitant increase in physiological arousal. In contrast, pre-sleep psychosocial stress deteriorated the same parameters during early sleep with a concomitant increase in physiological arousal. Our results show that presleep cognitions directly affect sleep in temporal proximity to the stressor. While physiological arousal mediates the effects of presleep stress on early sleep, we suggest that effects during late sleep originate from a repeated reactivation of mental concepts associated with the stressful event during sleep.

Our thoughts alter our sleep, but the underlying mechanisms are still unknown. We propose that mental processes are active to a greater or lesser extent during sleep and that this degree of activation affects our sleep depth. We examined this notion by activating the concept of “relaxation” during sleep using relaxation-related words in 50 healthy participants. In support of our hypothesis, playing relaxing words during non-rapid eye movement sleep extended the time spent in slow-wave sleep, increased power in the slow-wave activity band after the word cue, and abolished an asymmetrical sleep depth during the word presentation period. In addition, participants reported a higher sleep quality and elevated subjective alertness. Our results support the notion that the activation of mental concepts during sleep can influence sleep depth. They provide a basis for interventions using targeted activations to promote sleep depth and sleep quality to foster well-being and health.

Re-exposure of newly acquired vocabulary during sleep improves later memory recall in healthy adults. The success of targeted memory reactivation (TMR) during sleep presumably depends on the presence of slow oscillations (i.e., EEG activity at a frequency of about 0.75 Hz). As slow oscillating activity is at its maximum during adolescence, we hypothesized that TMR is even more beneficial at this developmental stage. In the present study, adolescents aged 11 to 13 learnt Dutch vocabulary in the evening and were tested on recall performance the next morning. Half of the words were presented via loudspeakers during post-learning periods of NREM (Non Rapid Eye Movement) sleep in order to stimulate memory reactivation. Unexpectedly, TMR during sleep did not improve memory on the behavioral level in adolescents. On the oscillatory level, successful reactivation during sleep resulted in the characteristic increase in theta power over frontal brain regions, as reported in adults. However, we observed no increase in spindle power during successful reactivation. Possible factors that may explain the lacking effect of TMR in adolescents in this study such as differences in learning abilities and pre-sleep performance levels are discussed.

Purpose: Sleep, in particular slow-wave sleep, is beneficial for memory consolidation. In two recent studies, a hypnotic suggestion to sleep more deeply increased the amount of slow-wave sleep in both a nap and a night design. In spite of these increases in slow-wave sleep, no beneficial effect on declarative memory consolidation was found. As coupling of slow-waves and sleep spindles is assumed to be critical for declarative memory consolidation during sleep, we hypothesized that the missing memory benefit after increased SWS could be related to a decrease in slow-wave/spindle coupling. Participants and Methods: Data from 33 highly hypnotizable subjects were retrieved from a nap (n = 14) and a night (n = 19) study with a similar design and procedure. After an adaptation session, subjects slept in the sleep laboratory for two experimental sessions with polysomnography. Prior to sleep, a paired-associate learning task was conducted. Next, subjects either listened to a hypnotic suggestion to sleep more deeply or to a control text in a randomized order according to a within-subject design. After sleep, subjects performed the recall of the memory task. Here, we conducted a fine-grained analysis of the sleep data on slow-waves, spindles and their coupling. Results: In line with our hypothesis, listening to a hypnosis tape decreased the percentage of spindles coupled to slow-waves. Slow-wave parameters were consistently increased, but sleep spindles remained unaffected by the hypnotic suggestion. Conclusion: Our results suggest that selectively enhancing slow-waves without affecting sleep spindles might not be sufficient to improve memory consolidation during sleep.