<h2 class="secHeading" id="section_abstract">Abstract</h2><p id="spar0005">The multifaceted concept of impulsivity implies that different impulsivity aspects, mediated by different neural processes, influence behavior at different levels. The nucleus accumbens (NAc) is a key component of the neural processes regulating impulsivity. In this review, we discuss the findings of lesion studies in animals and functional imaging studies in humans focusing on the role of the NAc in impulsivity. Evidence supports that the extent and pattern of involvement of the NAc, and its subregions, the core and the shell, vary among different facets of impulsivity. Data from imaging studies reviewed in this article suggest the involvement of the ventral striatum/NAc in impulsive choice. Findings of animal studies indicate that lesions of the NAc core subregion facilitated impulsivity in tasks involving intertemporal choice, and promoted a risk-averse, less impulsive, tendency in tasks involving options with probability differences. Modification of neurotransmitter activity, especially of dopamine, which is proposed to underlie the changes observed in functional imaging studies, has been shown to influence afferent input pattern in the NAc and the generation of the behavioral output. Parameters of behavioral tasks reflecting response inhibition function are altered by neurochemical interventions and local electrical stimulation in both the core and the shell subregions. <em>In toto</em>, NAc's pattern of neuronal activity, either genetically determined or acquired, has a critical impact on the interindividual variation in the expression of impulsivity. Nevertheless, the NAc is not the only substrate responsible for impulsivity and it is not involved in each facet of impulsivity to the same extent.</p><h4 id="secGabs_N1a48a868N7eacd808">Research highlights</h4><p>? The nucleus accumbens (NAc) is a key component of the neural processes regulating impulsivity. ? The extent and pattern of involvement of the NAc, and its subregions, the core and the shell, vary among different facets of impulsivity. ? There is strong evidence supporting the involvement of the NAc core in impulsive choice, but only limited evidence supports its involvement in response inhibition.</p>

<h2 class="secHeading" id="section_abstract">Abstract</h2><p id="">Most theories of choice assume that decisions derive from an assessment of the future outcomes of various options and alternatives through some type of cost-benefit analyses. The influence of emotions on decision-making is largely ignored. The studies of decision-making in neurological patients who can no longer process emotional information normally suggest that people make judgments not only by evaluating the consequences and their probability of occurring, but also and even sometimes primarily at a gut or emotional level. Lesions of the ventromedial (which includes the orbitofrontal) sector of the prefrontal cortex interfere with the normal processing of &ldquo;somatic&rdquo; or emotional signals, while sparing most basic cognitive functions. Such damage leads to impairments in the decision-making process, which seriously compromise the quality of decisions in daily life. The aim of this paper is to review evidence in support of &ldquo;The Somatic Marker Hypothesis,&rdquo; which provides a systems-level neuroanatomical and cognitive framework for decision-making and suggests that the process of decision-making depends in many important ways on neural substrates that regulate homeostasis, emotion, and feeling. The implications of this theoretical framework for the normal and abnormal development of the orbitofrontal cortex are also discussed.</p>

Early childhood is a period of dramatic change in sleep and emotion processing, as well as a time when disturbance in both domains are first detected. Although sleep is recognized as central in emotion processing and psychopathology, the great majority of experimental data have been collected in adults. We examined the effects of acute sleep restriction (nap deprivation) on toddlers emotion expression. Ten healthy children (seven females; 3036 months old) followed a strict sleep schedule (=12.5 h time in bed per 24-h) for 5 days, before each of two randomly assigned afternoon emotion assessments following Nap and No-Nap conditions (resulting in an 11-day protocol). Children viewed emotion-eliciting pictures (five positive, three neutral, three negative) and completed puzzles (one solvable, one unsolvable). Childrens faces were video-recorded, and emotion displays were coded. When sleep restricted, children displayed less confusion in response to neutral pictures, more negativity to neutral and negative pictures, and less positivity to positive pictures. Sleep restriction also resulted in a 34% reduction in positive emotion responses (solvable puzzle), as well as a 31% increase in negative emotion responses and a 39% decrease in confused responses (unsolvable puzzle). These findings suggest sleep is a key factor in how young children respond to their world. When sleep restricted, toddlers are neither able to take full advantage of positive experiences nor are they as adaptive in challenging contexts. If insufficient sleep consistently taxes young childrens emotion responses, they may not manage emotion regulation challenges effectively, potentially placing them at risk for future emotional/behavioral problems.

The causes of workplace deviance are of increasing interest to organizations. We integrate psychological and neurocognitive perspectives to examine the effects of sleep deprivation on workplace deviance. Utilizing self-regulatory resource theories, we argue that sleep deprivation decreases individuals' self-control while increasing hostility, resulting in increased workplace deviance. We test our hypotheses using two samples: one comprised of nurses from a large medical center and another comprised of undergraduate students participating in a lab study. Results from both samples largely converge in supporting our hypotheses.

Purpose: Over 8,000 American adolescents ages 14-15 years require medical attention owing to pedestrian injury annually. Cognitive factors contributing to pedestrian safety include reaction time, impulsivity, risk taking, attention, and decision making. These characteristics are also influenced by sleep restriction. Experts recommend that adolescents obtain 8.5 hours of unin-terrupted sleep each night, but most American adolescents do not. Inadequate sleep may place adolescents at risk for pedestrian injury.<br/>Methods: Using a within-subjects design, 55 14- and 15-year-olds engaged in a virtual reality pedestrian environment under two conditions, scheduled a week apart: sleep-restricted (4 hours' sleep the previous night) and adequate sleep (8.5 hours). Sleep was assessed using actigraphy and pedestrian behavior via four outcome measures: time to initiate crossing, time before contact with vehicle while crossing, virtual hits or close calls and attention to traffic (looks left and right).<br/>Results: While acutely sleep restricted, adolescents took more time to initiate pedestrian crossings, crossed with less time before contact with vehicles, experienced more virtual hits or close calls, and looked left and right more often compared with when adequately rested. Results were maintained after controlling for age, gender, ethnicity, and average total sleep duration before each condition.<br/>Conclusions: Adolescent pedestrian behavior in the simulated virtual environment was markedly different, and generally more risky, when acutely sleep restricted compared with adequately rested. Inadequate sleep may influence cognitive functioning to the extent that pedestrian safety is jeopardized among adolescents capable of crossing streets safely when rested. Policy decisions might be educated by these results. (C) 2013 Society for Adolescent Health and Medicine. All rights reserved.

<h2 class="secHeading" id="section_abstract">Summary</h2><p id="simple-para0100">Insufficient sleep, poor sleep quality and sleepiness are common problems in children and adolescents being related to learning, memory and school performance. The associations between sleep quality (<em>k</em>&#xA0;=&#xA0;16 studies, <em>N</em>&#xA0;=&#xA0;13,631), sleep duration (<em>k</em>&#xA0;=&#xA0;17 studies, <em>N</em>&#xA0;=&#xA0;15,199), sleepiness (<em>k</em>&#xA0;=&#xA0;17, <em>N</em>&#xA0;=&#xA0;19,530) and school performance were examined in three separate meta-analyses including influential factors (e.g., gender, age, parameter assessment) as moderators. All three sleep variables were significantly but modestly related to school performance. Sleepiness showed the strongest relation to school performance (<em>r</em>&#xA0;=&#xA0;&minus;0.133), followed by sleep quality (<em>r</em>&#xA0;=&#xA0;0.096) and sleep duration (<em>r</em>&#xA0;=&#xA0;0.069). Effect sizes were larger for studies including younger participants which can be explained by dramatic prefrontal cortex changes during (early) adolescence. Concerning the relationship between sleep duration and school performance age effects were even larger in studies that included more boys than in studies that included more girls, demonstrating the importance of differential pubertal development of boys and girls. Longitudinal and experimental studies are recommended in order to gain more insight into the different relationships and to develop programs that can improve school performance by changing individuals' sleep patterns.</p>

Complex dynamic behaviour involves reciprocal influences between emotion and cognition. On the one hand, emotion is a "double-edged sword" that may affect various aspects of our cognition and behaviour, by enhancing or hindering them and exerting both transient and long-term influences. On the other hand, emotion processing is also susceptible to cognitive influences, typically exerted in the form of emotion regulation. Noteworthy, both of these reciprocal influences are subjective to individual differences that may affect the way we perceive, experience, and eventually remember emotional experiences, or respond to emotionally challenging situations. Understanding these relationships is critical, as unbalanced emotion-cognition interactions may lead to devastating effects, such as those observed in mood and anxiety disorders. The present review analyses the reciprocal relationships between emotion and cognition, based on evidence derived from brain imaging investigations focusing on three main topics: (1) the impact of emotion on cognition, (2) the impact of cognition on emotion, and (3) the role of individual differences in emotion-cognition interactions. This evidence will be discussed in the context of identifying aspects that are fundamental to understanding the mechanisms underlying emotion-cognition interactions in healthy functioning, and to understanding changes associated with affective disorders.

Appropriate interpretation of pleasurable, rewarding experiences favors decisions that enhance survival. Conversely, dysfunctional affective brain processing can lead to life-threatening risk behaviors (e. g., addiction) and emotion imbalance (e. g., mood disorders). The state of sleep deprivation continues to be associated with maladaptive emotional regulation, leading to exaggerated neural and behavioral reactivity to negative, aversive experiences. However, such detrimental consequences are paradoxically aligned with the perplexing antidepressant benefit of sleep deprivation, elevating mood in a proportion of patients with major depression. Nevertheless, it remains unknown how sleep loss alters the dynamics of brain and behavioral reactivity to rewarding, positive emotional experiences. Using functional magnetic resonance imaging (fMRI), here we demonstrate that sleep deprivation amplifies reactivity throughout human mesolimbic reward brain networks in response to pleasure-evoking stimuli. In addition, this amplified reactivity was associated with enhanced connectivity in early primary visual processing pathways and extended limbic regions, yet with a reduction in coupling with medial frontal and orbitofrontal regions. These neural changes were accompanied by a biased increase in the number of emotional stimuli judged as pleasant in the sleep-deprived group, the extent of which exclusively correlated with activity in mesolimbic regions. Together, these data support a view that sleep deprivation not only is associated with enhanced reactivity toward negative stimuli, but imposes a bidirectional nature of affective imbalance, associated with amplified reward-relevant reactivity toward pleasure-evoking stimuli also. Such findings may offer a neural foundation on which to consider interactions between sleep loss and emotional reactivity in a variety of clinical mood disorders.

Performance decrements after sleep loss have been extensively studied and are usually attributed to generic attentional deficits. This claim, however, is based on the view of attention as a unitary construct, despite evidence that it should be considered a multidimensional cognitive ability. The aim of the present study was to evaluate the impact of one night of sleep deprivation on the efficiency of three attentional networks, defined by Posner and Raichle (1994) in anatomical and functional terms, as alerting, orienting, and executive control. Thirty participants performed the Attention Network Test at 9:00 a.m. following two different sleep conditions: baseline (a normal night of sleep) and deprivation (24 hrs of wakefulness). Results showed an overall slowing in reaction times and a significant decrease in accuracy after sleep deprivation. Sleep deprivation selectively affected the three attentional networks, given that only executive control efficacy significantly decreased after sleep deprivation. By contrast, phasic alerting and orienting showed no differences in the two sleep conditions. Thus, performance deficits following sleep deprivation do not reflect global attentional deficits.

<h2 class="secHeading" id="section_abstract">Abstract</h2><h4 id="absSec_N44463f70N443704e0">Background</h4><p id="simple-para0020">Sleep loss leads to temporary changes in mood and cognition, and is associated with reduced cerebral metabolism within the prefrontal cortex, similar to findings observed in some psychiatric disorders. However, the extent to which sleep deprivation may be associated with the emergence of clinical symptoms of psychopathology in healthy normal individuals is not clear.</p><h4 id="absSec_N44463f70N44370540">Methods</h4><p id="simple-para0025">The Personality Assessment Inventory (PAI) was administered to 25 healthy adults at rested baseline and again after 56&#xA0;h of continuous wakefulness.</p><h4 id="absSec_N44463f70N443705a0">Results</h4><p id="simple-para0030">Comparisons showed a significant global increase in PAI psychopathology scores from baseline to sleep-deprived sessions, particularly for somatic complaints, anxiety, depression, and paranoia. Mean elevations for the clinical scales remained within normal limits, however. In contrast, sleep loss was not associated with significant changes in anxiety-related disorders, manic symptoms, borderline, schizophrenic, or antisocial features.</p><h4 id="absSec_N44463f70N44370600">Conclusions</h4><p id="simple-para0035">Two nights without sleep may lead to a sub-clinical increase in self-reported affective symptoms of psychopathology while having little effect on symptoms of thought disorder, psychotic processes, or behavioral dysregulation. These data suggest that sleep loss may be differentially disruptive to regions of the brain involved in affective regulation and may, therefore, serve as a model for understanding the brain dysfunction associated with affective psychopathology.</p>

<h2 class="secHeading" id="section_abstract">Abstract</h2><p id="spar0010">To better understand the reward circuitry in human brain, we conducted activation likelihood estimation (ALE) and parametric voxel-based meta-analyses (PVM) on 142 neuroimaging studies that examined brain activation in reward-related tasks in healthy adults. We observed several core brain areas that participated in reward-related decision making, including the nucleus accumbens (NAcc), caudate, putamen, thalamus, orbitofrontal cortex (OFC), bilateral anterior insula, anterior cingulate cortex (ACC) and posterior cingulate cortex (PCC), as well as cognitive control regions in the inferior parietal lobule and prefrontal cortex (PFC). The NAcc was commonly activated by both positive and negative rewards across various stages of reward processing (e.g., anticipation, outcome, and evaluation). In addition, the medial OFC and PCC preferentially responded to positive rewards, whereas the ACC, bilateral anterior insula, and lateral PFC selectively responded to negative rewards. Reward anticipation activated the ACC, bilateral anterior insula, and brain stem, whereas reward outcome more significantly activated the NAcc, medial OFC, and amygdala. Neurobiological theories of reward-related decision making should therefore take distributed and interrelated representations of reward valuation and valence assessment into account.</p><h4 id="secGabs_N1bafdab0N262132e0">Research highlights</h4><p>? We conducted two sets of coordinate-based meta-analyses on 142 fMRI studies of reward. ? The core reward circuitry included the nucleus accumbens, insula, orbitofrontal, cingulate, and frontoparietal regions. ? The nucleus accumbens was activated by both positive and negative rewards across various reward processing stages. ? Other regions showed preferential responses toward positive or negative rewards, or during anticipation or outcome.</p>

<h2 class="secHeading" id="section_abstract">Abstract</h2><p id="sp010">A substantial body of literature supports the intuitive notion that a good night&rsquo;s sleep can facilitate human cognitive performance the next day. Deficits in attention, learning &amp; memory, emotional reactivity, and higher-order cognitive processes, such as executive function and decision making, have all been documented following sleep disruption in humans. Thus, whilst numerous clinical and experimental studies link human sleep disturbance to cognitive deficits, attempts to develop valid and reliable rodent models of these phenomena are fewer, and relatively more recent. This review focuses primarily on the cognitive impairments produced by sleep disruption in rodent models of several human patterns of sleep loss/sleep disturbance. Though not an exclusive list, this review will focus on four specific types of sleep disturbance: total sleep deprivation, experimental sleep fragmentation, selective REM sleep deprivation, and chronic sleep restriction. The use of rodent models can provide greater opportunities to understand the neurobiological changes underlying sleep loss induced cognitive impairments. Thus, this review concludes with a description of recent neurobiological findings concerning the neuroplastic changes and putative brain mechanisms that may underlie the cognitive deficits produced by sleep disturbances.</p><h4 id="secGabs_N2aa38350N1aaf0728">Highlights</h4><p>? Cognitive impairments produced by sleep disruption in rodent models are reviewed. ? Rodent models of four specific types of sleep disturbance are described. ? Sleep disturbance impairs attention, executive function, emotion, learning &amp; memory. ? Sleep disruption alters neuroplasticity. ? The effects of sleep loss on humans and nonhuman animals are compared.</p>

Objective. To examine associations between insufficient sleep (<8 h on average school nights) and health-risk behaviors.<br/>Methods. 2007 national Youth Risk Behavior Survey data of U.S. high school students (n = 12,154) were analyzed. Associations were examined on weighted data using multivariate logistic regression.<br/>Results. Insufficient sleep on an average school night was reported by 68.9% of students. Insufficient sleep was associated with higher odds of current use of cigarettes (age-adjusted odds ratio [AOR], 1.67; 95% confidence interval [CI], 1.45-1.93), marijuana (AOR, 1.52; 95% CI, 1.31-1.76), and alcohol (AOR, 1.64: 95% CI. 1.46-1.84); current sexual activity (AOR, 1.41; 95% CI, 1.25-1.59); seriously considered attempting suicide (AOR, 1.86; 95% CI, 1.60-2.16); feeling sad or hopeless (AOR, 1.62; 95% CI, 1.43-1.84); physical fighting (AOR, 1.40; 95% CI, 1.24-1.60), not being physically active at least 60 min >= 5 days in the past 7 days (AOR. 1.16; 95% CI, 1.04-1.29), using the computer >= 3 h/day (AOR, 1.58; 95% CI, 1.38-1.80), and drinking soda/pop >1 time/day (AOR, 1.14; 95% CI, 1.03-1.28).<br/>Conclusion. Two-thirds of adolescent students reported insufficient sleep, which was associated with many health-risk behaviors. Greater awareness of the impact of sleep insufficiency is vital. Published by Elsevier Inc.

Stress often co-occurs with inadequate sleep duration, and both are believed to impact mood and emotion. It is not yet known whether inadequate sleep simply increases the intensity of subsequent stress responses or interacts with stressors in more complicated ways. To address this issue, we investigated the effects of one night of total sleep deprivation on subjective stress and mood in response to low-stress and high-stress cognitive testing conditions in healthy adult volunteers in two separate experiments (total N = 53). Sleep was manipulated in a controlled, laboratory setting and stressor intensity was manipulated by changing difficulty of cognitive tasks, time pressure, and feedback about performance. Sleep-deprived participants reported greater subjective stress, anxiety, and anger than rested controls following exposure to the low-stressor condition, but not in response to the high-stressor condition, which elevated negative mood and stress about equally for both sleep conditions. These results suggest that sleep deprivation lowers the psychological threshold for the perception of stress from cognitive demands but does not selectively increase the magnitude of negative affect in response to high-stress performance demands.

This study aims to investigate the role of age gender sensation-seeking self esteem and locus of control in predicting low and high-risk-taking behaviors of Turkish adolescents Participants (n = 867) were from three state high schools in Ankara The Risk Involvement Questionnaire (RIQ) Arnett Inventory of Sensation-Seeking (AISS) Rosenberg Self-Esteem Scale (RSES) and Rotter Internal-External Locus of Control Scale (IELOC) were used to collect data Hierarchical multiple regression analyses indicated that except self-esteem all other variables were significantly related to adolescent low-risk behaviors Results also revealed that sensation-seeking age and locus of control explained only 5% of the variance of high-risk behaviors of Turkish adolescents (C) 2010 Elsevier Ltd All rights reserved

Risk-taking behavior involves making choices with uncertain positive or negative outcomes. Evidence suggests that risk-taking behavior is influenced by emotional state. One such emotional experience is social anxiety, which has been related to both risk-avoidant and risk-seeking decision making. The present study examined a community sample of 34 adolescents grouped into low (Low SA Group) and high (High SA Group) social anxiety (SA). Both groups were compared on changes in performance on a risk taking task (Balloon Analogue Risk Task) between a social threat condition (modified Trier Social Stress Test, High Stress) and a control condition (Low Stress). These conditions were administered on different days, and the order was counterbalanced across subjects. A group x condition interaction revealed that the High SA Group showed greater risk-taking behavior when exposed to the High Stress Condition compared to the Low Stress Condition, while the Low SA Group evidenced no difference between the two conditions. Interpretations for the increased risk behavior under the condition of social stress for those high in social anxiety are discussed as well as implications for understanding the complex relationship between social anxiety and risk behavior. (C) 2013 Elsevier Ltd. All rights reserved.

Study Objectives: To assess the stability of the multiple sleep latency test (MSLT) in primary insomnia and its relation to total sleep time.<br/>Design: Randomized, double-blind, placebo controlled, clinical trial.<br/>Setting: Outpatient with sleep laboratory assessments in months 1 and 8 of treatment.<br/>Participants: Ninety-five primary insomniacs, 32-64 years old and 55 age-and sex-matched general population-based, representative controls.<br/>Interventions: After a screening nocturnal polysomnograms (NPSG) and MSLT the following day, participants with primary insomnia were randomized to take zolpidem 10 mg (n = 50) or placebo (n = 45) nightly for 12 months. During months 1 and 8, while taking their prescribed treatments, NPSGs and MSLTs the following day were conducted. A population-based sample served as controls and received a single NPSG followed by MSLT.<br/>Results: Mean daily sleep latency on the screening MSLT of insomniacs was normally distributed across the full range of MSLT scores and significantly higher than those of a population-based representative control sample (P < 0.006). The insomniacs with the highest screening MSLTs had the shortest screening total sleep times (P < 0.05). The MSLTs of insomniacs during treatment in study month 1 were correlated (r = 0.44, P < 0.001) with their month 8 MSLT. The mean MSLT score of the zolpidem group did not differ from that of the placebo group, and the stability within treatment groups also did not differ.<br/>Conclusions: These data support the hypothesis that some insomniacs show a reliable disorder of hyperarousal with increased wake drive both at night and during the day.

In humans, activity patterns in the ventromedial prefrontal cortex (vmPFC) have been found to be predictive of subsequent fear memory consolidation. Pioneering work in rodents has further shown that vmPFC-amygdala theta synchronization is correlated with fear memory consolidation. We aimed to evaluate whether vmPFC activity during fear conditioning is (1) correlated with fear expression the subsequent day and whether (2) this relationship is mediated by rapid eye movement (REM) sleep. We analyzed data from 17 young healthy subjects undergoing a fear conditioning task, followed by a fear extinction task 24 h later, both recorded with simultaneous skin conductance response (SCR) and functional magnetic resonance imaging measurements, with a polysomnographically recorded night sleep in between. Our results showed a correlation between vmPFC activity during fear conditioning and subsequent REM sleep amount, as well as between REM sleep amount and SCR to the conditioned stimulus 24 h later. Moreover, we observed a significant correlation between vmPFC activity during fear conditioning and SCR responses during extinction, which was no longer significant after controlling for REM sleep amount. vmPFC activity during fear conditioning was further correlated with sleep latency. Interestingly, hippocampus activity during fear conditioning was correlated with stage 2 and stage 4 sleep amount. Our results provide preliminary evidence that the relationship between REM sleep and fear conditioning and extinction observed in rodents can be modeled in healthy human subjects, highlighting an interrelated set of potentially relevant trait markers.

Sleep problems often co-occur with psychopathological conditions and affective dysregulation. Individuals with mood disorders have significantly higher rates of sleep disturbances than healthy individuals, and among those with mood disorders, sleep problems are associated with lower rates of remission and response to treatment. Sleep disruption may itself be a risk factor for various forms of psychopathology, as experimental sleep deprivation has been found to lead to increased affective, cognitive, and somatic symptoms within healthy volunteers. However, little is known about the relationship between recurring sleep complaints in a naturalistic environment and symptoms of psychopathology among healthy individuals. In the present study, 49 healthy adults (21 males and 28 females) reported sleep quality and completed the Personality Assessment Inventory, a standardized self-report assessment of symptoms of psychopathology. Consistent with prior published findings during total sleep deprivation, individuals endorsing self-reported naturally occurring sleep problems showed higher scores on scales measuring somatic complaints, anxiety, and depression. Furthermore, the reported frequency of sleep disturbance was closely linked with the severity of self-reported symptoms. While causal directionality cannot be inferred, these findings support the notion that sleep and emotional functioning are closely linked.

Employees are getting less sleep, which has been shown to deplete self-regulatory resources and increase unethical behavior (Barnes, Schaubroeck, Huth, & Ghumman, 2011; Christian & Ellis, 2011). In this study, we extend the original mediated model by examining the role of 2 moderators in the relationship between sleep deprivation, depletion, and deceptive behavior. First, we derive psychological arguments from the psychopharmacology literature to hypothesize that caffeine moderates the relationship between sleep deprivation and depletion by replenishing self-regulatory resources. Second, we draw from recent research in social psychology to hypothesize that social influence moderates the relationship between depletion and deceptive behavior, such that depleted individuals are less able to resist the negative influence of others. Results of a laboratory study provide support for our expanded model combining mediation and moderation, adding to our understanding of the role of sleep deprivation in the incidence of workplace deception.

Experience-dependent plasticity, the ability of the brain to constantly adapt to an ever-changing environment, has been suggested to be highest during childhood and to decline thereafter. However, empirical evidence for this is rather scarce. Slow-wave activity (SWA; EEG activity of 1-4.5 Hz) during deep sleep can be used as a marker of experience-dependent plasticity. For example, performing a visuomotor adaptation task in adults increased SWA during subsequent sleep over a locally restricted region of the right parietal cortex, which is known to be involved in visuomotor adaptation. Here, we investigated whether local experience-dependent changes in SWA vary as a function of brain maturation. Three age groups (children, adolescents, and adults) participated in a high-density EEG study with two conditions (baseline and adaptation) of a visuomotor learning task. Compared with the baseline condition, sleep SWA was increased after visuomotor adaptation in a cluster of eight electrodes over the right parietal cortex. The local boost in SWA was highest in children. Baseline SWA in the parietal cluster and right parietal gray matter volume, which both indicate region-specific maturation, were significantly correlated with the local increase in SWA. Our findings indicate that processes of brain maturation favor experience-dependent plasticity and determine how sensitive a specific brain region is for learning experiences. Moreover, our data confirm that SWA is a highly sensitive tool to map maturational differences in experience-dependent plasticity.