Night Of Sleep Deprivation Research Articles

Sleep deprivation impairs molecular clearance from the human brain.

It remains an enigma why human beings spend one-third of their life asleep. Experimental data suggest that sleep is required for clearance of waste products from brain metabolism. This has, however, never been verified in humans. The primary aim of the present study was to examine in vivo whether one night of total sleep deprivation affects molecular clearance from the human brain. Secondarily, we examined whether clearance was affected by subsequent sleep. Multiphase MRI with standardized T1 sequences was performed up to 48 h after intrathecal administration of the contrast agent gadobutrol (0.5 ml of 1 mmol/ml), which served as a tracer molecule. Using FreeSurfer software, we quantified tracer enrichment within 85 brain regions as percentage change from baseline of normalized T1 signals. The cerebral tracer enrichment was compared between two cohorts of individuals; one cohort (n = 7) underwent total sleep deprivation from Day 1 to Day 2 (sleep deprivation group) while an age and gender-matched control group (n = 17; sleep group) was allowed free sleep from Day 1 to Day 2. From Day 2 to 3 all individuals were allowed free sleep. The tracer enriched the brains of the two groups similarly. Sleep deprivation was the sole intervention. One night of sleep deprivation impaired clearance of the tracer substance from most brain regions, including the cerebral cortex, white matter and limbic structures, as demonstrated on the morning of Day 2 after intervention (sleep deprivation/sleep). Moreover, the impaired cerebral clearance in the sleep deprivation group was not compensated by subsequent sleep from Day 2 to 3. The present results provide in vivo evidence that one night of total sleep deprivation impairs molecular clearance from the human brain, and that humans do not catch up on lost sleep.

Heart Rate Variability: Influence of Pre-processing Methods in Identifying Single-Night Sleep-Deprived Subjects

Autonomic nervous system (ANS) activity can be non-invasively estimated from the heart rate variability (HRV) signal obtained from the electrocardiogram (ECG). The aim of this work is to find useful parameters that allow to establish the presence of a single night sleep deprivation in healthy subjects. The study included two experimental groups of subjects: Non-sleep-deprived (sleep ≥ 4 h, N = 13) and sleep-deprived (sleep <4 h, N = 10). The RR series extracted from 5 min resting ECG signals were pre-processed using four different algorithms to detect and edit artifacts. The RR series were analyzed in terms of time-domain, frequency-domain and using the Poincare plot, in order to determine differences in HRV indexes across domains and subject groups. Statistical analyses were performed with the Friedman and Mann–Whitney tests, along, with correlation analysis. Pre-processing methods showed a moderate level of agreement. In subjects with 4 h of single-night sleep deprivation, results differed according to the selected method. SD21 index derived from the Poincare plot was the only HRV index showing differences between sleep-deprived and non-deprived subjects.

Effects of Repeated Low-dose Caffeine Ingestion During a Night of Total Sleep Deprivation on Physical Performance and Psychological State in Young Recreational Runners

Background: Caffeine is frequently consumed by athletes to maintain alertness in conditions of sleep loss. However, the effect of caffeine ingestion during total sleep deprivation during aerobic exercise remains questionable. Objectives: The present study aimed to assess the effects of repeated intake of low-dose caffeine during a night of total sleep deprivation on endurance performance and psychological states. Methods: Twelve recreational runners performed four test sessions in a double-blind randomized order after a placebo or 6 mg/kg of caffeine ingestion after a baseline night (BN) or three doses of 2 mg/kg of caffeine during a night of total sleep deprivation (TSD). At each session, they completed an exhaustive run around a 400 m athletics track and performed the Feeling Scale test. ANOVA with repeated measures followed by paired t-tests was used to analyze the data. Results: In comparison with BN, the TSD condition significantly impaired running performance (P &lt; 0.001). On the contrary, caffeine administration improved endurance running performance (P &lt; 0.001) and increased feeling of well-being (P &lt; 0.05) after TSD night as compared to placebo. Conclusions: Repeated ingestion of low-dose caffeine is an effective way to mitigate the negative effects of total sleep deprivation on endurance performance and mood states.

The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment.

Chronic sleep loss is a potent catabolic stressor, increasing the risk of metabolic dysfunction and loss of muscle mass and function. To provide mechanistic insight into these clinical outcomes, we sought to determine if acute sleep deprivation blunts skeletal muscle protein synthesis and promotes a catabolic environment. Healthy young adults (N = 13; seven male, six female) were subjected to one night of total sleep deprivation (DEP) and normal sleep (CON) in a randomized cross‐over design. Anabolic and catabolic hormonal profiles were assessed across the following day. Postprandial muscle protein fractional synthesis rate (FSR) was assessed between 13:00 and 15:00 and gene markers of muscle protein degradation were assessed at 13:00. Acute sleep deprivation reduced muscle protein synthesis by 18% (CON: 0.072 ± 0.015% vs. DEP: 0.059 ± 0.014%·h‐1, p = .040). In addition, sleep deprivation increased plasma cortisol by 21% (p = .030) and decreased plasma testosterone by 24% (p = .029). No difference was found in the markers of protein degradation. A single night of total sleep deprivation is sufficient to induce anabolic resistance and a procatabolic environment. These acute changes may represent mechanistic precursors driving the metabolic dysfunction and body composition changes associated with chronic sleep deprivation.

The effect of one-night sleep deprivation on cognitive functions in healthy young adults.

IntroductionThe effects of acute sleep deprivation on cognitive function have not been clearly elucidated. The purpose of this study was to evaluate changes in cognitive function in healthy adults after one night of sleep deprivation.Material and MethodsTwenty-one healthy young adults (aged 18-30 years) underwent assessment of cognitive functions before and after one night of total sleep deprivation and an age- and gender-matched control group was assessed before and after a normal night sleep. Cognitive functions were assessed using the Montreal cognitive assessment (MOCA) and trail making test (TMT) parts A and B.ResultsGeneral linear model repeated measures demonstrated an insignificant effect for time × group (sleep deprivation) interaction for MOCA, TMT Part A, and TMT Part B scores after one-night sleep deprivation (p>.05 for all).ConclusionA single night of sleep deprivation, which can be inevitable in modern society, had no significant effect on cognitive performance in healthy adults.

Gradually Increased Interhemispheric Functional Connectivity During One Night of Sleep Deprivation.

BackgroundIt is well known that circadian rhythms and sleep homeostasis contribute to a pronounced trough in sleepiness and behavioral performance at night. However, the underlying neuroimaging mechanisms remain unclear. How brain-function connectivity is modulated during sleep deprivation (SD) has been rarely examined.MethodsBy increasing the number of scanning sessions during SD, the current study used voxel-mirrored homotopic connectivity (VMHC) to investigate dynamic changes in interhemispheric communication during one night of SD. Every 2 hours from 10 pm to 06 am (session 1, 10 pm; session 2, 12 am; session 3, 2 am; session 4, 4 am; session 5, 6 am), functional magnetic resonance–imaging data and Stanford Sleepiness Scale (SSS) scores were collected from 36 healthy participants with intermediate chronotype. Dynamic changes in SSS scores and VMHC were determined using one-way repeated-measure ANOVA with the false discovery–rate method to correct for multiple comparisons.ResultsSignificant time effects for VMHC were found mainly in the bilateral thalamus, bilateral superior temporal gyrus, and bilateral precentral gyrus. SSS scores and VMHC in these areas were both found to be monotonously increased during SD. Furthermore, significant positive associations were found between SSS valu and VMHC values in the left superior temporal and right superior gyri.ConclusionThese findings might represent the dynamic modulation of circadian rhythm merely or the interaction effects of both circadian rhythm and sleep homeostasis on interhemispheric connectivity within the thalamus, default-mode network, and sensorimotor network. Our study provides more comprehensive information on how SD regulates brain connectivity between hemispheres and adds new evidence of neuroimaging correlates of increased sleepiness after SD.

Vulnerability in Executive Functions to Sleep Deprivation Is Predicted by Subclinical Attention-Deficit/Hyperactivity Disorder Symptoms

BackgroundSleep loss results in state instability of cognitive functioning. It is not known whether this effect is more expressed when there is an increased cognitive demand. Moreover, while vulnerability to sleep loss varies substantially among individuals, it is not known why some people are more affected than others. We hypothesized that top-down regulation was specifically affected by sleep loss and that subclinical inattention and emotional instability traits, related to attention-deficit/hyperactivity disorder symptoms, predict this vulnerability in executive function and emotion regulation, respectively. MethodsHealthy subjects (ages 17–45 years) rated trait inattention and emotional instability before being randomized to either a night of normal sleep (n = 86) or total sleep deprivation (n = 87). Thereafter, they performed a neutral and emotional computerized Stroop task, involving words and faces. Performance was characterized primarily by cognitive conflict reaction time and reaction time variability (RTV), mirroring conflict cost in top-down regulation. ResultsSleep loss led to increased cognitive conflict RTV. Moreover, a higher level of inattention predicted increased cognitive conflict RTV in the neutral Stroop task after sleep deprivation (r = .30, p = .0055) but not after normal sleep (r = .055, p = .65; interaction effect β = 6.19, p = .065). This association remained after controlling for cognitive conflict reaction time and emotional instability, suggesting domain specificity. Correspondingly, emotional instability predicted cognitive conflict RTV for the emotional Stroop task only after sleep deprivation, although this effect was nonsignificant after correcting for multiple comparisons. ConclusionsOur findings suggest that sleep deprivation affects cognitive conflict variability and that less stable performance in executive functioning may surface after sleep loss in vulnerable individuals characterized by subclinical symptoms of inattention.

Effects of two nights of sleep deprivation on executive function and central and peripheral fatigue during maximal voluntary contraction lasting 60s

PurposeːThe current study aimed at assessing the effect of a trial of two nights of sleep deprivation (SDT) on mood, sleepiness, motivation and cognitive and motor performance. MethodsːThirty-six healthy young and physically active adult men (17 in the control group and 19 in the SDT group) completed a 48-h control or 48-h SDT. For the SDT, participants did not sleep for 48 h. Executive function (attention and inhibitory control) in the Go/No-Go and Stroop tests, mood, sleepiness, motivation, heart rate variability (HRV), motor performance in a hand grip strength test, and 60-s maximal isometric contraction (MVC-60 s) of knee extension were evaluated at 9–11 am on consecutive days 1, 2, and 3. ResultsOne night of sleep deprivation increased sleepiness, decreased mood, motivation and motor endurance but did not affect executive function (as measured in the Stroop and Go/No-Go tests), the MVC for hand and leg knee extensor muscles, and peripheral motor fatigue in the leg MVC-60 s task. However, the central activation ratio (CAR) decreased significantly during the MVC-60 s. The SDT significantly contributed to the decrease in these functions. That is, the SDT reduced executive function (increased reaction time during Go/No-Go test), MVC of knee extension, and the CAR before and after the MVC-60 s. By contrast, the SDT did not increase CAR immediately after the MVC-60 s and did not decrease the rate of torque development (RTD). ConclusionsːThe SDT significantly impaired mood, motivation and increased sleepiness and HRV, reduced MVC of knee extensor muscles (but not RTD) and motor performance during the MVC-60 s and worsened executive function (attention and inhibitory control) only during the Go/No-Go task. However, the SDT did not reduce hand grip strength and CAR immediately after the MVC-60 s of knee extensor muscles.

Optimising sleep and performance during night float: A systematic review of evidence and implications for graduate medical education trainees.

Graduate medical education (GME) training commonly requires residents and fellows to engage in night float shift work. This review aims to assess the effectiveness of interventions for trainees when preparing for, completing, and recovering from working night float shifts. We reviewed all available studies published prior to September 2019 using PubMed, Scopus, CINAHL, the Cochrane library, PsycINFO, and Google Scholar databases. We included all original, primary research articles assessing either non-pharmacological or pharmacological interventions on the chronobiological and physiological effects of night float shift work among GME trainees. Five studies (n=179 patients) met inclusion criteria. Interventions included melatonin in the morning before sleep after night float shifts, napping during night float shifts, modafinil after a night of sleep deprivation, and caffeinated energy drinks after 6 consecutive night float shifts. Melatonin improved one measure of attention. A 2-hr nap was associated with improved speed related to task switching. Modafinil improved performance in tests of cognition. Caffeinated energy drinks led to improvement in select driving performance variables and reaction time. Effect sizes for outcome variables were calculated. Heterogeneity among the studies precluded combining the data in a meta-analysis. According to GRADE criteria, the quality of the evidence in these studies was low or very low. Our findings suggest GME trainees may benefit from utilising a limited number of interventions when preparing for or recovering from night float shift work. More investigation is needed to identify interventions that could help GME trainees adapt to and recover from working night float shifts.

Indices of cortical plasticity after therapeutic sleep deprivation in patients with major depressive disorder

BackgroundTherapeutic sleep deprivation (SD) presents a unique paradigm to study the neurobiology of major depressive disorder (MDD). However, the rapid antidepressant mechanism, which differs from today's slow first-line treatments, is not sufficiently understood. We recently integrated two prominent hypotheses of MDD and sleep, the synaptic plasticity hypothesis of MDD and the synaptic homeostasis hypothesis of sleep-wake regulation, into a synaptic plasticity model of therapeutic SD in MDD. Here, we further tested this model positing that homeostatically elevating net synaptic strength through therapeutic SD shifts the initially deficient inducibility of associative synaptic long-term potentiation (LTP)-like plasticity in patients with MDD into a more favorable window of associative plasticity. MethodsWe used paired associative stimulation (PAS), a transcranial magnetic stimulation protocol (TMS), to quantify cortical LTP-like plasticity after one night of therapeutic sleep deprivation in 28 patients with MDD. ResultsWe demonstrate a significantly different inducibility of associative plasticity in clinical responders to therapeutic SD (> 50% improvement on the 6-item Hamilton-Rating-Scale for Depression, n=13) compared to non-responders (n=15), which was driven by a long-term depression (LTD)-like response in SD-non-responders. Indices of global net synaptic strength (wake EEG theta activity, intracortical inhibition and BDNF serum levels) were increased after SD in both groups, with responders showing a generally lower intracortical inhibition than non-responders. LimitationsRepetitive assessments prior to and after treatment would be needed to further determine potential mechanisms. ConclusionAfter a night of therapeutic SD, clinical responders show a significantly higher inducibility of associative LTP-like plasticity than non-responders.

Alteration of Brain Gray Matter Density After 24 h of Sleep Deprivation in Healthy Adults.

It has been reported that one night of acute sleep deprivation (SD) could induce brain structural changes at the synaptic and neuronal levels in animal studies, and could lead to white matter microstructure and cortical thickness change in human neuroimaging studies. In this study, we focused on changes of brain gray matter density (GMD) after one night of acute SD, which has not been explored previously. Twenty-three normal young participants completed the experiment. Each participant underwent twice T1-weighted structural image scanning with one at 08:00 after normal sleep [resting wakeful (RW)] and the other at 08:00 after 24 h of SD. Using voxel-based morphometry (VBM) analysis by FSL-VBM software, we compared GMD between RW and SD. In addition, the gray matter volume (GMV) and cortical thickness (CT) were also calculated based on volumetric and surface measures with FreeSurfer software. The psychomotor vigilance test (PVT) and the Karolinska Sleepiness Scale (KSS) were performed and evaluated for correlation analysis with GMD, GMV, and CT of the significant regions. Our results showed that the GMD in the right frontal pole (FP), right superior frontal gyrus (SFG), and right middle frontal gyrus significantly increased and GMV and CT in the right temporal pole (TP) significantly decreased after 24 h of acute SD. SD-induced changes in GMD in the right middle frontal gyrus were positively correlated with the changes of KSS scores (Spearman’s correlation r = 0.625, p = 0.0014, Bonferroni correction with p < 0.05/25). Taken together, our findings suggested that one night of acute SD could induce substantial brain structure changes and the alterations in GMD in the right middle frontal gyrus (MFG) might be implicated in sleepiness after SD.

Effects of a 30 min nap opportunity on cognitive and short-duration high-intensity performances and mood states after a partial sleep deprivation night

ABSTRACT This study evaluated the effects of partial-sleep-deprivation (SDN) and a 30 min nap opportunity on physical and cognitive performances and mood states. Fourteen physically active students (BMI = 232.8 ± 0.4 kg/m2) performed the reaction time, the number cancellation (i.e., assessing vigilance) and the 5-m shuttle run tests and responded to the Profile of Mood States (POMS-f) questionnaire at 18h00 after a normal-sleep (NSN) and a SDN) and after two nap conditions (Nap and no-Nap) realized between 13h00 and 13h30. Vigilance and the reaction time were better after Nap compared to no-Nap opportunity following NSN and SDN and during NSN compared to SDN only during no-Nap. Total and peak distance during the 5-m shuttle run test were higher and the fatigue index was lower during Nap compared to no-Nap condition after NSN and SDN and during NSN compared to SDN during Nap and no-Nnap. Anxiety, fatigue, confusion, and depression were lower and vigour was higher during Nap compared to no-Nap after NSN and SDN and during NSN compared to SDN during Nap and no-Nap. In conclusion, a 30-min of nap opportunity helps to overcome the negative effect of SDN on mood states as well as physical and cognitive performances.

Examining the Causal Effects of Sleep Deprivation on Emotion Regulation and Its Neural Mechanisms.

Cognitive reappraisal (CR) is a strategy used to regulate emotions that is thought to be effective but effortful, relying on higher-order cognitive control systems to engage in active regulation. Sleep deprivation is believed to impair the functioning of these control systems, suggesting that it may impede the ability to implement CR effectively. This study tested the causal effects of sleep deprivation on emotional reactivity and the neurobiological systems underlying CR. We employed a within-subject crossover design in which participants underwent fMRI scanning twice, once when fully rested and once after a night of total sleep deprivation. During scans, participants passively viewed or used CR to down-regulate their emotional response to negative and neutral images. Contrary to hypotheses, both self-reported negative affect ratings and neural responses to the images indicated no difference in the way participants implemented CR when sleep deprived and when fully rested. Meanwhile, neural regions that showed distinct reactivity responses to negative relative to neutral images lost this specificity under deprived conditions. Negative affect ratings and heart rate deceleration, a physiological response typically evoked by aversive pictures, exhibited a similar blunting. Together, these results suggest that, although sleep deprivation may reduce the discrimination between emotional reactivity responses to negative and neutral stimuli, it does not impact CR the way it is presently studied.

Sleep in highly automated driving: Takeover performance after waking up

Takeover performance in automated driving is subject to investigation in the context of a variety of driver states such as distraction or drowsiness. New driver states will emerge with increasing automation level with drivers potentially being allowed to sleep while driving a highly automated vehicle. Still at some point during a drive, drivers will be required to or voluntarily take back control of the vehicle. A simulator study was conducted to investigate drivers’ ability to take over the vehicle control after sleeping. In a within-subjects study design N = 25 test drivers completed a drive using a highly automated driving system a) during day time after a full night of sleep and b) early in the morning after a night of partial sleep deprivation. During the second drive, sleep was measured in drivers according to the American Academy of Sleep Medicine (AASM) standard using electroencephalography (EEG). In total, the participants had to handle four takeover requests (TORs) from the system, two while being awake (day drive) and two when being awakened from sleep stage N2 (morning drive). The objective criticality of the situations was assessed performing the Takeover Controllability rating (TOC-rating). The results indicate that the applied takeover time of 60 s was sufficient for drivers to reengage in driving after sleeping. Reaction times were extended by about 3 s after sleep compared to the wake condition. Takeover performance assessed with the TOC-rating however was clearly worse after sleep than after wakefulness which was also reflected in the drivers’ subjective perception of the criticality of the situation. Further research is needed on how to deal with performance impairments after waking up from sleep during automated driving.

Effects of caffeine ingestion on 8-km run performance and cognitive function after 26 hours of sleep deprivation

ABSTRACT The current study aimed to examine the effects of caffeine consumption on physical and cognitive performance after an endurance race following one night of sleep deprivation. Ten recreational runners performed four test sessions in a randomized order at 09:00 h after placebo or 5 mg/kg of caffeine ingestion during a baseline night (BN) (bedtime: from 22:30 h to 07:00 h) or a night of total sleep deprivation (TSD) (26 hours of continuous wakefulness). At each session, they completed an 8-km running competition around a 400 m outdoor athletics track, and they performed the correct detection and the reaction-time tasks. In comparison with BN, performance-time and reaction-time increased, and correct detections decreased after TSD condition. Compared to placebo, caffeine ingestion improved 8-km performance-time by 48 sec (2.8%) after BN and 108 sec (4.9%) after TSD, increased correct detections after BN (p < 0.01) and TSD (p < 0.05), and decreased reaction-time after BN (p < 0.001) and TSD (p < 0.05). Therefore, caffeine is an effective strategy to mitigate the adverse effects of total sleep deprivation on physical and cognitive performance.

Effects of sleep deprivation on arterial vasculature in university students

Abstract Introduction Sleep plays an essential role in the mental, emotional, physical and psychological well-being of an individual and a poor quality of this leads to psychological changes, also affecting the cardiovascular system. The current society demands more and more hours of work, which leads to a decrease in the quantity and quality of sleep, and this has already been associated in several studies with risk factors for cardiovascular diseases such as hypertension, obesity, diabetes, among others, but was never considered a risk factor by its own. Objectives Understand if partial sleep deprivation for 4 nights causes vascular changes in healthy university students. Methodology The sample consisted of 20 healthy university students, who underwent 3 nights in which they slept the ideal for their age group, being evaluated at the end of those nights. At the next night they were subjected to partial sleep deprivation and were evaluated the next day. The third evaluation occurred after 4 nights of partial sleep deprivation. Evaluations consisted in carotid evaluation, flow-mediated dilation (FMD), blood pressure (BP) and temperature monitoring. From the first night, the participants used an actigraphy during the daily routine for 7 nights. An initial questionnaire was completed and also the Epworth Sleepiness Scale (ESE) and the Pittsburgh Sleep Quality Index (PSQI). Results Partial sleep deprivation causes a decrease in the diameter of the right brachial artery and the common carotid artery (CCA). There was also an increase in the SBP of CCA, in pulsatility and endurance indexes and on β-stiffness. With sleep deprivation, sleep efficiency also decreased. Conclusion Sleep deprivation leads to an increase in inflammatory markers that act on the endothelium and end up promoting the existence of cardiovascular events.

Two nights of recovery sleep restores hippocampal connectivity but not episodic memory after total sleep deprivation

Sleep deprivation significantly impairs a range of cognitive and brain function, particularly episodic memory and the underlying hippocampal function. However, it remains controversial whether one or two nights of recovery sleep following sleep deprivation fully restores brain and cognitive function. In this study, we used functional magnetic resonance imaging (fMRI) and examined the effects of two consecutive nights (20-hour time-in-bed) of recovery sleep on resting-state hippocampal connectivity and episodic memory deficits following one night of total sleep deprivation (TSD) in 39 healthy adults in a controlled in-laboratory protocol. TSD significantly reduced memory performance in a scene recognition task, impaired hippocampal connectivity to multiple prefrontal and default mode network regions, and disrupted the relationships between memory performance and hippocampal connectivity. Following TSD, two nights of recovery sleep restored hippocampal connectivity to baseline levels, but did not fully restore memory performance nor its associations with hippocampal connectivity. These findings suggest that more than two nights of recovery sleep are needed to fully restore memory function and hippocampal-memory associations after one night of total sleep loss.

Drosophila as a Model to Study the Relationship Between Sleep, Plasticity, and Memory.

Humans spend nearly a third of their life sleeping, yet, despite decades of research the function of sleep still remains a mystery. Sleep has been linked with various biological systems and functions, including metabolism, immunity, the cardiovascular system, and cognitive functions. Importantly, sleep appears to be present throughout the animal kingdom suggesting that it must provide an evolutionary advantage. Among the many possible functions of sleep, the relationship between sleep, and cognition has received a lot of support. We have all experienced the negative cognitive effects associated with a night of sleep deprivation. These can include increased emotional reactivity, poor judgment, deficit in attention, impairment in learning and memory, and obviously increase in daytime sleepiness. Furthermore, many neurological diseases like Alzheimer’s disease often have a sleep disorder component. In some cases, the sleep disorder can exacerbate the progression of the neurological disease. Thus, it is clear that sleep plays an important role for many brain functions. In particular, sleep has been shown to play a positive role in the consolidation of long-term memory while sleep deprivation negatively impacts learning and memory. Importantly, sleep is a behavior that is adapted to an individual’s need and influenced by many external and internal stimuli. In addition to being an adaptive behavior, sleep can also modulate plasticity in the brain at the level of synaptic connections between neurons and neuronal plasticity influences sleep. Understanding how sleep is modulated by internal and external stimuli and how sleep can modulate memory and plasticity is a key question in neuroscience. In order to address this question, several animal models have been developed. Among them, the fruit fly Drosophila melanogaster with its unparalleled genetics has proved to be extremely valuable. In addition to sleep, Drosophila has been shown to be an excellent model to study many complex behaviors, including learning, and memory. This review describes our current knowledge of the relationship between sleep, plasticity, and memory using the fly model.

0058 Effects of Acute Total Sleep Deprivation on Human Plasma N-glycans

Abstract Introduction There is a need for a novel biomarker that can be used to measure sleep sufficiency as it pertains to fitness for duty. As glycans (polysaccharides) are known to be involved in modifying protein effectiveness, we are exploring these as biomarkers that may be sensitive to differences between sleep deprivation and normal healthy adult sleep duration. We have measured one major class of glycans, called N-glycans, which are covalently linked to asparagine residues of polypeptide chains of membrane-bound and secreted proteins. We compared the plasma N-glycan profiles of participants before and after they participated in a total sleep deprivation protocol. Methods 10 healthy participants (6 male, 4 female) aged 30–44 went through 88 hours of total sleep deprivation. Hourly blood draws were taken via forearm catheter throughout the protocol. N-glycan analysis was performed using plasma samples collected at 17:35 prior to the first night of sleep deprivation and at 17:35 following 82.5 hours of continuous wakefulness. N-glycans were first cleaved from peptides and isolated from plasma, and profiles were then measured using Matrix-Assisted Laser Desorption/Ionization-Time of Flight (MALDI-TOF) mass spectrometry. Results 66 N-glycans were observed in our profiles. Of these, the relative abundance of 17 N-glycans were significantly different following sleep deprivation (paired t-test, 13 with p&amp;lt;0.05, 4 with p&amp;lt;0.01). In each case, the relative abundance was lower in the sleep deprivation time point. We found two structures, Hex6HexNAc5NeuAc3 and Hex7HexNAc6NeuAc2, which were also significant in one of our previous chronic sleep restriction protocols. Conclusion While we observed that many N-glycans decreased in relative abundance, it is unclear whether these changes represent a shift in glycan synthesis or result from decreased expression of the proteins they are bound to. Our next steps involve exploring the functions of the proteins associated with Hex6HexNAc5NeuAc3 and Hex7HexNAc6NeuAc2, and measuring their expression levels. Support NIH/HL75501; NIH/National Center for Research Resources UL1-RR02758 and M01-RR01032 to the Harvard Clinical and Translational Science Center.

0314 Resilience to Inhibitory Deficits During Sleep Deprivation is Predicted by Gray Matter Volume in the Ventrolateral and Ventromedial Prefrontal Cortex

Abstract Introduction Stable, trait-like inter-individual resilience to sleep loss has been demonstrated for psychomotor vigilance, mood, subjective sleepiness, and some reasoning tasks, some of which have been associated with specific genetic or neurobiological markers. Resilience to executive control deficits induced by sleep deprivation (SD) has not been explored in terms of neurobiological markers. We, therefore, collected magnetic resonance imaging (MRI) scans of healthy individuals when well rested and correlated gray matter volume with resistance to inhibitory declines during 29 hours of SD. Methods Forty-five healthy individuals (22 female) ranging in age from 20 to 43 underwent structural MRI. Within 2-4 days after scanning, participants returned to the lab to undergo one night of SD, during which they completed a standard go/no-go task involving inhibitory processing every 4 hours. Scores were calculated as throughput (correct responses per working minute). The difference between performance in the evening (22:45) versus the performance the next morning (06:45) was calculated as an index of “inhibitory resilience.” Gray matter volume was regressed against the inhibitory resilience measure. Based on prior research, regions were constrained to the ventrolateral prefrontal cortex and ventromedial prefrontal cortex. Results Greater resilience against declines in inhibitory capacity during SD was predicted by 1) larger gray matter volume within the ventrolateral prefrontal cortex and 2) reduced volume within the ventromedial prefrontal cortex (p&amp;lt;.05, FWE cluster corrected). These two clusters contributed significant unique explanatory variance to the model (R2=.45, p&amp;lt;.0001). Conclusion The ability to sustain performance during an inhibitory go/no-go task during SD was predicted by greater gray matter volume within the ventrolateral prefrontal cortex, a region that has been previously associated with inhibitory capacity, and reduced volume within an area of the ventromedial prefrontal cortex, which is often related to the default mode network. Findings suggest that specific brain networks may confer task-specific resistance to SD. Support Defense Advanced Research Projects Agency, DARPA Young Faculty Award: DARPA-12-12-11-YFA-FP-029