Sleep Deprivation Condition Research Articles

Vestibular control of standing balance following 24h of sleep deprivation.

Sleep deprivation alters cognitive and sensorimotor function, but its effects on the control of standing balance are inconclusive. The vestibular system is critical for standing balance, and is modified by sleep deprivation; however, how sleep deprivation affects vestibular-evoked balance responses is unknown. Thus, this study aimed to examine the effect of 24h of sleep deprivation on the vestibular control of standing balance. During both a well-rested (i.e., control) and sleep deprivation condition, nine females completed two 90-s trials of bilateral, binaural stochastic electrical vestibular stimulation (EVS) and two 120-s trials of quiet stance on a force plate. Quiet stance performance was assessed by center of pressure displacement parameters. Mediolateral ground reaction force (ML force) and surface electromyography (EMG) of the right medial gastrocnemius (MG) were sampled simultaneously with the EVS signal to quantify vestibular control of balance within the frequency (gain and coherence) and time (cumulant density) domains. Twenty-four hours of sleep deprivation did not affect quiet stance performance. Sleep deprivation also had limited effect on EVS-MG EMG and EVS-ML Force coherence (less than control at 8-10.5Hz, greater at ~ 16Hz); however, gain of EVS-MG EMG (< 8, 11-24Hz) and EVS-ML force (0.5-9Hz) was greater for sleep deprivation than control. Sleep deprivation did not alter peak-to-peak amplitude of EVS-MG EMG (p = 0.51) or EVS-ML force (p = 0.06) cumulant density function responses. Despite no effect on quiet stance parameters, the observed increase in vestibular-evoked balance response gain suggests 24-h sleep deprivation may lead to greater sensitivity of the central nervous system when transforming vestibular-driven signals for standing balance control.

Sleep Deprivation Triggers the Excessive Activation of Ovarian Primordial Follicles via β2 Adrenergic Receptor Signaling.

Sleep deprivation (SD) is observed to adversely affect the reproductive health of women. However, its precise physiological mechanisms remain largely elusive. In this study, using a mouse model of SD, it is demonstrated that SD induces the depletion of ovarian primordial follicles, a phenomenon not attributed to immune-mediated attacks or sympathetic nervous system activation. Rather, the excessive secretion of stress hormones, namely norepinephrine (NE) and epinephrine (E), by overactive adrenal glands, has emerged as a key mediator. The communication pathway mediated by the KIT ligand (KITL)-KIT between granulosa cells and oocytes plays a pivotal role in primordial follicle activation. SD heightened the levels of NE/E that stimulates the activation of the KITL-KIT/PI3K and mTOR signaling cascade in an β2 adrenergic receptor (ADRB2)-dependent manner, thereby promoting primordial follicle activation and consequent primordial follicle loss in vivo. In vitro experiments further corroborate these observations, revealing that ADRB2 upregulates KITL expression in granulosa cells via the activation of the downstream cAMP/PKA pathway. Together, these results reveal the significant involvement of ADRB2 signaling in the depletion of ovarian primordial follicles under sleep-deprived conditions. Additionally, ADRB2 antagonists are proposed for the treatment or prevention of excessive activation of primordial follicles induced by SD.

How to quantify sleepiness during an attempt to sleep?

Background. Sleepiness assessment tools were mostly developed for detection of an elevated sleepiness level in the condition of sleep deprivation and several medical conditions. However, sleepiness occurs in various other conditions including the transition from wakefulness to sleep during an everyday attempt to get sleep.Objective. We examined whether objective sleepiness indexes can be implicated in detection of fluctuations in sleepiness level during the polysomnographically-monitored attempt to sleep, i.e. in the absence of self-reports on perceived sleepiness level throughout such an attempt.Approach. The polysomnographic signals were recorded in the afternoon throughout 106 90 min napping attempts of 53 university students (28 females). To calculate two objective sleepiness indexes, the electroencephalographic (EEG) spectra were averaged on 30 s epochs of each record, assigned to one of 5 sleep-wake stages, and scored using either the frequency weighting curve for sleepiness substate of wake state or loadings of each frequency on the 2nd principal component of variation in the EEG spectrum (either sleepiness score or PC2 score, respectively).Main results. We showed that statistically significant fluctuations in these two objective sleepiness indexes during epochs assigned to wake stage can be described in terms of the changes in verbally anchored levels of subjective sleepiness assessed by scoring on the 9-step Karolinska Sleepiness Scale.Significance. The results afford new opportunities to elaborate importance of intermediate substates between wake and sleep states for sleep-wake dynamics in healthy individuals and patients with disturbed sleep.

Tracking Vigilance Fluctuations in Real-Time: A Sliding-Window HRV-based Machine-Learning Approach.

Heart rate variability (HRV)-based machine learning models hold promise for real-world vigilance evaluation, yet their real-time applicability is limited by lengthy feature extraction times and reliance on subjective benchmarks. This study aimed to improve the objectivity and efficiency of HRV-based vigilance evaluation by associating HRV and behavior metrics through a sliding-window approach. Forty-four healthy adults underwent psychomotor vigilance tasks under both well-rested and sleep-deprived conditions, with simultaneous electrocardiogram recording. A sliding-window approach (30s length, 10s step) was used for HRV feature extraction and behavior assessment. Repeated-measures ANOVA was used to examine how HRV related to objective vigilance levels. Stability selection technique was applied for feature selection, and the vigilance ground truth-high (fastest 40%), intermediate (middle 20%), and low (slowest 40%)-were determined based on each participant's range of performance. Four machine-learning classifiers-k-nearest neighbours, support vector machine (SVM), AdaBoost, and random forest-were trained and tested using cross-validation. Fluctuated vigilance performance indicated pronounced state instability, particularly after sleep deprivation. Temporary decrements in performance were associated with a decrease in heart rate and an increase in time-domain heart rate variability. SVM achieved the best performance, with a cross-validated accuracy of 89% for binary classification of high versus low vigilance epochs. Overall accuracy dropped to 72% for three-class classification in leave-one-participant-out cross-validation, but SVM maintained a precision of 84% in identifying low-vigilance epochs. Sliding-window-based HRV metrics would effectively capture the fluctuations in vigilance during task execution, enabling more timely and accurate detection of performance decrement.

Prolonged Sleep Deprivation Induces a Reprogramming of Circadian Rhythmicity with the Hepatic Metabolic Transcriptomic Profile.

Sleep disturbances can disrupt the overall circadian rhythm. However, the impact of sleep deprivation on the circadian rhythm of the liver and its underlying mechanisms still requires further exploration. In this study, we subjected male mice to 5 days of sleep deprivation and performed liver transcriptome sequencing analysis at various time points within a 24-h period. Subsequently, we monitored the autonomic activity and food intake in these male mice for six days post-sleep deprivation. We observed alterations in sleep-wake and feeding rhythms in the first two days following sleep deprivation. Additionally, we also observed a decrease in 24-h serum-glucose levels. Liver transcriptome sequencing has shown that sleep deprivation induces the rhythmic transcription of a large number of genes, or alters the rhythmic properties of genes, which were then significantly enriched in the carbohydrate, lipid, and protein metabolism pathways. Our findings suggest that under conditions of prolonged sleep deprivation, the expression of metabolic-related genes in the liver was reset, leading to changes in the organism's metabolic state to ensure energy supply to sustain prolonged wakefulness.

Visual light flicker stimulation: enhancing alertness in sleep-deprived rats.

In the evolving field of neurophysiological research, visual light flicker stimulation is recognized as a promising non-invasive intervention for cognitive enhancement, particularly in sleep-deprived conditions. This study explored the effects of specific flicker frequencies (40 Hz and 20-30 Hz random flicker) on alertness recovery in sleep-deprived rats. We employed a multidisciplinary approach that included behavioral assessments with the Y-maze, in vivo electrophysiological recordings, and molecular analyses such as c-FOS immunohistochemistry and hormone level measurements. Both 40 Hz and 20-30 Hz flicker significantly enhanced behavioral performance in the Y-maze test, suggesting an improvement in alertness. Neurophysiological data indicated activation of neural circuits in key brain areas like the thalamus and hippocampus. Additionally, flicker exposure normalized cortisol and serotonin levels, essential for stress response and mood regulation. Notably, increased c-FOS expression in brain regions related to alertness and cognitive functions suggested heightened neural activity. These findings underscore the potential of light flicker stimulation not only to mitigate the effects of sleep deprivation but also to enhance cognitive functions. The results pave the way for future translational research into light-based therapies in human subjects, with possible implications for occupational health and cognitive ergonomics.

Effect of creatine supplementation on cognitive function and mood

Background: Creatine, a naturally occurring compound plays a crucial role in cellular energy metabolism, particularly in tissues with high energy demands like muscles and the brain. Beyond its well-established role in physical performance enhancement, recent research has revealed its potential benefits for cognitive functions and mood regulation. This review paper aims to comprehensively analyze the existing literature on creatine supplementation's effects on cognitive functions and mood. State of Knowledge: Findings suggest that creatine supplementation enhances memory, attention, and executive functions, especially under conditions of stress or sleep deprivation. Moreover, it exhibits mood-stabilizing effects, potentially offering relief for symptoms of depression and fatigue. Creatine's ability to augment brain energy metabolism, alongside its neuroprotective properties, underlies its cognitive and mood-enhancing effects. While generally safe, caution is advised, particularly in populations with kidney diseases or those using medications affecting kidney function. Summary: Creatine emerges as a promising adjunct therapy for enhancing cognitive functions and promoting emotional well-being beyond its traditional role in physical performance.The review underscores the need for further research to elucidate the precise mechanisms of creatine's effects and explore its synergistic potential with other cognitive-enhancing supplements.

Effects of sleep deprivation on food-related Pavlovian-instrumental transfer: a randomized crossover experiment.

Recent research suggests that insufficient sleep elevates the risk of obesity. Although the mechanisms underlying the relationship between insufficient sleep and obesity are not fully understood, preliminary evidence suggests that insufficient sleep may intensify habitual control of behavior, leading to greater cue-elicited food-seeking behavior that is insensitive to satiation. The present study tested this hypothesis using a within-individual, randomized, crossover experiment. Ninety-six adults underwent a one-night normal sleep duration (NSD) condition and a one-night total sleep deprivation (TSD) condition. They also completed the Pavlovian-instrumental transfer paradigm in which their instrumental responses for food in the presence and absence of conditioned cues were recorded. The sleep × cue × satiation interaction was significant, indicating that the enhancing effect of conditioned cues on food-seeking responses significantly differed across sleep × satiation conditions. However, this effect was observed in NSD but not TSD, and it disappeared after satiation. This finding contradicted the hypothesis but aligned with previous literature on the effect of sleep disruption on appetitive conditioning in animals-sleep disruption following learning impaired the expression of appetitive behavior. The present finding is the first evidence for the role of sleep in Pavlovian-instrumental transfer effects. Future research is needed to further disentangle how sleep influences motivational mechanisms underlying eating.

Room Steering Temperature Determination with Variable Concerned of Driver Conditions Who are Sleep Deprived and Road Condition

Among the main reasons for the high death rate worldwide are traffic accidents. The most common cause of road accidents is driver fatigue. Not getting enough sleep is one thing that makes people tired. A study on how sleep-deprived sleep-deprived drivers felt about themselves was conducted, and the results showed that they were tired. A potential preventive measure against the driver's extreme weariness is the room steering temperature. The goal of this research is to find the room temperature range that produces the most minor drowsiness is this research's goal. The research used six treatments in a 40-minute driving simulator: hot, cold, pleasant room temperature steering, and monotonous and non-monotonous road conditions. With the Electroencephalogram, one may measure one's state of sleepiness by monitoring brain wave activity. Six treatments were administered to each of the study's four young adult male participants. Teta, alpha, and beta wave powers are derived by processing data from brain wave activity using Matlab R2009A. An ANOVA test is used to discover which factors affect the degree of drowsiness by using the ratio of sleepiness level, which is determined using the equation (θ + α) /β. ANOVA test results indicated that while road conditions and room steering temperature impacted sleepiness, their interaction had no effect. Just the hot-cold level is found to be significantly different by the Tukey and Newman Keuls tests. For sleep-deprived drivers, the temperature differences between hot and cold conditions result in varying drowsiness. The research's practical conclusion is that, for sleep-deprived drivers, a hot temperature range (&gt;26°C–29°C) can result in the lowest level of tiredness.

The dynamics of neurobehavioral impairment and recovery sleep: improved biomathematical modeling for fatigue risk management in operational settings

Adequate sleep is essential for maintaining health, safety, and neurobehavioral functioning in 24/7 operational settings. Loss of sleep causes fatigue, which results in neurobehavioral impairment. Neurobehavioral impairment builds up disproportionately under conditions of total sleep deprivation compared to sustained sleep restriction; and recuperation due to recovery sleep is disproportionately fast after total sleep deprivation compared to sustained sleep restriction. These sleep schedule-dependent dynamics have been captured in a previously published, biomathematical model of fatigue, which includes positive feedback regulation of a relatively fast (hours to days) sleep/wake homeostatic process by a slower (days to weeks) allostatic process—a feature that suggests adenosinergic mechanisms are involved. However, the previously published model underestimates the rate of recuperation due to recovery sleep after acute total sleep deprivation as well as after consecutive days of sleep restriction. The objective of the present research is to modify the model to improve the accuracy of its predictions for recuperation due to recovery sleep. This can be accomplished by including in the model an additional, reciprocal feedback mechanism, presumed to be predominantly adenosinergic in nature, which provides feedback from the faster homeostatic process back onto the slower allostatic process. Adding a single new model parameter and refitting three existing model parameters significantly improves the predictions for recuperation due to recovery sleep after both acute total sleep deprivation and sustained sleep restriction. This model modification also improves the predictions of the build-up of neurobehavioral impairment across days of sustained sleep restriction, without adversely affecting the accuracy of the model in other scenarios including circadian misalignment and sleep inertia. The modified model preserves the previously developed capability to predict the differential dynamics of fatigue for objective performance impairment and subjective sleepiness. With the improved predictions for recuperation due to recovery sleep, the expanded model can be used to provide quantitative estimates for potentially impactful work scheduling decisions, such as the duration of time off needed before workers would be safe to return to the work floor. This enhances the usefulness of the model as a tool for predicting and managing neurobehavioral functioning and safety in 24/7 operational settings.

Interactions between neurotrophins, mood, and physical activity under the conditions of sleep deprivation

Sleep deprivation (DS) is the forced elimination of sleep. While brain-derived neurotrophic factor (BDNF) has been extensively studied in the context of in mood changes following DS, the role of other neurotrophins remains elusive. This study explores the impact of DS on BDNF, glial cell line-derived neurotrophic factor (GDNF), neurotrophin-3 (NT3), and neurotrophin-4 (NT4) at mRNA and protein level, considering their potential links to mood disturbances. The study involved 81 participants subjected to polysomnography (PSG) and DS. Blood samples, mood assessments, and actigraphy data were collected twice, after PSG and DS. NT mRNA expression and serum protein concentrations of BDNF, GDNF, NT3, and NT4 were measured. Participants were divided into Responders and Non-Responders based on mood improvement after DS. DS reduced BDNF mRNA expression in all participants, with no change in serum BDNF protein. GDNF protein decreased in Non-Responders, while Responders exhibited reduced GDNF mRNA. NT3 protein increased in both groups, while NT3 mRNA decreased in Respondents. NT4 protein rose universally post-DS, but NT4 mRNA remained unchanged. Physical activity (PA) negatively correlated with mRNA expression of BDNF, GDNF, and NT3 post-DS. The study’s short DS duration and exclusion of immature NT forms limit comprehensive insights. GDNF, together with NT3, might play an important role in mood response to DS. PA during DS seems to impair the mRNA expression of NTs in leukocytes. Future studies on the subject of sleep deprivation might consider investigating the relationship between BDNF and NT4 in the context of their apparent redundancy.

Exploring the therapeutic potential of cannabidiol for sleep deprivation-induced hyperalgesia

Hyperalgesia resulting from sleep deprivation (SD) poses a significant a global public health challenge with limited treatment options. The nucleus accumbens (NAc) plays a crucial role in the modulation of pain and sleep, with its activity regulated by two distinct types of medium spiny neurons (MSNs) expressing dopamine 1 or dopamine 2 (D1-or D2) receptors (referred to as D1-MSNs and D2-MSNs, respectively). However, the specific involvement of the NAc in SD-induced hyperalgesia remains uncertain. Cannabidiol (CBD), a nonpsychoactive phytocannabinoid, has demonstrated analgesic effects in clinical and preclinical studies. Nevertheless, its potency in addressing this particular issue remains to be determined. Here, we report that SD induced a pronounced pronociceptive effect attributed to the heightened intrinsic excitability of D2-MSNs within the NAc in Male C57BL/6N mice. CBD (30 mg/kg, i.p.) exhibited an anti-hyperalgesic effect. CBD significantly improved the thresholds for thermal and mechanical pain and increased wakefulness by reducing delta power. Additionally, CBD inhibited the intrinsic excitability of D2-MSNs both in vitro and in vivo. Bilateral microinjection of the selective D2 receptor antagonist raclopride into the NAc partially reversed the antinociceptive effect of CBD. Thus, these findings strongly suggested that SD activates NAc D2-MSNs, contributing heightened to pain sensitivity. CBD exhibits antinociceptive effects by activating D2R, thereby inhibiting the excitability of D2-MSNs and promoting wakefulness under SD conditions.

A sleepless night disrupts the resolution of emotional conflicts: Behavioural and neural evidence.

The present study aims to investigate the influence of 24-hr sleep deprivation on implicit emotion regulation using the emotional conflict task. Twenty-five healthy young adults completed a repeated-measures study protocol involving a night of at-home normal sleep control and a night of in-laboratory sleep deprivation. Prior to the experimental session, all participants wore an actigraph watch and completed the sleep diary. Following each condition, participants performed an emotional conflict task with electroencephalographic recordings. Emotional faces (fearful or happy) overlaid with words ("fear" or "happy") were used as stimuli creating congruent or incongruent trials, and participants were instructed to indicate whether the facial expression was happy or fearful. We measured the accuracy and reaction time on the emotional conflict task, as well as the mean amplitude of the P300 component of the event-related potential at CPz. At the behavioural level, sleep-deprived participants showed reduced alertness with overall longer reaction times and higher error rates. In addition, participants in the sleep deprivation condition made more errors when the current trial followed congruent trials compared with when it followed incongruent trials. At the neural level, P300 amplitude evoked under the sleep-deprived condition was significantly more positive compared with the normal sleep condition, and this effect interacted with previous-trial and current-trial congruency conditions, suggesting that participants used more attentional resources to resolve emotional conflicts when sleep deprived. Our study provided pioneering data demonstrating that sleep deprivation may impair the regulation of emotional processing in the absence of explicit instruction among emerging adults.

Cognitive performance of air personnel following sleep deprivation.

Air forces have developed several methods for reducing fatigue-related accidents. In the Israeli Air Force, the "Dead Tired" workshop was developed with the purpose of presenting aircrew with their objective performance under sleep deprivation conditions. The aim of this study was to examine the cognitive abilities of both aircrew and unmanned aerial vehicle operators, both objectively and subjectively. All Israeli aircrew and unmanned aerial vehicle operators participated in a "Dead Tired" workshop. During the workshop, the participants performed the Psychomotor Vigilance Task, a task that tests their attention abilities, while gathering information on their subjective sleepiness in the form of a Karolinska Sleepiness Scale. Data of 366 participants (25 females), of whom 187 were unmanned aerial vehicle operators and 179 were aircrew, were obtained; and the mean age was 21.8 ± 1.2 years (range 19-26 years). A significant decline in task performance was seen following 20 hr of wakefulness in both unmanned aerial vehicle operators and aircrew (p < 0.001). Unmanned aerial vehicle operators' performance was significantly better throughout the majority of the workshop (p < 0.001). Recovery after the full-night's sleep was seen for unmanned aerial vehicle operators, but not for aircrew (p = 0.008). A high correlation was seen between Psychomotor Vigilance Task performance and Karolinska Sleepiness Scale responses (correlation coefficient = 0.93). Sleep deprivation negatively impacted the performance of both groups of participants. Unmanned aerial vehicle operators were found to be more resilient to the effects of sleep deprivation and were quicker to recover in comparison to aircrew.

Sleep deprivation causes gut dysbiosis impacting on systemic metabolomics leading to premature ovarian insufficiency in adolescent mice.

Rationale: Currently, there are occasional reports of health problems caused by sleep deprivation (SD). However, to date, there remains a lack of in-depth research regarding the effects of SD on the growth and development of oocytes in females. The present work aimed to investigate whether SD influences ovarian folliculogenesis in adolescent female mice. Methods: Using a dedicated device, SD conditions were established in 3-week old female mice (a critical stage of follicular development) for 6 weeks and gut microbiota and systemic metabolomics were analyzed. Analyses were related to parameters of folliculogenesis and reproductive performance of SD females. Results: We found that the gut microbiota and systemic metabolomics were severely altered in SD females and that these were associated with parameters of premature ovarian insufficiency (POI). These included increased granulosa cell apoptosis, reduced numbers of primordial follicles (PmFs), correlation with decreased AMH, E2, and increased LH in blood serum, and a parallel increased number of growing follicles and changes in protein expression compatible with PmF activation. SD also reduced oocyte maturation and reproductive performance. Notably, fecal microbial transplantation from SD females into normal females induced POI parameters in the latter while niacinamide (NAM) supplementation alleviated such symptoms in SD females. Conclusion: Gut microbiota and alterations in systemic metabolomics caused by SD induced POI features in juvenile females that could be counteracted with NAM supplementation.

Evaluation of cognitive and psychomotor faculties in relation to mood-related symptoms under the conditions of sleep deprivation.

Deprivation of sleep (DS) has been associated with changes in mood and cognitive function, rapidly but transiently improving the severity of depression symptoms. However, it remains unclear whether there are differences in performance between DS responders and non-responders. The relationship between DS, mood, cognitive, and psychomotor function is also poorly understood. Participants (n = 77) underwent a baseline assessment of sleep under the control of polysomnography (PSG). Later they were subjected to DS with actigraphy monitoring. Evaluation of mood as well as completing a battery of tests assessing cognitive functions and eye-hand coordination was conducted four times, pre/post PSG and DS. Participants were further divided into respondents (RE, n = 48) and non-respondents (NR, n = 29) depending on alleviation of depression symptoms severity following DS. All participants exhibited increased response speed to visual triggers after DS compared to baseline (p = 0.024). Psychomotor vigilance test (PVT) results remained intact in the RE, whereas it was increased in the NR (p = 0.008). Exposure time in the eye-hand coordination test improved in both groups, but total error duration was reduced only in RE individuals (p < 0.001, p = 0.009 for RE and NR, respectively). All subjects were more proficient at trail-making test (p ≤ 0.001 for Part 1 and 2 in all, NR, RE). Stroop test also improved regardless of mood changes after DS (p = 0.007, p = 0.008 for Part 1 and 2, respectively); cognitive interference remained at a similar level within groups (p = 0.059, p = 0.057 for NR and RE, respectively). A positive correlation was observed between the difference in PSG morning/DS morning depression severity and vigilance (R = 0.37, p = 0.001, R = 0.33, p = 0.005, for error duration eye-hand coordination test and PVT total average score, respectively). RE tend to maintain or improve cognitive function after DS, oppositely to NR. Vigilance in particular might be tightly associated with changes in depression symptoms after DS. Future studies should examine the biological basis behind the response to sleep loss.

Cognitive impairment after sleep deprivation: The role of precuneus related connectivity on the intra-individual variability changes

ObjectiveIntra-individual variability (IIV) in cognitive performance is thought to reflect the efficiency with which attentional resources are allocated in different circumstances requiring cognitive control. IIV in cognitive performance is associated with the strength of the negative correlation between task-positive network and default mode network (DMN) activity. In this study, we investigated the impact of sleep deprivation (SD) on functional connectivity (FC) between the DMN and psychomotor vigilance task-related network (PVT-RN), and its relationship with IIV in cognitive performance. MethodsTwo analyses, network-level independent component analysis (NL-ICA) and region-level (RL)-ICA, were employed to compare the coefficient of variation (CV) of the PVT between normal sleep and SD conditions across 67 healthy participants. ResultsAfter SD, in NL-ICA, the FC between the PVT-RN and DMN was positively correlated with the CV of the PVT, as well as the changes therein, compared with normal sleep. Using a mask derived from the DMN and PVT-RN, the RL-ICA revealed that 12 edges/connections between DMN and PVT independent components were associated with the CV of the PVT, with nine of these connections involving the precuneus. ConclusionsThese findings suggest that the precuneus may play a crucial role in the interactions of various brain functions during the PVT, with the connections between the precuneus and frontoparietal and somatosensory networks being significantly altered after SD. Moreover, following SD, weakened negative FC between the precuneus and bilateral inferior parietal lobule may disrupt the balance between cognitive and executive control functions, leading to a decline in cognitive performance.

Effect of Acute and Chronic Sleep Deficit on Working and Long-Term Memory in Rats

It is known that insufficient sleep or diurnal rhythm disturbances of sleep and wakefulness exert a detrimental effect on cognitive functions. It was thought for a long period that memory consolidation is the most vulnerable link, i.e., information transfer from short-term/working memory to long-term memory. However, there is a progressive number of studies indicating that the most negative consequences of sleep loss are observed in working memory. In our study, we undertook an effort to assess possible disturbances in working memory and long-term memory following sleep loss impact with different protocols in acute and chronic experiment in rats. Sleep in Wistar rats was deprived/restricted by swinging platform technique according to the following protocols: 1 – total sleep deprivation for 18 h; 2 – partial sleep restriction for 24 h (3 h of sleep deprivation alternated with 1 h of sleep opportunity – totally 18 h of sleep deprivation); 3 – chronic partial sleep restriction (conditions 2 for five consistent days). Total sleep deprivation in Y-maze test was shown to result in a significant decrease in spontaneous alternations of maze arms that indicates working memory impairment. This impact in Barnes test did not exert an effect on long-term memory – time spent for seeking a shelter did not change in this task. Acute and chronic sleep restriction induced no changes in working memory and long-term memory. The results obtained allow us to come to conclusion that working memory (in contrast to long-term memory) is a vulnerable component of cognitive function under total sleep deprivation conditions. This negative effect was abolished if periods of sleep deprivation alternated with short periods of sleep opportunities that indicate protective significance of short sleep periods for cognitive functions during sleep deficit. Hence, short-term sleep is helpful for cognitive health and protects working memory, whereas continuous long-term wakefulness impairs it.

O033 Is Sleeping and Waking Important for the Cortisol Awakening Response?

Abstract Introduction The rapid rise in cortisol after waking is known as the cortisol awakening response (CAR). However, as part of its normal circadian rhythm cortisol also rises in the morning independent of awakening. If CAR is a direct response to awakening, it should be eliminated in conditions of sleep deprivation (SD). Given that an atypical CAR is associated with several psychiatric and medical disorders, understanding the factors that influence CAR is of clinical relevance. This study explored cortisol during the normal waking period prior, during, and post-SD. Methods N=21 (11F 22.80±4.40y) completed 62h of SD in the laboratory. Salivary cortisol was collected across 5-time-points (07:00h, 07:15h, 07:30h, and 07:45h) on 2-pre-at-home-study days, 4-in-lab-study days, and 2-post-at-home-study days. Mixed-effects ANOVAs tested for fixed effects of day, time, and their interactions on cortisol, and cortisol area under the curve (AUCi, AUCg). Results SD produced significant effects of time*day (p&amp;lt;0.001). Cortisol levels at +30 and +45min post-awakening were lower on SD days. Cortisol levels on awakening (0mins) did not differ between any study days. There were significant effects of day (p&amp;lt;0.001). AUCi and AUCg were greater on in-laboratory-baseline and recovery days compared to other study days. Discussion This study found CAR is not present during periods of SD when there is no ‘waking’ from sleep. It showed for the first time that CAR recovers to baseline levels following recovery sleep. While the role of the CAR remains unclear this study identified factors that future research should consider to advance understanding of its purpose.

Plasma Aβ level alterations after sleep deprivation correspond to brain structural remodeling in medical night shift workers

The relationship between brain structure alteration and metabolic product clearance after night shift work with total sleep deprivation (SD) remains unclear. Twenty-two intensive care unit staff on regularly rotating shift work were implemented with structural and diffusion MRI under both rest wakefulness (RW) and SD conditions. Peripheral blood samples were collected for the measurement of cerebral metabolites. Voxel-based morphometry and diffusion tensor imaging analysis were used to investigate the alterations in the gray matter density (GMD) and mean diffusivity (MD) within the participants. Furthermore, correlation analysis was performed to investigate the relationship between the neuroimaging metrics and hematological parameters. A significant increase in the GMD values was observed in the anterior and peripheral areas of the brain under SD. In contrast, a decrease in the values was observed in the posterior regions, such as the bilateral cerebellum and thalamus. In addition, a significant reduction in the total cerebrospinal fluid volume was observed under SD. The Aβ42/Aβ40 levels in participants under SD were significantly lower than those under RW. The mean MD increment values extracted from the region of interest (ROI) of the anterior brain were negatively correlated with the increment of plasma Aβ42/Aβ40 levels (r = −0.658, P = 0.008). The mean GMD decrement values extracted from the posterior ROI were positively correlated with the increment of plasma Aβ-40 levels (r = 0.601, P = 0.023). The findings of this study suggest that one night of shift work under SD induces extensive and direction-specific structural alterations of the brain, which are associated with aberrant brain metabolic waste clearance.