Cortical miR-709 links glutamatergic signaling to NREM sleep EEG slow waves in an activity-dependent manner.

MicroRNAs (miRNAs) are key post-transcriptional regulators of gene expression that have been implicated in a plethora of neuronal processes. Nevertheless, their role in regulating brain activity in the context of sleep has so far received little attention. To test their involvement, we deleted mature miRNAs in post-mitotic neurons at two developmental ages, i.e., in early adulthood using conditional Dicer knockout (cKO) mice and in adult mice using an inducible conditional Dicer cKO (icKO) line. In both models, electroencephalographic (EEG) activity was affected and the response to sleep deprivation (SD) altered; while the rapid-eye-movement sleep (REMS) rebound was compromised in both, the increase in EEG delta (1 to 4 Hz) power during non-REMS (NREMS) was smaller in cKO mice and larger in icKO mice compared to controls. We subsequently investigated the effects of SD on the forebrain miRNA transcriptome and found that the expression of 48 miRNAs was affected, and in particular that of the activity-dependent miR-709. In vivo inhibition of miR-709 in the brain increased EEG power during NREMS in the slow-delta (0.75 to 1.75 Hz) range, particularly after periods of prolonged wakefulness. Transcriptome analysis of primary cortical neurons in vitro revealed that miR-709 regulates genes involved in glutamatergic neurotransmission. A subset of these genes was also affected in the cortices of sleep-deprived, miR-709-inhibited mice. Our data implicate miRNAs in the regulation of EEG activity and indicate that miR-709 links neuronal activity during wakefulness to brain synchrony during sleep through the regulation of glutamatergic signaling.

Norepinephrine Drives Sleep Fragmentation Activation of Asparagine Endopeptidase, Locus Ceruleus Degeneration, and Hippocampal Amyloid-ß42 Accumulation.

Chronic sleep disruption (CSD), from insufficient or fragmented sleep and is an important risk factor for Alzheimer's disease (AD). Underlying mechanisms are not understood. CSD in mice results in degeneration of locus ceruleus neurons (LCn) and CA1 hippocampal neurons and increases hippocampal amyloid-ß42 (Aß42), entorhinal cortex (EC) tau phosphorylation (p-tau), and glial reactivity. LCn injury is increasingly implicated in AD pathogenesis. CSD increases NE turnover in LCn, and LCn norepinephrine (NE) metabolism activates asparagine endopeptidase (AEP), an enzyme known to cleave amyloid precursor protein (APP) and tau into neurotoxic fragments. We hypothesized that CSD would activate LCn AEP in an NE-dependent manner to induce LCn and hippocampal injury. Here, we studied LCn, hippocampal, and EC responses to CSD in mice deficient in NE [dopamine ß-hydroxylase (Dbh)-/-] and control male and female mice, using a model of chronic fragmentation of sleep (CFS). Sleep was equally fragmented in Dbh -/- and control male and female mice, yet only Dbh -/- mice conferred resistance to CFS loss of LCn, LCn p-tau, and LCn AEP upregulation and activation as evidenced by an increase in AEP-cleaved APP and tau fragments. Absence of NE also prevented a CFS increase in hippocampal AEP-APP and Aß42 but did not prevent CFS-increased AEP-tau and p-tau in the EC. Collectively, this work demonstrates AEP activation by CFS, establishes key roles for NE in both CFS degeneration of LCn neurons and CFS promotion of forebrain Aß accumulation, and, thereby, identifies a key molecular link between CSD and specific AD neural injuries.

Noradrenaline enhances Na-K ATPase subunit expression by HuR-induced mRNA stabilization and their transportation to the cell surface through PLC and PKC mediated pathway: Implications with REMS-loss associated disorders.

Rapid eye movement sleep (REMS) maintains brain excitability at least by regulating Na-K ATPase activity. Although REMS deprivation (REMSD)-associated elevated noradrenaline (NA) increases Na-K ATPase protein expression, its mRNA transcription did not increase. We hypothesized and confirmed both in vivo as well as in vitro that elevated mRNA stability explains the apparent puzzle. The mRNA stability was measured in control and REMSD rat brain with or without in vivo treatment with α1-adrenoceptor (AR) antagonist, prazosin (PRZ). Upon REMSD, Na-K ATPase α1-, and α2-mRNA stability increased significantly, which was prevented by PRZ. To decipher the molecular mechanism of action, we estimated NA-induced Na-K ATPase mRNA stability in Neuro-2a cells under controlled conditions and by transcription blockage using Actinomycin D (Act-D). NA increased Na-K ATPase mRNA stability, which was prevented by PRZ and propranolol (PRP, ß-AR antagonist). The knockdown assay confirmed that the increased mRNA stabilization was induced by elevated cytoplasmic abundance of Human antigen R (HuR) and involving (Phospholipase C) PLC-mediated activation of Protein Kinase C (PKC). Additionally, using cell-impermeable Enz-link sulfo NHS-SS-Biotin, we observed that NA increased Na-K ATPase α1-subunits on the Neuro-2a cell surface. We conclude that REMSD-associated elevated NA, acting on α1- and ß-AR, increases nucleocytoplasmic translocation of HuR and increases Na-K ATPase mRNA stability, resulting in increased Na-K ATPase protein expression. The latter then gets translocated to the neuronal membrane surface involving both PKC and (Protein Kinase A) PKA-mediated pathways. These findings may be exploited for the amelioration of REMSD-associated chronic disorders and symptoms.

Acute partial sleep deprivation attenuates blood pressure responses to cycling exercise.

Exaggerated blood pressure (BP) responses during exercise are independently associated with future development of hypertension. Partial sleep deprivation (PSD) can increase 24-hour ambulatory BP, but the effects on exercise BP are unclear. We hypothesized that acute PSD would augment the BP response to constant load cycling exercise and a 20-minute time trial. Twenty-two, healthy adults (22±3 years; 13 males; V̇O2peak: 43.6±8.2 ml.kg-1.min-1) completed a randomized crossover trial whereby they slept normally (normal sleep-wake schedule for each participant), or sleep was partially deprived (early awakening, 40% of normal sleep duration). Each participant completed a 12-minute warm-up consisting of two 6-minute steps (step 1: 62±25 W; step 2: 137±60 W) followed by a 20-minute time trial on a cycle ergometer. PSD did not alter power output during the 20-minute time trial ([control vs. PSD] 170±68 vs. 168±68 W, P=0.65). Systolic BP did not differ during step 1 of the warm-up (141±15 vs. 137±12 mmHg, P=0.39) but was lower following PSD during step 2 (165±21 vs. 159±22 mmHg, P=0.004) and the 20-minute time trial (171±20 vs. 164±23 mmHg, P<0.001). These results were maintained when V̇O2peak was included as a covariate. Systolic BP responses were modulated by sex (time x visit x sex interaction P=0.03), with attenuated systolic BP during the warm-up and the 20-minute time trial in males but not females. In contrast to our hypothesis, acute PSD attenuates systolic BP responses during constant load and 20-minute time trial cycling exercise, though these observations appear to be primarily driven by changes in males.

Effects of sleep deprivation on language-related brain functional connectivity: differences by gender and age.

Sleep deprivation (SD) negatively affects many cognitive functions, such as language performance. However, what remains unclear is whether and how SD affects the language-related brain network based on gender and age differences. The current study of 86 healthy adults used resting-state functional magnetic resonance imaging (rs-fMRI) to measure language-related functional connectivity after full sleep or partial SD. Gender and age differences in functional connectivity were assessed across four linguistic aspects: phonetics, morphology, semantics, and syntax. The results showed that SD can affect the connectivity status of language-related brain networks, especially syntax-related networks. Furthermore, the influence of SD on the functional connectivity in language-related networks differed between male and female groups, and between younger and older groups. Specifically, there were gender differences in the temporal association cortex and age differences in the parietal association cortex, during full sleep versus partial SD. These findings highlight changes in the brain's functional connectivity in response to SD as a potential source of gender and age differences in brain function.

Sleep Problems Among Black Youth Exposed to Police Violence on Digital Media.

Findings from a recent survey of a community-based sample of Black youth ages 12 through 21 in Baltimore City, Maryland (n = 345) reveal that viewing fatal police violence videos is associated with significant increases in the odds of youth sleep disturbances, and about 30% of this association is attributable to emotional distress after viewing the videos.

Assessing the influence of sleep and sampling time on metabolites in oral fluid: implications for metabolomics studies.

INTRODUCTION: The human salivary metabolome is a rich source of information for metabolomics studies. Among other influences, individual differences in sleep-wake history and time of day may affect the metabolome. OBJECTIVES: We aimed to characterize the influence of a single night of sleep deprivation compared to sufficient sleep on the metabolites present in oral fluid and to assess the implications of sampling time points for the design of metabolomics studies. METHODS: Oral fluid specimens of 13 healthy young males were obtained in Salivette® devices at regular intervals in both a control condition (repeated 8-hour sleep) and a sleep deprivation condition (total sleep deprivation of 8 h, recovery sleep of 8 h) and their metabolic contents compared in a semi-targeted metabolomics approach. RESULTS: Analysis of variance results showed factor 'time' (i.e., sampling time point) representing the major influencer (median 9.24%, range 3.02-42.91%), surpassing the intervention of sleep deprivation (median 1.81%, range 0.19-12.46%). In addition, we found about 10% of all metabolic features to have significantly changed in at least one time point after a night of sleep deprivation when compared to 8 h of sleep. CONCLUSION: The majority of significant alterations in metabolites' abundances were found when sampled in the morning hours, which can lead to subsequent misinterpretations of experimental effects in metabolomics studies. Beyond applying a within-subject design with identical sample collection times, we highly recommend monitoring participants' sleep-wake schedules prior to and during experiments, even if the study focus is not sleep-related (e.g., via actigraphy).

Chronic sleep deprivation impairs retinal circadian transcriptome and visual function.

Sleep loss is common in modern society and is increasingly associated with eye diseases. However, the precise effects of sleep loss on retinal structure and function, particularly on the retinal circadian system, remain largely unexplored. This study investigates these effects using a chronic sleep deprivation (CSD) model in mice. Our investigation reveals that CSD significantly alters the retinal circadian transcriptome, leading to remarkable changes in the temporal patterns of enriched pathways. This perturbation extends to metabolic and immune-related transcriptomes, coupled with an accumulation of reactive oxygen species in the retina. Notably, CSD rhythmically affects the thickness of the ganglion cell complex, along with diurnal shifts in microglial migration and morphology within the retina. Most critically, we observe a marked decrease in both scotopic and photopic retinal function under CSD conditions. These findings underscore the broad impact of sleep deprivation on retinal health, highlighting its role in altering circadian gene expression, metabolism, immune response, and structural integrity. Our study provides new insights into the broader impact of sleep loss on retinal health.

Differential effects of sleep deprivation on behavior and microglia in a brain-region-specific manner in young and aged male mice.

Microglia, resident immune cells in the central nervous system, constantly monitor the state of the surrounding brain activity. The animal model induced by sleep deprivation (SD) is widely used to study the pathophysiological mechanisms of insomnia and bipolar disorder. However, it remains unclear whether SD affects behaviors in young and aged male mice and microglia in various brain regions. In this study, we confirmed brain region-specific changes in microglial density and morphology in the accumbens nucleus (Acb), amygdala (AMY), cerebellum (Cb), corpus callosum (cc), caudate putamen, hippocampus (HIP), hypothalamus (HYP), medial prefrontal cortex (mPFC), and thalamus (TH) of young mice. In addition, the density of microglia in old mice was higher than that in young mice. Compared with young mice, old mice showed a markedly increased microglial size, decreased total length of microglial processes, and decreased maximum length. Importantly, we found that 48-h SD decreased microglial density and morphology in old mice, whereas SD increased microglial density and morphology in most observed brain regions in young mice. SD-induced hyperactivity was observed only in young mice but not in old mice. Moreover, microglial density (HIP, AMY, mPFC, CPu) was significantly positively correlated with behaviors in SD- and vehicle-treated young mice. Contrarily, negative correlations were shown between the microglial density (cc, Cb, TH, HYP, Acb, AMY) and behaviors in vehicle-treated young and old mice. These results suggest that SD dysregulates the homeostatic state of microglia in a region- and age-dependent manner. Microglia may be involved in regulating age-related behavioral responses to SD.

Sleep-wake behavior and responses to sleep deprivation and immune challenge of protein kinase RNA-activated knockout mice.

Protein Kinase RNA-activated (PKR) is an enzyme that plays a role in many systemic processes, including modulation of inflammation, and is implicated in neurodegenerative diseases, such as Alzheimer's disease (AD). PKR phosphorylation results in the production of several cytokines involved in the regulation / modulation of sleep, including interleukin-1ß, tumor necrosis factor-α and interferon-γ. We hypothesized targeting PKR would alter spontaneous sleep of mice, attenuate responses to sleep deprivation, and inhibit responses to immune challenge. To test these hypotheses, we determined the sleep-wake phenotype of mice lacking PKR (knockout; PKR-/-) during undisturbed baseline conditions; in responses to six hours of sleep deprivation; and after immune challenge with lipopolysaccharide (LPS). Adult male mice (C57BL/6J, n = 7; PKR-/-, n = 7) were surgically instrumented with EEG recording electrodes and an intraperitoneal microchip to record core body temperature. During undisturbed baseline conditions, PKR -/- mice spent more time in non-rapid eye movement sleep (NREMS) and rapid-eye movement sleep (REMS), and less time awake at the beginning of the dark period of the light:dark cycle. Delta power during NREMS, a measure of sleep depth, was less in PKR-/- mice during the dark period, and core body temperatures were lower during the light period. Both mouse strains responded to sleep deprivation with increased NREMS and REMS, although these changes did not differ substantively between strains. The initial increase in delta power during NREMS after sleep deprivation was greater in PKR-/- mice, suggesting a faster buildup of sleep pressure with prolonged waking. Immune challenge with LPS increased NREMS and inhibited REMS to the same extent in both mouse strains, whereas the initial LPS-induced suppression of delta power during NREMS was greater in PKR-/- mice. Because sleep regulatory and immune responsive systems in brain are redundant and overlapping, other mediators and signaling pathways in addition to PKR are involved in the responses to acute sleep deprivation and LPS immune challenge.

Cyclooxygenase-2 (COX-2)-dependent mechanisms mediate sleep responses to microbial and thermal stimuli.

Prostaglandins (PGs) play a crucial role in sleep regulation, yet the broader physiological context that leads to the activation of the prostaglandin-mediated sleep-promoting system remains elusive. In this study, we explored sleep-inducing mechanisms potentially involving PGs, including microbial, immune and thermal stimuli as well as homeostatic sleep responses induced by short-term sleep deprivation using cyclooxygenase-2 knockout (COX-2 KO) mice and their wild-type littermates (WT). Systemic administration of 0.4 µg lipopolysaccharide (LPS) induced increased non-rapid-eye movement sleep (NREMS) and fever in WT animals, these effects were completely absent in COX-2 KO mice. This finding underscores the essential role of COX-2-dependent prostaglandins in mediating sleep and febrile responses to LPS. In contrast, the sleep and fever responses induced by the pro-inflammatory cytokine tumor necrosis factor α, a proinflammatory cytokine which activates COX-2, were preserved in COX-2 KO animals, indicating that these effects are independent of COX-2-related signaling. Additionally, we examined the impact of ambient temperature on sleep. The sleep-promoting effects of moderate warm ambient temperature were suppressed in COX-2 KO animals, resulting in significantly reduced NREMS at ambient temperatures of 30 °C and 35 °C compared to WT mice. However, rapid-eye-movement sleep responses to moderately cold or warm temperatures did not differ between the two genotypes. Furthermore, 6 h of sleep deprivation induced rebound increases in sleep with no significant differences observed between COX-2 KO and WT mice. This suggests that while COX-2-derived prostaglandins are crucial for the somnogenic effects of increased ambient temperature, the homeostatic responses to sleep loss are COX-2-independent. Overall, the results highlight the critical role of COX-2-derived prostaglandins as mediators of the sleep-wake and thermoregulatory responses to various physiological challenges, including microbial, immune, and thermal stimuli. These findings emphasize the interconnected regulation of body temperature and sleep, with peripheral mechanisms emerging as key players in these integrative processes.

Dual deficiency of melatonin and dihydrotestosterone promotes stromal cell damage and mediates prostatitis via the cGAS-STING pathway in sleep-deprived mice.

PURPOSE: Prostatitis is a highly prevalent condition that seriously affects men's physical and mental health. Although epidemiological investigations have provided evidence of a correlation between insufficient sleep and prostatitis, the pathogenesis of prostatitis remains unclear. We sought to identify the underlying mechanism involved and identify a promising therapeutic target. METHODS: Sleep deprivation (SD) was utilized to establish a mouse model of insufficient sleep in a special device. Prostatitis was observed at different time points post-SD. The degree of prostatitis was evaluated by pathological section and behavioural tests. Using immunofluorescence, western blot, and proteomic analyses, the underlying mechanism of SD-related prostatitis was investigated, and the development and therapeutic target of prostatitis were elucidated. RESULTS: SD, as an initial pathological trigger, resulted in a reduction in dihydrotestosterone and melatonin levels. Proteomic analysis revealed that the cGAS-STING pathway may play a significant role in inducing prostatitis. The subsequent results illustrated that the dual reduction in dihydrotestosterone and melatonin led to an accumulation of reactive oxygen species and the release of mitochondrial DNA (mt-DNA). The accumulation of mt-DNA activated the cGAS-STING pathway, which recruited inflammatory cells into the prostatic stroma through the secretion of interferon-ß. Consequently, an inflammatory microenvironment was formed, ultimately promoting the development of prostatitis. Notably, mice with SD-induced prostatitis gradually recovered to a normal state within 7 days of recovery sleep. However, after being subjected to SD again, these mice tended to have a more pronounced manifestation of prostatitis within a shorter timeframe, which suggested that prostatitis is prone to relapse. CONCLUSIONS: The cGAS-STING pathway activated by dual deficiency of dihydrotestosterone and melatonin plays a comprehensive inflammatory role in SD-related prostatitis. This research provides valuable insights into the pathogenesis, therapeutic targets, and prevention strategies of prostatitis.

Transcranial Irradiation Mitigates Paradoxical Sleep Deprivation Effect in an Age-Dependent Manner: Role of BDNF and GLP-1.

The growing prevalence of aged sleep-deprived nations is turning into a pandemic state. Acute sleep deprivation (SD) accompanies aging, changing the hippocampal cellular pattern, neurogenesis pathway expression, and aggravating cognitive deterioration. The present study investigated the ability of Near Infra Red (NIR) light laser to ameliorate cognitive impairment induced by SD in young and senile rats. Wistar rats ≤ 2 months (young) and ≥ 14 months (senile) were sleep-deprived for 72 h with or without transcranial administration of NIR laser of 830 nm. Our results showed that NIR photobiomodulation (PBM) attenuated cognitive deterioration made by SD in young, but not senile rats, while both sleep-deprived young and senile rats exhibited decreased anxiety (mania)-like behavior in response to PBM. NIR PBM had an inhibitory effect on AChE, enhanced the production of ACh, attenuated ROS, and regulated cell apoptosis factors such as Bax and Bcl-2. NIR increased mRNA expression of BDNF and GLP-1 in senile rats, thus facilitating neuronal survival and differentiation. The present findings also revealed that age exerts an additive factor to the cellular assaults produced by SD where hippocampal damages made in 2-month rats were less severe than those of the aged one. In conclusion, NIR PBM seems to promote cellular longevity of senile hippocampal cells by combating ROS, elevating neurotrophic factors, thus improving cognitive performance. The present findings provide NIR as a possible candidate for hippocampal neuronal insults accompanying aging and SD.

Extended wakefulness alters the relationship between EEG oscillations and performance in a sustained attention task.

During drowsiness, maintaining consistent attention becomes difficult, leading to behavioural lapses. Bursts of oscillations in the electroencephalogram (EEG) might predict such lapses, given that alpha bursts increase during inattention and theta bursts increase with time spent awake. Paradoxically, however, alpha bursts decrease with time awake and theta bursts increase during focussed attention and cognitive tasks. Therefore, we investigated to what extent theta and alpha bursts predicted performance in a sustained attention task, either when well rested (baseline, BL) or following 20 h of extended wakefulness (EW). High-density EEG was measured in 18 young adults, and the timing of bursts was related to trial outcomes (fast, slow, and lapse trials). To increase the likelihood of lapses, the task was performed under soporific conditions. Against expectations, alpha bursts were more likely before fast trials and less likely before lapses at baseline, although the effect was substantially reduced during extended wakefulness. Theta bursts showed no significant relationship to behavioural outcome either at baseline or extended wakefulness. However, following exploratory analyses, we found that large-amplitude theta and alpha bursts were more likely to be followed by lapse trials during extended wakefulness but not baseline. In summary, alpha bursts during baseline anticipated better trial outcomes, whereas large-amplitude theta and alpha bursts during extended wakefulness anticipated worse outcomes. Therefore, neither theta nor alpha bursts maintain a consistent relationship with behaviour under different levels of overall vigilance.

Alteration in neural oscillatory activity and phase-amplitude coupling after sleep deprivation: Evidence for impairment and compensation effects.

Insufficient sleep can significantly affect vigilance and increase slow-wave electroencephalographic power as homeostatic sleep pressure accumulates. Phase-amplitude coupling is involved in regulating the spatiotemporal integration of physiological processes. This study aimed to examine the functional associations of resting-state electroencephalographic power and delta/theta-gamma phase-amplitude coupling from the prefrontal cortex (PFC) to posterior regions with vigilance performance after sleep deprivation. Forty-six healthy adults underwent 24-hr sleep deprivation with resting-state electroencephalographic recordings, and vigilant attention was measured using the Psychomotor Vigilance Task. Power spectral and phase-amplitude coupling analyses were conducted, and correlation analysis was utilized to reveal the relationship between electroencephalographic patterns and changes in vigilance resulting from sleep deprivation. Sleep deprivation significantly declined vigilance performance, accompanied by increased resting-state electroencephalographic power in all bands and delta/theta-gamma phase-amplitude coupling. The increased theta activity in centro-parieto-occipital areas significantly correlated with decreased mean and slowest response speed. Conversely, the increased delta-low gamma and theta-high gamma phase-amplitude couplings negatively correlated with the deceleration of the fastest Psychomotor Vigilance Task reaction times. These findings suggest that sleep deprivation affects vigilance by altering electroencephalographic spectral power and information communication across frequency bands in different brain regions. The distinct effects of increased theta power and delta/theta-gamma phase-amplitude coupling might reflect the impairment and compensation of sleep deprivation on vigilance performance, respectively.

Chronic sleep deficiency and its impact on pain perception in healthy females.

Acute sleep deprivation in experimental studies has been shown to induce pain hypersensitivity in females. However, the impact of natural sleep deficiency and fluctuations across the week on pain perception remains unclear. A sleep-monitoring headband and self-reports were utilized to assess objective and subjective sleep in longer (> 6 hr) and short sleepers (< 6 hr). Pain sensitivity measures including heat, cold, pressure pain thresholds, pain inhibition (conditioned pain modulation) and facilitation (tonic pain summation) were assessed on Mondays and Fridays. Forty-one healthy young (23.9 ± 0.74 years) women participated. Short sleepers slept on average 2 hr less than longer sleepers (297.9 ± 8.2 min versus 418.5 ± 10.9 min) and experienced impaired pain inhibitory response (mean = -21.14 ± 7.9°C versus mean = 15.39 ± 9.5°C; p = 0.005). However, no effect was observed in pain thresholds and pain summation (p > 0.05). Furthermore, pain modulatory responses differed between Mondays and Fridays. Chronic sleep deficiency (< 6 hr) compromises pain responses, notably on Mondays. Maintaining a consistent sleep pattern with sufficient sleep (> 6 hr) throughout the week may protect against pain sensitization and the development of chronic pain in females. Further research is needed, especially in patients with chronic pain.

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.

Insufficient sleep blunts positive, but not negative, affective response to emotionally complex film clips.

The effects of sleep deprivation on emotional function are not yet fully understood. Although sleep deprivation has been shown to have larger effects on positive emotional reactivity than on negative, this research has been limited by the use of separate stimuli for positive and negative emotion elicitation. Different sets of stimuli represent a confound that makes it difficult to interpret this difference with confidence. The study reported here was designed to overcome this limitation by using film clips that elicit both positive and negative emotional responses at the same time. Undergraduate participants (33 female, 2 male) completed a laboratory-based emotion elicitation procedure using these film clips. Differences in sleep deprivation, estimated by subjective sleepiness and reaction times, were used to predict responses to these emotion probes. Greater subjective sleepiness was associated with significantly lesser positive responses to the film clips (rs = -0.37, p = 0.03). The relationship between subjective sleepiness and negative responses to the same clips was smaller and not significant (rs = -0.11, p = 0.51). Reaction times were not related to subjective emotional responses in this sample (all p > 0.40). These results support the theory that sleepiness has asymmetrical effects on positive and negative emotional functioning.

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 restriction alters the integration of multiple information sources in probabilistic decision-making.

The detrimental effects of sleep loss on overall decision-making have been well described. Due to the complex nature of decisions, there remains a need for studies to identify specific mechanisms of decision-making vulnerable to sleep loss. Bayesian perspectives of decision-making posit judgement formation during decision-making occurs via a process of integrating knowledge gleaned from past experiences (priors) with new information from current observations (likelihoods). We investigated the effects of sleep loss on the ability to integrate multiple sources of information during decision-making by reporting results from two experiments: the first implementing both sleep restriction (SR) and total sleep deprivation (TSD) protocols, and the second implementing an SR protocol. In both experiments, participants were administered the Bayes Decisions Task on which optimal performance requires the integration of Bayesian prior and likelihood information. Participants in Experiment 1 showed reduced reliance on both information sources after SR, while no significant change was observed after TSD. Participants in Experiment 2 showed reduced reliance on likelihood after SR, especially during morning testing sessions. No accuracy-related impairments resulting from SR and TSD were observed in both experiments. Our findings show SR affects decision-making through altering the way individuals integrate available sources of information. Additionally, the ability to integrate information during SR may be influenced by time of day. Broadly, our findings carry implications for working professionals who are required to make high-stakes decisions on the job, yet consistently receive insufficient sleep due to work schedule demands.