Role Of Sleep Research Articles

Role of Sleep in Formation of Relational Associative Memory.

Relational memory, the ability to make and remember associations between objects, is an essential component of mammalian reasoning. In relational memory tasks, it has been shown that periods of offline processing, such as sleep, are critical to making indirect associations. To understand biophysical mechanisms behind the role of sleep in improving relational memory, we developed a model of the thalamocortical network to test how slow-wave sleep affects performance on an unordered relational memory task. First, the model was trained in the awake state on a paired associate inference task, in which the model learned to recall direct associations. After a period of subsequent slow-wave sleep, the model developed the ability to recall indirect associations. We found that replay, during sleep, of memory patterns learned in awake increased synaptic connectivity between neurons representing the item that was overlapping between tasks and neurons representing the unlinked items of the different tasks; this forms an attractor that enables indirect memory recall. Our study predicts that overlapping items between indirectly associated tasks are essential for relational memory, and sleep can reactivate pathways to and from overlapping items to the unlinked objects to strengthen these pathways and form new relational memories.SIGNIFICANCE STATEMENT Experimental studies have shown that some types of associative memory, such as transitive inference and relational memory, can improve after sleep. Still, it remains unknown what specific mechanisms are responsible for these sleep-related changes. In this new work, we addressed this problem by building a thalamocortical network model that can learn relational memory tasks and that can be simulated in awake or sleep states. We found that memory traces learned in awake were replayed during slow waves of NREM sleep and revealed that replay increased connections to and from overlapping memory items to form new relational memories. Our work discovered specific mechanisms behind the role of sleep in associative memory and made testable predictions about how sleep augments associative learning.

0276 Sleep EEG Changes in a Transgenic Mouse Model of Spinocerebellar Ataxia Type 3

Abstract Introduction Spinocerebellar ataxia type 3 (SCA3) or Machado-Joseph disease is a fatal, incurable, dominantly inherited ataxia, typically of adult-onset, and the most frequent type of SCA worldwide. SCA3 patients show progressive neuronal loss in several brain areas reflecting a broad spectrum of motor and non-motor symptoms, including ataxia, parkinsonism, and sleep disorders. In other neurodegenerative diseases, sleep disturbances alter brain homeostatic mechanisms, including DNA repair, synaptic function, and network activity, leading to deterioration of neurologic function. Sleep research has provided insights into their pathophysiology, disease prediction, and symptom management. Such studies have not been performed in SCA3. The aim of this study is to characterize sleep EEG in an SCA3 transgenic mouse model. Methods We used homozygous, hemizygous, and wild-type YACMJD84.2 littermate mice. To confirm the expected disease phenotype, we assessed for locomotor and exploratory activity in the morning and evening when the mice were 22 to 31 weeks old. We then implanted 6 electrodes in the frontal, parietal, and cerebellar areas. About two weeks after, we recorded their sleep activity for 15 hours (ZT0-15) per day for three consecutive days. We analyzed the data from the open-field testing and the EEG from the third day of recordings using SPSS and Matlab and a p<0.05 was considered for statistical significance. Results As expected, homozygous SCA3 mice showed statistically significant decreased locomotor and exploratory activities compared with wild-type littermates. In terms of sleep architecture we did not observe any significant differences between the different genotypes. Moreover, compared with wild-type, homozygous SCA3 mice displayed increased β spectral power band activity during REM. They also had decreased θ band activity, β band activity, spindle activity, and γ band acitivity during wake. Conclusion Our data suggest that EEG spectral power is dysregulated in homozygous SCA3 mice. Changes in β band have been observed in SCA3 patients during wake, and in patients with REM sleep behavior disorder. Therefore, future studies analyzing the sleep EEG of SCA3 patients are needed to confirm whether our findings are translatable. Further studies should also investigate the causal relationship between the observed differences in sleep and disease progression. Gaining greater insight into the role of sleep in SCA3 could provide translatable biomarkers and lead to improved assessment of the disease progression and therapeutic interventions. Support (If Any) NHLBI 5T32HL110952

0200 Does Sleep Predict Antibody Response and Maintenance to the COVID-19 Vaccine?

IntroductionThere is growing evidence that insufficient sleep can negatively impact the immune system, including vaccination response. Prior laboratory studies have shown that acute sleep restriction can result in impaired antibody resposne to the hepatitis A and influenza vaccine. Similarly, prospective studies have shown that short sleep duration, measured by self-report and wrist actigraphy, is associated with muted antibody responses. These prior findings have critical implications for the COVID-19 pandemic and the efficacy and durability of the COVID-19 vaccines currently available. Whether sleep accounts for variability in response to the COVID-19 vaccination series has not been investigated.MethodsWe recruited 530 healthy participants (mean age= 52.4, SD=12.1, range: 18-88 years; 64.1% female) who were naive to the COVID-19 vaccination series. Participants completed self-report questionaires (e.g., Pittsburgh Sleep Quality Index) and morning sleep diaries for 7-consecutive days surrounding COVID-19 vaccine administrations. Additionally, 198 participants wore a sleep tracking device (Oura ring) continuously for ~2 months beginning prior to vaccination, which provides behavioral sleep data on days prior to and following the COVID-19 vaccination series. Blood samples were collected prior to vaccination, +1 month after their final vaccine shot (peak response), and +6 months after their final vaccine shot (maintenance); neutralization assays using pseudotype virus will be carried out to quantify antibody titers.ResultsData collection concludes December 2021, with antibody assays to be completed February 2022. Initial baseline data indicates that most participants reported poor overall global sleep quality (PSQI mean=6.3, SD=3.6; 52% PSQI>5). Linear mixed models will be conducted to test associations between habitual sleep duration (averaged over the measurement time points), sleep efficiency, and subjective sleep quality with antibody responses over time. Additionally, we will report on the relevance of sleep timing (midpoint) and vaccination timing (receiving the vaccine in the morning vs afternoon vs evening), and the role of self-reported sleep disorders (e.g., obstructive sleep apnea) and shift worker status. Covariates in these analyses will include age, gender, race, body mass index, prior COVID infection, and vaccine type (Moderna, Pfizer, Johnson and Johnson).ConclusionThese analyses will provide new knowledge about the role of sleep in mounting and maintaining antibody response to the COVID-19 vaccination series. These findings may provide novel insights into when and for whom improvements in sleep may result in better vaccine efficacy.Support (If Any)R24AG048024

0028 Network Analysis of Adipokines in Sleep Disorders and Metabolic Dysregulation

Abstract Introduction Adipokines are a growing group of secreted proteins that play important roles in metabolism. Accumulating evidence suggests that adipokines may mediate the close association between sleep disturbance and metabolic derangements. Due to the extensive crosstalk between adipokines and metabolic pathways, an integrated approach is required to better understand the significance of adipokines in sleep disorders and associated metabolic dysregulation. In the current study, we employed network analysis, a set of concepts and methods derived from graph theory, to obtain novel insights into the roles of adipokines in sleep disorders and associated metabolic dysregulation. Methods A network of six adipokines and their molecular targets is constructed based on current understanding of their roles in sleep and metabolic disorders using an adjacency matrix. The network is then visualized and analyzed using an open source platform Gephi to derive network-level metrics, including degree and centrality measures. These metrics are used to explore the relationship between sleep disturbance and associated metabolic dysregulation in several disease processes. Results 94 nodes and 264 edges were identified in the network, representing regulatory factors, adipokines, molecular pathways, and disease processes. Two adipokines, leptin and adiponectin, were found to have higher degrees than other adipokines, indicating their central roles in connecting sleep disturbance to metabolic dysregulations. Among the regulatory factors, obesity and obstructive sleep apnea were found to be major drivers for the sleep associated metabolic dysregulation based on their higher degrees. The important pathways adipokines act on in the network included insulin signaling, inflammation, food intake, and energy expenditure. The main disease processes adipokines act on included cardiovascular, reproductive, and autoimmune diseases. Leptin, AMPK, and fatty acid oxidation were found to have global influence in the network based on their high betweenness. Conclusion Adipokines are important players in the metabolic dysregulations associated with sleep disturbance. Adipokines such as leptin and adiponectin act on diverse metabolic pathways in response to sleep disturbance, obesity, insulin resistance, and inflammation.They play important roles in cardiovascular, reproductive, and autoimmune diseases. Adipokines and their targets, such as leptin, AMPK, and fatty acid oxidation are likely important interventional/pharmaceutical targets for these disease processes. Support (If Any) none

0813 Post-Pinealectomy Insomnia and Melatonin Therapy

Abstract Introduction Melatonin is a hormone produced in the pineal gland that has an important role in sleep; immune, neurologic, psychiatric, metabolic, and endocrinologic function; cardiac-autonomic regulation and even cancer risk. We present a case of insomnia, somnambulism, dream enactment, and periodic limb movements of sleep (PLMS) after a pinealectomy. Report of Cases: A 40-year-old woman with a history of a complete pinealectomy due to a pineal cyst presented to the sleep medicine clinic. Shortly after the pinealectomy, she developed sleep onset and maintenance insomnia. Two years later she developed somnambulism, and four years later she developed dream enactment and PLMS. She reported no prior treatments for her sleep issues, including no history of melatonin use. On average, her total sleep time (TST) was 2-8 hours/night with awakenings every 2 hours. Sleep latency was 10-45 minutes. Polysomnograghy demonstrated an apnea-hypopnea index of 0.6/hr, PLM index of 68.1/hr, normal REM atonia, and no complex behaviors. The patient started 1mg immediate release (IR) melatonin, which did not help her insomnia, but parasomnias resolved. She had improvement in her PLMS with iron supplementation and melatonin. The melatonin dose was increased to 3mg IR which helped increase her TST to 4-8 hours. She was switched to 3mg extended release (ER) melatonin, and then increased to 4mg ER. She obtained the most benefit for her insomnia with 1mg IR plus 4mg ER with sleep latency reduced to 5-10 minutes and TST improved up to 7.5 hours with rare awakenings. Conclusion Pinealectomy in humans is rarely reported. Most data about the consequences of pinealectomy and pathophysiology of melatonin come from animal research. Melatonin level after pinealectomy is often undetectable or severely diminished. Current limited literature on patients with pinealectomy consists of case reports about patients who experienced insomnia, non-24-hour sleep-wake rhythm disorder [SSM1] and mood disorders. Melatonin doses ranging from 0.5mg to 14mg IR and up to 5mg ER have been trialed with most patients having symptomatic improvement with doses above 3mg. We found that a combination of 1mg immediate and 4mg extended release melatonin was the most beneficial for our patient. Support (If Any)

0436 Effect of sleep on the relationship between pain related disability and neural correlates of pain processing in adults with fibromyalgia and insomnia

Abstract Introduction Up to 80% of adults with fibromyalgia experience insomnia. While sleep and pain are known to be associated, sleep's role in the association between pain related disability and neural correlates of pain processing is unknown. We evaluated whether sleep moderates the association between brain activity in response to painful stimuli and pain related disability in adults with fibromyalgia and insomnia (FMI). Methods Twenty-nine adults with FMI (Mage=57.2, SD=13.1) wore Actiwatch 2s over 14 days, completed the Pain Disability Index (PDI), and underwent fMRI using a quantitative sensory testing (QST) protocol involving thermal stimuli. Twelve brain regions with significant activation changes to QST (identified previously, PMID34310276) were included as dependent variables, PDI score as independent variable and actigraphic sleep variables (Sleep Onset Latency (SOL), Total Sleep Time (TST), Sleep Efficiency (%SE)) as moderators in the analysis. For moderation at significance levels of p<0.05 (and trends at p<0.1), significance of simple slopes at high (1 SD above), average and low (1 SD below) sleep levels were examined. Results %SE moderated the relationship between right cingulate gyrus (rCG) activity and PDI score (B=0.0009, SE=0.0003, p=.016, R^2=0.22). At lower values of %SE (but not at average or higher levels), there was a negative association between rCG activity and PDI score (B=-0.0166, SE=0.0064, p=0.016). Moderating impact of SOL (B=-0.0002, SE=0.0001, p=.05, R^2=0.14) and TST (B=0.0002, SE=0.0001, p=.06, R^2=0.15) trended towards significance. [MCS1] PDI and rCG activity showed negative associations at highest levels of SOL, while PDI and right inferior frontal gyrus activity showed positive associations at highest levels of TST. Conclusion Since the rCG is involved in gating, integration and classification of pain signals, decreased activation in rCG could reflect reduced modulation of pain processing in the region. Preliminary results indicate that at lower levels of sleep efficiency, this decrease in modulation of pain processing is associated with greater perceptions of disability related to pain. Further studies in larger samples are warranted to understand the causal effects, if any, of sleep on pain related disability and the neural correlates of pain processing. Support (If Any) NIAMS-R01AR055160/S1; PI-McCrae

0121 Sleep facilitates memory, but not navigation across the pubertal transition in the novel Minecraft Memory and Navigation Task

Abstract Introduction The hippocampus uniquely supports the acquisition and retention of spatial information, and sleep supports the consolidation of hippocampal-dependent memories. However, support for the role of sleep in spatial memory and navigation is mixed. We developed and tested a novel Minecraft Memory and Navigation (MMN) task in adults which showed that sleep uniquely supports the memory for spatial locations, but navigation improved regardless of delay condition (Simon et al., submitted). Here, we tested participants during the developmental transition from childhood to adolescence, a time known for structural and functional hippocampal maturation. Methods Thirty-one youth (Mage = 10.6, SD = 1.56, 9-13 years, grouped: child, early adolescent, adolescent) were administered the MNN task. Training included two free-explorations trials to learn 12 unique object-locations associations in an open-field Minecraft environment. At test, participants were cued to place objects from randomly teleported locations. They were tested twice, immediately and 12-hours later, after a period of sleep or wake. Conditions and environments were counterbalanced in a within-subject design. Each step-by-step movement was recorded for navigation analyses including path length, orientation angle, and search behaviors. Results We found a significant benefit of sleep, compared to wake, on the spatial location accuracy when accounting for age group (F(1,27) = 6.153, p = .02), such that similar to young adults, youth’s metric accuracy of spatial locations improved. We found no change in navigation performances from Test 1 to Test 2 in either condition. Between the start and target locations, youth initiated and maintained similar trajectory angles with similar total path lengths (p’s > .068). Spatial location memory did not correlate with any navigation metrics (p’s > .361). Navigation metrics correlated among themselves, which withstood correction (p’s < .005). Conclusion Youth demonstrated similar sleep-dependent benefits for the metric accuracy of the spatial locations. In contrast to adults, youth’s navigation performance did not improve over delay, regardless condition. Our findings are in line with sleep’s promotion of hippocampal-dependent information, with retention of the spatial locations. Our data are consistent with the hypothesis that sleep does not facilitate navigation, and points to potential developmental maturation required to support navigation behaviors. Support (If Any)

0499 Sleep and Neurocognition in Adolescents with ADHD: A Polysomnographic Study

Abstract Introduction Sleep disturbances are common among adolescents with ADHD; however, few studies have characterized the nature of ADHD-related sleep problems using the gold-standard sleep measure, polysomnography (PSG), in adolescence. Additionally, although similar cognitive deficits are common across ADHD and sleep-disordered populations, the potential role of sleep in contributing to cognitive impairment in adolescent ADHD is unknown. This study investigates differences in PSG-measured sleep among adolescents with ADHD versus healthy controls without psychiatric disorders (HC) and associations with cognition. Methods Sixty-two adolescents aged 13-17 (31 ADHD, mean age=15.3, 50% female) completed a psychiatric evaluation and 3 nights of ambulatory PSG. Following the third night, participants completed the Cambridge Neuropsychological Test Automated Battery (CANTAB). Sleep variables were averaged over 3 nights. Linear regressions controlling for age and sex examined group differences in a range of traditional PSG and spectral EEG indices as well as relationships between PSG/spectral indices and cognition (two summary scores derived from CANTAB: response accuracy and response time) within the ADHD group. Results Adolescents with ADHD displayed reduced SWS% (F(3,51)=9.67, p=.003), increased N2% (F(3,51)=10.35, p=.002), increased relative sigma (F(3,47)=6.55, p=.01) and beta (F(3,47)=4.10, p<.05) power, and a trend toward reduced relative delta power (F(3,47)=2.95, p=.09) compared to HC. Within the ADHD group, greater REM% (r=.43), reduced N2% (r=-.55), greater relative delta power (r=.52), higher delta power peak (r=.56), steeper delta decline overnight (r=-.56), and reduced relative theta (r=-.53), beta (r=-.74), and gamma (r=-.67) power were associated with better response accuracy (p’s<.05). Greater relative delta (r=-.51), and reduced relative theta (r=.55) and beta (r=.63), power were associated with faster response times. Conclusion Although adolescents with ADHD did not differ from HC on traditional PSG measures (TST, WASO), they exhibited abnormalities in sleep stage distribution and non-REM EEG frequency spectral indices, including reduced SWS and low frequency power and increased stage 2 sleep and high frequency power overnight. Notably, similar parameters were associated with impaired cognition, suggesting sleep may contribute to cognitive deficits in ADHD. Future studies may clarify whether sleep plays a causal role in cognitive impairments in adolescent ADHD and if sleep treatments result in improved cognition in this population. Support (If Any) K23MH108704

Sleep Deprivation During Memory Consolidation, but Not Before Memory Retrieval, Widens Threat Generalization to New Stimuli.

Past aversive experiences shape our ability to deal with future dangers, through the encoding of implicit and explicit memory traces and through the ability to generalize defensive reactions to new stimuli resembling learned threats. Numerous evidence demonstrate that sleep is important for the consolidation of memories related to threatening events. However, there is a lack of studies examining the effects of sleep deprivation on the retrieval of consolidated threat memories, and previous studies on the role of sleep in threat generalization have produced mixed results. To address these issues, here we adopted a differential threat conditioning and a delayed (second half of the night) sleep deprivation during the first or the seventh night after learning. We found no effects of sleep deprivation on either implicit or explicit threat memories, regardless of its occurrence timing. Conversely, implicit but not explicit responses to novel cues similar to a learned threat displayed a widened generalization pattern, but only if sleep deprivation took place during the first night after conditioning and not if it occurred during the seventh night after conditioning. Therefore, we propose that sleeping after exposure to danger may support optimal implicit discrimination processes to evaluate new signals in the future and that even a brief period of sleeplessness may widen threat generalization to new stimuli, which is a hallmark of several threat-related disorders.

Evaluation of a Circadian Rhythm and Sleep-Focused Mobile Health Intervention for the Prevention of Accelerated Summer Weight Gain Among Elementary School-Age Children: Protocol for a Randomized Controlled Feasibility Study.

BackgroundThe i♥rhythm project is a mobile health adaptation of interpersonal and social rhythm therapy designed to promote healthy sleep and behavioral rhythms among 5-8-year olds during summer for the prevention of accelerated summer weight gain.ObjectiveThis pilot study will examine the feasibility, acceptability, and preliminary efficacy of the i♥rhythm intervention. This will ensure that the research protocol and procedures work as desired and are acceptable to families in preparation for the fully powered randomized controlled trial. The proposed study will examine the willingness of participants to participate in the intervention and determine whether modifications to the intervention, procedures, and measures are needed before conducting a fully powered study. We will assess our ability to (1) recruit, consent, and retain participants; (2) deliver the intervention; (3) implement the study and assessment procedures; (4) assess the reliability of the proposed measures; and (5) assess the acceptability of the intervention and assessment protocol.MethodsThis study will employ a single-blinded 2-group randomized control design (treatment and no-treatment control) with randomization occurring after baseline (Time 0) and 3 additional evaluation periods (postintervention [Time 1], and 9 months [Time 2] and 12 months after intervention [Time 3]). A sample of 40 parent-child dyads will be recruited.ResultsThis study was approved by the institutional review board of Baylor College of Medicine (H-47369). Recruitment began in March 2021. As of March 2022, data collection and recruitment are ongoing.ConclusionsThis study will address the role of sleep and circadian rhythms in the prevention of accelerated summer weight gain and assess the intervention’s effects on the long-term prevention of child obesity.Trial RegistrationClinicalTrials.gov NCT04445740; https://clinicaltrials.gov/ct2/show/NCT04445740.International Registered Report Identifier (IRRID)DERR1-10.2196/37002

Sleep enhances reconsolidation-based strengthening of visuospatial memories

Consolidated memories can be returned to a labile state upon reactivation. The re-stabilization of reactivated memories, or reconsolidation, can allow for change in previously established memories. Given the role of sleep in the initial consolidation of memories, sleep may be important for reconsolidation as well. However, effects of sleep on reconsolidation and specific aspects of sleep that may contribute are unclear. Here, participants learned 30 picture-location pairs. After overnight sleep, initial consolidation was tested. Following either one day (Experiment 1) or one week (Experiment 2), participants were tested again to reactivate their memory and then learned 30 novel picture-location pairs. Control groups (Experiment 1) received no reactivation prior to new learning. Twelve hours later, after daytime wakefulness or overnight sleep, participants completed a final memory test. Sleep participants underwent polysomnography between reactivation and final tests. In Experiment 1, reactivation led to preservation of memory compared to no reactivation. Sleep was associated with less post-reactivation memory decline than waking, with memory preservation positively related to time spent in non-rapid-eye movement sleep. In Experiment 2, sleep was associated with greater post-reactivation memory improvement than waking, with improvement positively related to sigma activity. These results suggest sleep enhances reconsolidation-based strengthening of episodic memories.

Loss of Estrogen‐Related Receptor Alpha (ESRRA) Impairs Neuronal Mitochondrial Function and Results in Disturbed Sleep and Neural Oscillatory Patterns

ESRRA is an orphan nuclear receptor enriched in metabolically active tissues and has been known to affect the transcription of a set of genes that regulate mitochondrial bioenergetics in peripheral organs. Of note, ESRRA is also abundantly expressed in the brain, but the functional role of brain ESRRA remains poorly understood. To test the role of ESRRA on energy metabolism in neurons, we performed the Seahorse assay in mouse primary cortical neurons with or without ESRRA expression and found that neurons lacking ESRRA have significantly reduced cellular respiration compared to control neurons, indicating that loss of ESRRA decreases mitochondrial oxidative capacity and thus neuronal energy production. We have previously reported that global ESRRA null (KO) displayed markedly reduced locomotor activity (home cage vibration plate p<0.05, wheel running p<0.001), suggesting that these mice do display an energy deficit as a result of this manipulation. Based on the commonly appreciated role of sleep in the replenishment of energy stores for normal brain function, we hypothesized that reduced brain energy levels caused by genetic loss of ESRRA would lead to hypersomnia and diminished neural oscillations, which may underlie hypolocomotion seen in ESRRA KO mice. To test this hypothesis, wireless electroencephalography/electromyography (EEG/EMG) devices were implanted in a cohort of ESRRA KO and wildtype (WT) mice and 24hr sleep state was recorded and scored. Sleep architecture analysis from 24‐hour wireless EEG/EMG recording revealed that ESRRA KO mice exhibit significantly increased non‐rapid eye movement (NREM) (p<0.05) sleep as well as disrupted circadian pattern of rapid eye movement (REM) (p<0.01) sleep compared to WT littermates. Power spectral analysis further revealed that high range gamma (40‐100Hz) (p<0.001) and alpha (9‐13Hz) (p<0.05) oscillations are significantly decreased while low range gamma (25‐40Hz) (p<0.05) and beta (13‐25Hz) (p<0.05) oscillations are increased in ESRRA KO mice. Our findings not only reveal a previously unappreciated role of ESRRA in regulating neuronal mitochondrial function, sleep‐wake cycle, and neural oscillations, but also support a novel concept that a single molecular cause of diminished brain energy levels can prolong sleep duration and results in aberrant REM sleep pattern.

Melatonin and Alzheimer’s Disease: A Mini-Review

Melatonin is a hormone with neuroregulatory, antioxidant and anti-inflammatory properties. Its benevolent effects on Alzheimer’s disease (AD) has been replicated in both animal models and clinical studies. Melatonin was effective in deterring the toxic effects of amyloid beta (Aβ) and reducing tau phosphorylation. Conflicting results exist for the clinical effectiveness of melatonin administration in AD patients. The positive effects of melatonin in AD have mainly been viewed from its role in sleep and circadian rhythm. Several limitations exist in the previous research on the relationship between melatonin and AD. Future research should focus on sharpening methodology, and adopting more expanded, multi-faceted approach, with consideration for melatonin’s antioxidant and anti-inflammatory properties.

Role of Sleep in the Formation of False Memory Using Category Associates

Role of Sleep in the Formation of False Memory Using Category Associates

Sleep loss impairs cognitive performance and alters song output in Australian magpies

Sleep maintains optimal brain functioning to facilitate behavioural flexibility while awake. Owing to a historical bias towards research on mammals, we know comparatively little about the role of sleep in facilitating the cognitive abilities of birds. We investigated how sleep deprivation over the full-night (12 h) or half-night (6 h) affects cognitive performance in adult Australian magpies (Cracticus tibicen), relative to that after a night of undisturbed sleep. Each condition was preceded and followed by a baseline and recovery night of sleep, respectively. Prior to each treatment, birds were trained on an associative learning task; on the day after experimental treatment (recovery day), birds were tested on a reversal learning task. To glean whether sleep loss affected song output, we also conducted impromptu song recordings for three days. Ultimately, sleep-deprived magpies were slower to attempt the reversal learning task, less likely to perform and complete the task, and those that did the test performed worse than better-rested birds. We also found that sleep-deprived magpies sang longer yet fewer songs, shifted crepuscular singing to mid-day, and during the post-recovery day, song frequency bandwidth narrowed. These results collectively indicate that sleep loss impairs motivation and cognitive performance, and alters song output, in a social adult songbird.

Roles of Neuropeptides in Sleep-Wake Regulation.

Sleep and wakefulness are basic behavioral states that require coordination between several brain regions, and they involve multiple neurochemical systems, including neuropeptides. Neuropeptides are a group of peptides produced by neurons and neuroendocrine cells of the central nervous system. Like traditional neurotransmitters, neuropeptides can bind to specific surface receptors and subsequently regulate neuronal activities. For example, orexin is a crucial component for the maintenance of wakefulness and the suppression of rapid eye movement (REM) sleep. In addition to orexin, melanin-concentrating hormone, and galanin may promote REM sleep. These results suggest that neuropeptides play an important role in sleep–wake regulation. These neuropeptides can be divided into three categories according to their effects on sleep–wake behaviors in rodents and humans. (i) Galanin, melanin-concentrating hormone, and vasoactive intestinal polypeptide are sleep-promoting peptides. It is also noticeable that vasoactive intestinal polypeptide particularly increases REM sleep. (ii) Orexin and neuropeptide S have been shown to induce wakefulness. (iii) Neuropeptide Y and substance P may have a bidirectional function as they can produce both arousal and sleep-inducing effects. This review will introduce the distribution of various neuropeptides in the brain and summarize the roles of different neuropeptides in sleep–wake regulation. We aim to lay the foundation for future studies to uncover the mechanisms that underlie the initiation, maintenance, and end of sleep–wake states.

Resting-state functional connectivity of the sensory/somatomotor network associated with sleep quality: evidence from 202 young male samples.

Previous neuroimaging studies have demonstrated that sleep is associated with brain functional changes in some specific brain regions. However, few studies have examined the relationship between all possible functional connectivities (FCs) within the sensory/somatomotor network (SSN) and the sleep quality of young male samples. The SSN consists of two motor cortices and is known to play a critical role in sleep. Poor sleep quality may be associated with increased sensory/somatomotor functional connectivity during rest. Hence, 202 young male participants underwent a resting-state functional magnetic resonance imaging (fMRI) scan and completed the Pittsburgh Sleep Quality Index (PSQI). Results indicated that increased functional connectivity within the SSN was associated with poor sleep quality. Specifically, the total PSQI score was positively correlated with the increased functional connectivity of the left paracentral lobule (PCL), bilateral precentral gyrus (PreCG), supplementary motor area (SMA) and bilateral postcentral gyrus (PoCG). Additionally, our findings also exhibited that (a) the subjective sleep quality factor of PSQI was positively correlated with FC between the bilateral PoCG and the bilateral PCL as well as between the left PreCG and the right SMA; (b) the sleep latency factor of PSQI was positively correlated with FC between the left PoCG and the right precuneus (PCUN); (c) the sleep disturbances factor of PSQI was positively correlated with FC between the left PCL and the right PoCG, and (d) the daytime dysfunction factor of PSQI was positively correlated with FC between the bilateral PoCG and the left PCL as well as between the bilateral PreCG and the SMA. In short, our findings can be comprehensively understood as neural mechanisms of intrinsic SSN connectivity are associated with sleep quality of man. Meanwhile, it may expand our knowledge and provide new insight into a deeper understanding of the neurobiological mechanisms of sleep or sleep problems.

The Role of Sleep in Human Psychosocial Behavior

The Role of Sleep in Human Psychosocial Behavior

Goodnight, astrocyte: waking up to astroglial mechanisms in sleep.

Astrocytes mediate many important aspects of neural homeostasis, but until recently, their role in sleep was largely unknown. The situation has dramatically changed in the last decade. The use of transgenic animals, optogenetics, chemogenetics, brain imaging and sophisticated molecular assays has led to exciting discoveries. Astrocytes dynamically change their activity across the sleep-wake cycle and may encode sleep need via changes in intracellular signalling pathways. Astrocytes also exocytose/secrete sleep-inducing molecules which modulate brain activity, sleep architecture and sleep regulation. Many of these observations have been made in mice and Drosophila melanogaster, indicating that astroglial sleep mechanisms are evolutionarily conserved. We review recent findings and discuss future directions.

Functioning of K channels during sleep

The functioning of voltage-dependent K channels (Kv) may correlate with the physiological state of brain in organisms, including the sleep in Drosophila. Apparently, all major types of K currents are expressed in CNS of this model organism. These are the Shab-Kv2, Shaker-Kv1, Shal-Kv4, and Shaw-Kv3 α subunits and can be deciphered by patch-clamp technique. Although it is plausible that some of these channels may play a prevailing role in sleep or wakefulness, several of recent data are not conclusive. It needs to be defined that indeed the frequency of action potentials in large ventral lateral pacemaker neurons is either higher or lower during the morning or night because of an increased Kv3 and Kv4 currents, respectively. The outcomes of dynamic-clamp approach in combination with electrophysiology in insects are unreliable in contrast to those in mammalian neurons. Since the addition of virtual Kv conductance during any Zeitgeber time should not significantly alter the resting membrane potential. This review explains the Drosophila sleep behavior based on neural activity with respect to K current-driven action potential rate.