Sleep Deprivation Group Research Articles

Camphor alters occipital electrocorticographic patterns during sleep deprivation in Wistar rats

IntroductionSleep disorders are common in the general population, necessitating the search for new strategies to address this public health challenge. The study aims to describe the electrocorticographic and behavioral changes in sleep deprived Wistar rats exposed to varying doses of camphor, to assess its effects on sleep and its potential as a sleep-inducing drug.Materials and MethodsFor the electrocorticographic evaluation, seventy-two rats were randomly assigned to distinct groups: a control group, a sleep-deprived group, three sleep-deprived groups receiving 10, 20, and 30 mg/kg i.p. of camphor respectively, and three groups that received these doses without sleep deprivation. For the behavioral analysis, twenty-seven rats were divided into three groups, each receiving the same doses as the previous test.Results and DiscussionOur results showed that there was a decrease in the frequency of brain oscillatory patterns when camphor was administered at 10 mg/kg i.p. whereas there was a dose-dependent increase in the spectral power and distribution following the administration of 20 and 30 mg/kg i.p., with the emergence of Delta, Theta, Alpha, and Beta waves. As for the behavioral analysis, it was demonstrated that testicular relaxation, decreased motility, and light sleep induction also occurred in a dose-dependent manner. Thus, we conclude that camphor administration intensifies occipital electrocorticographic patterns in sleep-deprived rats, and its electrocorticographic and behavioral analysis could indicate a potential as a supporting agent in the insomnia treatment.

Examining the impact of sleep deprivation on medical reasoning’s performance among anaesthesiology residents and doctors: a prospective study

BackgroundWorking long consecutive hours’ is common for anaesthesia and critical care physicians. It is associated with impaired medical reasoning’s performance of anaesthesiology and serious medical errors. However, no study has yet investigated the impact of working long consecutive hours’ on medical reasoning.ObjectiveThe present study evaluated the impact of working long consecutive hours’ on the medical reasoning’s performance of anaesthesiology and intensive care physicians (residents and seniors).MethodsThis multicentric, prospective, cross-over study was conducted in 5 public hospitals of Normandy region. Two groups of anaesthesia and critical care physicians were formed. One was in a rest group, RG (after a 48-hours weekend without hospital work) and the other in Sleep Deprivation Group (SDG) after a 24 h-consecutives-shift. Changes in medical reasoning’s performance were measured by 69-items script concordance tests (SCT) through to the two tests. Group A completed the first part of the assessment (Set A) after a weekend without work and the second part (Set B) after a 24 h-shift; group B did the same in reverse order. The primary outcome was medical reasoning’s performance as measured by SCT in RG and SDG. The secondary outcomes included association between the performance with the demographic data, variation of the KSS (Karolinska sleepiness scale) daytime alertness score, the number of 24 h-shift during the previous 30 days, the vacations during the previous 30 days, the presence of more or less than 4 h consecutives hours slept, the management of a stressful event during the shift, the different resident years, the place where the shift took place (University hospital or general hospitals) and the type of shift (anaesthesia or intensive care).Results84 physicians (26 physicians and 58 residents) were included. RG exhibited significantly higher performance scores than SDG (68 ± 8 vs. 65 ± 9, respectively; p = 0.008). We found a negative correlation between the number of 24 h-shifts performed during the previous month and the variation of medical reasoning’s performance and no significant variation between professionals who slept 4 h or less and those who slept more than 4 h consecutively during the shift (-4 ± 11 vs. -2 ± 11; p = 0.42).ConclusionOur study suggests that medical reasoning’ performance of anaesthesiologists, measured by the SCT, is reduced after 24 h-shift than after rest period. Working long consecutive hours’ and many shifts should be avoided to prevent the occurrence of medical errors.

Exploring the protective role of green tea extract against cardiovascular alterations induced by chronic REM sleep deprivation via modulation of inflammation and oxidative stress

BackgroundChronic Rapid eye movement (REM) sleep deprivation has been associated with various cardiovascular alterations, including disruptions in antioxidant defense mechanisms, lipid metabolism, and inflammatory responses. This study investigates the therapeutic potential of green tea extract (GTE) in mitigating these adverse effects.MethodsA total of 24 male Wistar albino rats were used in this study and divided into the control group (n = 8), Chronic-REM Sleep Deprivation (CRSD) Group (n = 8) and Chronic-REM SD + Green Tea 200 (CRSD + GTE200) Group (n = 8). After 21 days, a comprehensive analysis of paraoxonase (PON1), arylesterase (ARE), malondialdehyde (MDA), glutathione (GSH), nitric oxide (NOx), proinflammatory cytokines, and lipid profiles in aortic tissue, heart tissue, and serum was conducted in a sleep-deprived rat model.ResultsChronic REM sleep deprivation led to a significant reduction in PON1 and ARE levels in aortic (p = 0.046, p = 0.035 respectively) and heart tissues (p = 0.020, p = 0.019 respectively), indicative of compromised antioxidant defenses. MDA levels increased, and NOx levels decreased, suggesting oxidative stress and impaired vascular function. Lipid profile alterations, including increased triglycerides and total cholesterol, were observed in serum. Elevated levels of inflammatory cytokines (IL-6 and TNF-alpha) further indicated an inflammatory response (p = 0.007, p = 0.018 respectively). GTE administration demonstrated a protective role, restoring antioxidant enzyme levels, suppressing lipid peroxidation, and improving NOx levels.ConclusionThese findings suggest the therapeutic potential of GTE in alleviating the cardiovascular impairments of chronic REM sleep deprivation, emphasizing its candidacy for further clinical exploration as a natural intervention in sleep-related disorders and associated cardiovascular risks.

Electroacupuncture inhibits hippocampal oxidative stress and autophagy in sleep-deprived rats through the protein kinase B and mechanistic target of rapamycin signaling pathway.

To investigate the effects of acupuncture on learning and memory impairment, oxidative stress and autophagy induced by sleep depriv ation in rats, and to analyze the related mechanism. Thirty Wistar rats were randomly divided into a normal group, sleep deprivation group and acupuncture group. The rat model of sleep deprivation was established by a modified multiplatform sleep deprivation method. The Baihui (GV20), Shenmen (HT7) and Sanyinjiao (SP6) acupoints of rats were located to give electroacupuncture (density wave, frequency 20 Hz, intensity 1 mA) to maintain the needle feeling, and to keep the needle for 15 min and continuous acupuncture for 7 d. The spatial learning and memory abilities of the rats were detected by the water maze test. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPX) in the brain were detected by an assay kit, and the autophagy related proteins light chain 3 alpha (LC3A), light chain 3 beta (LC3B) and Beclin 1 and the activation of the protein kinase B (PKB/AKT) and mechanistic target of rapamycin (mTOR) signaling pathway in the rat's brain were detected by Western blotting. Compared with the normal group, the time spent in the target quadrant (P < 0.05) and the number of times entering the target quadrant (P < 0.05) in the rats of sleep deprivation group were significantly reduced, and the content of MDA was significantly increased (P < 0.01), while the activities of SOD and GPX (P < 0.01) in the brain were significantly decreased, and LC3A Ⅱ/Ⅰ, LC3B Ⅱ/Ⅰ and Beclin 1 increased significantly (P < 0.01), while p-AKT (ser473)/AKT, p-mTOR (ser2448)/mTOR and p-p70s6K (thr389)/p70S6 decreased significantly (P < 0.01). Compared with the sleep deprivation group, the time spent in the target quadrant and the times of entering the target quadrant (P < 0.05) in the rats of acupuncture group after 7 d of treatment were significantly increased, Additionally, the content of MDA was significantly decreased (P < 0.05), while the activities of SOD and GPX (P < 0.05) in the brain were significantly increased. Moreover, the levels of LC3A Ⅱ/Ⅰ, LC3BⅡ/Ⅰ and Beclin 1 decreased significantly (P < 0.05), and that of p-AKT (ser473)/AKT, p-mTOR (ser2448)/mTOR and p-p70s6K (thr389)/p70s6k increased significantly (P < 0.05). Acupuncture can significantly improve the learning and memory damage caused by sleep deprivation and inhibit oxidative stress and autophagy, and its effect is related to the activation of AKT/mTOR signaling.

Safflower Improves Memory, Learning, and Behavior in Rats Subjected to Sleep Deprivation.

Sleep is a physiological process that provides the body with a window for recovery and restoration. Intriguingly, even short-term sleep deprivation can impair brain memory, emotional capacity, information processing, and attention. Safflower (Carthamus tinctorius L.) has been shown to attenuate memory loss and improve anxiety and depression. This study aims to study the possible therapeutic effect of safflower on sleep deprivation-dependent effects on memory and behavior. Thirty young male Wistar albino rats were acclimatized, trained, and then assigned to three random groups: control (C), sleep-deprived (SD), and sleep-deprived Safflower-treated (SD+Sf) groups. Morris Water Maze (MWM) and Elevated Plus Maze (EPM) tests were used to study spatial memory and learningand anxiety-related behavior, respectively, in the study groups. There was a significant deterioration in learning and memory, as tested by the MWM in the SD group, compared to the C group. This included prolonged test duration, reduced average speed, and longer travel distance. Treatment with safflower significantly improved MWM test performance in the SD+Sf group when compared to the SD group. When compared to the C group, rats in the SD group demonstrated altered EPM test parameters suggestive of anxiety-like behavior. These included spending more time in the closed arms, spending less time in the open arms, and having fewer entries in the open arms. Rats in the SD+Sf group showed improved EPM test parameters when compared to the SD group. Safflower significantly ameliorated sleep deprivation induced by memory loss and altered behavior. Safflower supplementation may provide potential memory-enhancing and preserving, anxiolytic, and antidepressant therapeutic roles.

Modifications in the Composition of the Gut Microbiota in Rats Induced by Chronic Sleep Deprivation: Potential Relation to Mental Disorders.

Sleep deprivation(SD) has numerous negative effects on mental health. A growing body of research has confirmed the implication of gut microbiota in mental disorders. However, the specific modifications in mammalian gut microbiota following SD exhibit variations across different studies. Male specific-pathogen-free Wistar rats were given a modified multiple-platform exposure for 7 days of SD. Fecal samples were obtained from the control and SD groups both at baseline and after 7 days of SD. We utilized 16S rDNA gene sequencing to investigate the gut microbial composition and functional pathways in rats. Analysis of the microbiota composition revealed a significant change in gut microbial composition after chronic SD, especially at the phylum level. The relative abundances of p_Firmicutes, g_Romboutsia, and g_Enterococcus increased, whereas those of p_Bacteroidetes, p_Verrucomicrobia, p_Fusobacteria, g_Akkermansia, and g_Cetobacterium decreased in animals after chronic SD compared with controls or animals before SD. The ratio of Firmicutes to Bacteroidetes exhibited an increase following SD. The relative abundance of gut microbiota related to the functional pathways of GABAergic and glutamatergic synapses was observed to be diminished in rats following SD compared to pre-SD. Collectively, these findings suggest that chronic SD causes significant alterations in both the structural composition and functional pathways of the gut microbiome. Further researches are necessary to investigate the chronological and causal connections among SD, the gut microbiota and mental disorders.

Abstract Tu063: Acute sleep deprivation induces cardiac remodeling via activation of AT1R/ERK/GSK-3β signaling

Background: Sleep deprivation (SD) has an adverse effect on cardiovascular system. However, whether acute SD contributes to the morphological and functional changes of the heart remains unclear. Approach and Results: The modified multiple platform method (MMPM) was used to establish the SD model in Sprague-Dawley rats. Acute SD significantly enhanced cardiac ejection fraction and fractional shortening in rats as observed by echocardiography. The elevated ratio of heart weight to body weight (HW/BW) and enlarged cross-section area of cardiomyocytes by WGA staining were detected in SD groups (3, 7,10 days). The upregulation of ANP and BNP was also detected by western blotting. Masson-trichrome staining showed significant fibrosis in the SD groups, which was confirmed by western blotting of the fibrosis markers α-SMA and collagen 1. Furthermore, SD increased the level of angiotensin II (Ang II) and angiotensin type 1 receptor (AT1R) in the heart tissue of SD groups accompanied by the activation of the ERK/GSK-3β pathway. Administration of valsartan and benazepril dramatically ameliorated SD-induced cardiac fibrosis and hypertrophy by downregulating Ang II/AT1R and phosphor-ERK/GSK-3β levels. Conclusion: Our results indicated that cardiac remodeling was induced by the acute and short duration of SD, in which the AT1R/ ERK/GSK3β signal pathway was involved. Our study demonstrates a novel complementary phenomenon induced by SD and provides detailed evidence for the risk of SD on the cardiovascular system.

Impact of chronic sleep deprivation on male reproductive health: Insights from testicular and epididymal responses in mice.

Sleep deprivation (SD) can cause damage to the male reproductive system. However, the duration required for such damage and the specific sequence and severity of damage to the testis and epididymis remain unclear. To investigate the effects of different durations of SD on different parts of the testis and epididymis caput, corpus, and cauda. Adult ICR mice were randomly assigned to five groups: the SD group (SD for 18h/day for 1, 2, 3, or 4weeks), the SD + Vit E group (supplemented with Vit E 50mg/kg/d during 4weeks of SD, the SD+NS group (saline supplementation during 4weeks of SD), the SD + RS group (5weeks of recovery sleep after 4weeks of SD), and a normal sleep control (Ctrl) group. Following the interventions, sperm parameters, testicular and epididymal histopathology, inflammatory response, and oxidative stress markers were compared between the groups. Compared to the Ctrl group, the SD group showed a decrease in sperm motility and concentration from SD 2W and SD 3W, respectively. Decreases in sperm concentration and motility were more pronounced in the cauda compared to the caput and corpus. Pathological damage was less severe in the epididymis caput than in the corpus and cauda. After 4weeks of SD, inflammation and oxidative stress increased in both testes and epididymis. Both sleep recovery and vitamin E supplementation showed significant improvements, though they did not fully reach the level of the Ctrl group. Chronic SD for more than 2weeks causes varying degrees of damage to the testis, epididymis caput, corpus, and cauda in male mice. This damage is not fully reversible after 5weeks of sleep recovery and antioxidant stress treatment. These findings help us to identify and prevent SD damage to the male reproduction at an early stage.

Effects of Schisandrae Chinensis Fructus Lignans on Alertness of Rats With Sleep Deprived by Treadmill Exercise

Objective To investigate the effects of Schisandrae Chinensis Fructus lignans on the alertness of the rats with sleep deprived by treadmill exercise and the underlying neurobiological mechanism. Methods According to the random number table method,SD male rats were assigned into control,sleep deprivation,low-,medium-,and high-dose Schisandrae Chinensis Fructus lignans,and atomoxetine hydrochloride groups,with 8 rats in each group.The rats in other groups except the control group were subjected to sleep deprivation by treadmill exercise for 3 d.During the deprivation period,each administration group was administrated with the corresponding drug by gavage,and a 5-9 hole tester was used to test the alertness performance of rats in each group. Furthermore,other SD male rats were selected and randomized into control,sleep deprivation,Schisandrae Chinensis Fructus lignans (67.2 mg/kg) and atomoxetine hydrochloride groups,with 10 rats in each group.The rats were modeled with the sleep deprivation method the same as that above and administrated with corresponding agents.ELISA was employed to measure the serum level of orexin A in each group of rats.The protein levels of c-Fos,orexin receptor 1,and orexin receptor 2 in the prefrontal cortex of rats in each group were observed by immunofluorescence and Western blotting. Results Compared with the control group,sleep deprivation reduced the choice accuracy (P<0.001) and increased the omission responses,omission percent,and mean correct response latency (P=0.002,P=0.003,P=0.020).Compared with the sleep deprivation group,medium- and high-dose Schisandrae Chinensis Fructus lignans and atomoxetine hydrochloride improved the alertness of rats,as demonstrated by the increased choice accuracy (P=0.001,P=0.006,P<0.001) and reduced omission responses (P=0.001,P=0.001,P<0.001),omission percent (P=0.001,P=0.002,P<0.001),and mean correct response latency (P=0.018,P=0.003,P=0.014).Compared with the control group,the sleep deprivation group showed elevated level of orexin A in the serum (P<0.001),up-regulated expression of c-Fos (P<0.001),and down-regulated expression of orexin receptor 1 (P=0.037) in the prefrontal cortex.Compared with the sleep deprivation group,Schisandrae Chinensis Fructus lignans (67.2 mg/kg) and atomoxetine hydrochloride lowered the orexin A level in the serum (P=0.005,P=0.029),down-regulated the expression of c-Fos (P=0.028,P=0.036),and up-regulated the expression of orexin receptor 1 (P=0.043,P=0.013) in the prefrontal cortex. Conclusion Schisandrae Chinensis Fructus lignans may antagonize the alertness decrease caused by sleep deprivation by regulating the secretion of orexin and the expression of orexin receptor 1 in the prefrontal cortex.

Chronic sleep deprivation, noise and high fat diet markedly induce C-reactive protein level in mice model

Background: C-reactive protein (CRP) is a circulating sign of systemic chronic inflammation that your liver produces if your body is inflamed. Stressful events over a long period of time are linked to inflammatory disorders. Stress pathways are triggered by noise and sleep deprivation, as well as unhealthy habits like fatty meals. Several studies have connected higher CRP levels with plasma levels. The current study aims to explore the potential association’s relationship between chronic sleep deprivation, noise, high fat diet, and CRP disorders.Methods: Three studies were carried out in our study to evaluate C-reactive protein levels in male Swiss albino mice groups after exposure to three different physical stressors for four weeks. The first study mice group were exposed to chronic sleep deprivation; second group was exposed to electrostatic speaker noise stressors; and the third group was fed a high fat diet. Quantitative estimation of C – reactive protein level in plasma using an ELISA kit.Results: Significant changes in inflammatory CRP levels in the examined plasma were detected in the sleep deprivation group. CRP levels were found to be steadily increasing after two weeks, reaching a significant peak in the fourth week (p &lt; 0.001). Moreover, in the fourth week, there were substantial increases in CRP plasma level with independent evidence, in the experimental noise group (p &lt; 0.001). As well, the biomarker of inflammation level increased across the dietary high density fat diet, reaching the highest level at the end of the study (p &lt; 0.05).Conclusion: Our findings contribute to the body of evidence indicating a link between external stress and subclinical inflammatory markers. Furthermore, CRP concentrations are triggered by chronic sleep deprivation and noise exposure, and their concentrations rise with prolonged dietary fatty acid consumption.Keywords: Sleep deprivation; Noise; High fat diet; Inflammation; CRP

Investigation of the structural changes in the hippocampus and prefrontal cortex using FTIR spectroscopy in sleep deprived mice

Sleep is a basic, physiological requirement for living things to survive and is a process that covers one third of our lives. Melatonin is a hormone that plays an important role in the regulation of sleep. Sleep deprivation affect brain structures and functions. Sleep deprivation causes a decrease in brain activity, with particularly negative effects on the hippocampus and prefrontal cortex. Despite the essential role of protein and lipids vibrations, polysaccharides, fatty acid side chains functional groups, and ratios between amides in brain structures and functions, the brain chemical profile exposed to gentle handling sleep deprivation model versus Melatonin exposure remains unexplored. Therefore, the present study, aims to investigate a molecular profile of these regions using FTIR spectroscopy measurement’s analysis based on lipidomic approach with chemometrics and multivariate analysis to evaluate changes in lipid composition in the hippocampus, prefrontal regions of the brain. In this study, C57BL/6J mice were randomly assigned to either the control or sleep deprivation group, resulting in four experimental groups: Control (C) (n = 6), Control + Melatonin (C + M) (n = 6), Sleep Deprivation (S) (n = 6), and Sleep Deprivation + Melatonin (S + M) (n = 6). Interventions were administered each morning via intraperitoneal injections of melatonin (10 mg/kg) or vehicle solution (%1 ethanol + saline), while the S and S + M groups underwent 6 h of daily sleep deprivation from using the Gentle Handling method. All mice were individually housed in cages with ad libitum access to food and water within a 12-hour light–dark cycle. Results presented that the brain regions affected by insomnia. The structure of phospholipids, changed. Yet, not only changes in lipids but also in amides were noticed in hippocampus and prefrontal cortex tissues. Additionally, FTIR results showed that melatonin affected the lipids as well as the amides fraction in cortex and hippocampus collected from both control and sleep deprivation groups.

Sleep deprivation increases the generalization of perceptual and concept-based fear: An fNIRS study

Insufficient sleep can initiate or exacerbate anxiety by triggering excessive fear generalization. In this study, a de novo paradigm was developed and used to examine the neural mechanisms governing the effects of sleep deprivation on processing perceptual and concept-based fear generalizations. A between-subject design was adopted, wherein a control group (who had a typical night's sleep) and a one-night sleep deprivation group completed a fear acquisition task at 9:00 PM on the first day and underwent a generalization test the following morning at 7:00 AM. In the fear acquisition task, navy blue and olive green were used as perceptual cues (P+ and P−, respectively), while animals and furniture items were used as conceptual cues (C+ and C−, respectively). Generalization was tested for four novel generalized categories (C+P+, C+P−, C−P+, and C−P−). Shock expectancy ratings, skin conductance responses, and functional near-infrared spectroscopy were recorded during the fear acquisition and generalization processes. Compared with the group who had a typical night's sleep, the sleep deprived group showed higher shock expectancy ratings (especially for P+ and C−), increased oxygenated hemoglobin in the dorsolateral prefrontal cortex, and increased activation in the triangular inferior frontal gyrus during the generalization test. These findings suggest that sleep deprivation increases the generalization of threat memories, thus providing insights into the overgeneralization characteristics of anxiety and fear-related disorders.

Comparison between sub-chronic and chronic sleep deprivation-induced behavioral and neuroimmunological abnormalities in mice: Focusing on glial cell phenotype polarization

BackgroundSleep disorders, depression, and Alzheimer’s disease (AD) are extensively reported as comorbidity. Although neuroinflammation triggered by microglial phenotype M1 activation, leading to neurotransmitter dysfunction and Aβ aggregation, is considered as the leading cause of depression and AD, whether and how sub-chronic or chronic sleep deprivation (SD) contribute to the onset and development of these diseases remains unclear. MethodsMemory and depression-like behaviors were evaluated in both SDs, and then circadian markers, glial cell phenotype polarization, cytokines, depression-related neurotransmitters, and AD-related gene/protein expressions were measured by qRT-PCR, enzyme-linked immunosorbent assay, high-performance liquid chromatography, and western-blotting respectively. ResultsBoth SDs induced give-up behavior and anhedonia and increased circadian marker period circadian regulator 2 (PER2) expression, which were much worse in chronic than in the sub-chronic SD group, while brain and muscle ARNT-like protein-1 only decreased in the chronic-SD. Furthermore, increased microglial M1 and astrocyte A1 expression and proinflammatory cytokines, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α was observed in both SDs, which were more significant in chronic SD. Similarly, decreased norepinephrine and 5-hydroxytryptamine/5-hydroxyindoleacetic acid ratio were more significant, which corresponds to the worse depression-like behavior in chronic than sub-chronic-SD. With regard to AD, increased amyloid precursor protein (APP) and soluble (s)-APPβ and decreased sAPPα in both SDs were more significant in the chronic. However, sAPPα/sAPPβ ratio was only decreased in chronic SD. ConclusionThese findings suggest that both SDs induce depression-like changes by increasing PER2, leading to neuroinflammation and neurotransmitter dysfunction. However, only chronic SD induced memory impairment likely due to severer circadian disruption, higher neuroinflammation, and dysregulation of APP metabolism

Sleep deprivation reduces the baroreflex sensitivity through elevated angiotensin (Ang) II subtype 1 receptor expression in the nucleus tractus solitarii.

Sleep insufficiency has been linked to an increased risk of high blood pressure and cardiovascular diseases. Emerging studies have demonstrated that impaired baroreflex sensitivity (BRS) is involved in the adverse cardiovascular effects caused by sleep deprivation, however, the underlying mechanisms remain unknown. Therefore, the present study aims to clarify the role of abnormal renin-angiotensin system in the nucleus tractus solitarii (NTS) in impaired BRS induced by sleep deprivation. Rats were randomly divided into two groups: normal sleep (Ctrl) and chronic sleep deprivation (CSD) group. Rats were sleep deprived by an automated sleep deprivation system. The blood pressure, heart rate, BRS, the number of c-Fos positive cells and the expression of angiotensin (Ang) II subtype 1 receptors (AT1R) in the NTS of rats were assessed. Compared to Ctrl group, CSD group exhibited a higher blood pressure, heart rate, and reduced BRS. Moreover, the number of c-Fos positive cells and local field potential in the NTS in CSD group were increased compared with the Ctrl group. It was shown that the expression of the AT1R and the content of Ang II and the ratio of Ang II to Ang-(1-7) were increased in the NTS of rats in CSD group compared to Ctrl group. In addition, microinjection of losartan into the NTS significantly improved the impaired BRS caused by sleep deprivation. In conclusion, these data suggest that the elevated AT1R expression in the NTS mediates the reduced BRS induced by chronic sleep deprivation.

Brain vital sign monitoring of sleep deprivation detects situational cognitive impairment.

Objective, rapid evaluation of cognitive function is critical for identifying situational impairment due to sleep deprivation. The present study used brain vital sign monitoring to evaluate acute changes in cognitive function for healthy adults. Thirty (30) participants were scanned using portable electroencephalography before and after either a night of regular sleep or a night of total sleep deprivation. Brain vital signs were extracted from three established event-related potential components: (1) the N100 (Auditory sensation); (2) the P300 (Basic attention); and (3) the N400 (Cognitive processing) for all time points. As predicted, the P300 amplitude was significantly reduced in the sleep deprivation group. The findings indicate that it is possible to detect situational cognitive impairment due to sleep deprivation using objective, rapid brain vital sign monitoring.

Differentially expressed genes of esophageal tissue in male acute and chronic sleep deprivation mice.

Gastroesophageal reflux disease (GERD) is associated with sleep disturbances. However, mechanisms underlying these interactions remain unclear. Male acute and chronic sleep deprivation (SD) mice were used for this study. Mice in the chronic SD group exhibited anxiety- and depression-like behaviors. We further performed high-throughput genome sequencing and bioinformatics analysis to screen for featured differentially expressed genes (DEGs) in the esophageal tissue. The acute SD group, comprised 25 DEGs including 14 downregulated and 11 upregulated genes. Compared with the acute SD group, more DEGs were present in the chronic SD group, with a total of 169 DEGs, including 88 downregulated and 81 upregulated genes. Some DEGs that were closely related to GERD and associated esophageal diseases were significantly different in the chronic SD group. Quantitative real-time polymerase chain reaction verified the downregulation of Krt4, Krt13, Krt15 and Calml3 and upregulation of Baxl1 and Per3. Notably, these DEGs are involved in biological processes, which might be the pathways of the neuroregulatory mechanisms of DEGs expression.

Effects of sleep deprivation and hazard types on the hazard perception of young novice drivers: An ERP study

ObjectiveThe present study aimed to explore the effects of sleep deprivation on young novice drivers’ cognitive neural processing of different hazard types. MethodA 2 (sleep deprivation group, control group) × 3 (no hazard, covert hazard, overt hazard) mixed experimental design was used. Twenty-eight young drivers were sleep-deprived (no sleep within the past 24 h), while 28 drivers were in the control group (maintaining a normal schedule throughout the week). Eighty pictures containing a covert hazard (20 pictures), overt hazard (20 pictures) and no hazard (40 pictures) were presented. Participants were asked to press the keyboard quickly if they detected a hazard situation. The reaction time, accuracy, and changes in the N1 (100–150 ms) and N2 (250–350 ms) components of event-related potentials (ERP) measured using electroencephalography (EEG) were obtained. ResultsCompared to the control group, the response accuracy of sleep-deprived drivers was higher in the cover-hazard situation and their N1 latency was longer in the no-hazard situation. Compared to the no-hazard and overt-hazard situations, the participants’ reaction times and N2 amplitudes were significantly greater, and the response accuracy was significantly lower in the covert-hazard situation. ConclusionHazard perception is compromised when drivers are sleep-deprived, especially when they are confronted with covert hazard situations. The findings help understand the negative effects of sleep deprivation in the early stage of young novice drivers’ hazard perception.

Sleep deprivation from mid-gestation leads to impaired of motor coordination in young offspring mice with microglia activation in the cerebellar vermis

ObjectiveTo investigate the effects of mid-pregnancy sleep deprivation (SD) in C57BL/6 J mice on the motor coordination of the offspring and to explore the potential mechanism of microglia activation in the cerebellar vermis of the offspring involved in the induction of impaired motor coordination development. MethodsC57BL/6 J pregnant mice were randomly divided into the SD and control groups. SD was implemented by the multi-platform method from first day of the middle pregnancy (gestation day 8, GD8). At postnatal day 21 (PND21), we measured the development of motor behavior and collected cerebellar vermis tissues to observe the activation of microglia by H&E staining, the expression of microglia-specific markers ionized calcium-binding adaptor molecule-1 (Iba-1) and cluster of differentiation 68 (CD68) by immunohistochemical, and interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor -α (TNF-α) by real-time quantitative PCR (RT-qPCR). ResultsIn the offspring of SD group, comparing to the control group, the total time of passage and the reverse crawl distance in the balance beam test, and the frequency of falls from the suspension cord was increased; with lower max rotational speed and shorter duration in the rotarod experiment. Further, we found that the microglia of cerebellar vermis tissues emerged an amoeba-like activation. The mean gray value of Iba-1 was lower, the density of positive cells of CD68 and the expression levels of IL-6 and TNF-α were increased. ConclusionsThe motor coordination of offspring is impaired, accompanying a SD from mid-pregnancy, and the cerebellar vermis showed microglia activation and pro-inflammatory response. It suggested the adverse effects of SD from mid-gestation on the development of motor coordination through the inflammatory response in the cerebellar vermis of the offspring.

Sleep Pattern Interference in the Cognitive Performance of Lusitano Horses.

Like most mammalian, polyphasic sleep, equine sleep can be divided into two phases: the REM (rapid eye movement) phase and the NREM (non-rapid eye movement) phase. For this study, a randomized crossover experiment was conducted using ten purebred Lusitano horses, all dressage athletes aged from three to seven years old. The horses were filmed before the intervention to characterize their sleep patterns. REM sleep deprivation was achieved by not letting the horses attain sternal or lateral recumbency for three consecutive days, totaling 72 h. A spatial memory task and a visual attention test were performed. A recording time of 48 h appeared to be long enough to characterize the sleep patterns of the stalled horses. The total recumbency time of the studied population was lower than that previously reported in horses. Although the recumbency times before and after the intervention were similar, there was a tendency shown by the delta (p = 0.0839) towards an increased time needed to resolve spatial memory tasks in the sleep-deprived group. Future studies may deepen the understanding of horse sleep requirements and patterns, and the effects of environmental changes on horse sleep.

Sleep deprivation effects on EGFR signaling in a zebrafish exposed to rotenone

The objective of this study was to investigate the effects of exposure to rotenone, sleep deprivation, and the epidermal growth factor receptor (EGFR) inhibitor on the locomotor activity of zebrafish larvae. Observations were conducted on control groups, sleep-deprived groups without interventions, groups treated with rotenone or the EGFR inhibitor alone, and also groups with combined exposures. The results showed that sleep deprivation alone led to a decrease of speed of the locomotor activity compared to the control groups. The treatment with rotenone alone resulted in varied effects on the locomotor activity. However, a combined exposure to rotenone and sleep deprivation further reduced the locomotor activity compared to the control and rotenone-treated groups. The groups treated with the EGFR inhibitor alone exhibited variable effects on the locomotor activity. Furthermore, the combined exposure to the EGFR inhibitor and sleep deprivation resulted in diverse changes in the locomotor activity. However, the combined treatment with rotenone and the EGFR inhibitor produced complex alterations in the locomotor activity.These findings demonstrate the distinct effects of exposure to rotenone, sleep deprivation, and the EGFR inhibitor on the locomotor activity of zebrafish larvae. The interaction between these factors further modulates locomotor activity, suggesting a potential interplay between the EGFR system, sleep regulation, and the dopaminergic system. Understanding the relationship between the EGFR system, sleep regulation, and neurological regulation may contribute to the development of therapeutic strategies to address such issues as sleep disorders and neurodegenerative conditions.