Total Sleep Deprivation Group Research Articles

Sleep recovery ameliorates submandibular salivary gland inflammation associated with paradoxical sleep deprivation in male Wistar rats.

Submandibular salivary gland inflammation has been suggested as one of the mechanisms underlying impaired salivary secretion associated with sleep deprivation (SD). However, whether the salivary inflammatory response occurs to the same extent in paradoxical sleep deprivation with or without sleep recovery remains unknown. This study evaluated the extent to which inflammation influences salivary impairments associated with paradoxical sleep deprivation with or without sleep recovery. Male Wistar rats were randomly assigned into three groups as control, partial SD (PSD) with sleep recovery for four hours a day and total SD (TSD). Paradoxical SD was carried out for seven days in the SD groups, after which saliva, blood, and submandibular gland samples were taken. Levels of interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), and nitrite were determined in saliva, serum, and the submandibular salivary gland. Leucocyte count and neutrophil-lymphocyte ratio were determined in all groups. One-way ANOVA and the Tukey's post hoc tests were used for data analysis. P-values < 0.05 were considered statistically significant. Levels of TNF-α, IL-6, and nitrite in the submandibular salivary glands were significantly higher in the TSD groups (p=0.04,p<0.001, p=0.03, respectively) than in the control. Saliva level of TNF-α was higher in the PSD and TSD groups (p=0.003 and p=0.01 respectively) than in the control. Neutrophil-lymphocyte ratio was significantly higher in both PSD and TSD groups than in the control (p<0.01 for both). While total SD produced higher inflammatory response in the submandibular salivary gland, four-hour sleep recovery ameliorated this impact. This finding suggests that sleep recovery is crucial to improve inflammatory salivary gland dysfunction induced by sleep deprivation.

Maternal total sleep deprivation causes oxidative stress and mitochondrial dysfunction in oocytes associated with fertility decline in mice.

Previous studies have shown sleep deprivation is increasingly reported as one of the causes of female infertility. However, how and by what relevant mechanisms it affects female fertility remains unclear. In this study, female mice underwent 72 hours of total sleep deprivation (TSD) caused by rotating wheel or 2 different controls: a stationary wheel, or forced movement at night. Even though, there was no significant difference in the number of eggs ovulated by the TSD mice compared to the control groups. Overall levels of estrogen and FSH were lower throughout the estrus cycle. A total of 42 genes showed significant differential expression in GV oocytes after TSD by RNA sequencing (RNA-Seq). These included genes were enriched in gene ontology terms of mitochondrial protein complex, oxidoreductase activity, cell division, cell cycle G1/S phase transition, as well as others. The increased concentrations of reactive oxygen species (ROS) in germinal vesicle (GV) and metaphase II (MII) oocytes from TSD mice were observed, which might be induced by impaired mitochondrial function caused by TSD. The GV oocytes displayed increased mitochondrial DNA (mtDNA) copy number and a significant transient increase in inner mitochondrial membrane potential (Δψm) from the TSD mice probably due to compensatory effect. In contrast, MII oocytes in the TSD group showed a decrease in the mtDNA copy number and a lower Δψm compared with the controls. Furthermore, abnormal distribution of mitochondria in the GV and MII oocytes was also observed in TSD mice, suggesting mitochondrial dysfunction. In addition, abnormal spindle and abnormal arrangement of chromosomes in MII oocytes were markedly increased in the TSD mice compared with the control mice. In conclusion, our results suggest that TSD significantly alters the oocyte transcriptome, contributing to oxidative stress and disrupted mitochondrial function, which then resulted in oocyte defects and impaired early embryo development in female mice.

Effect of Sleep Deprivation on the Number of Prefrontal Cortex Neuroglia Cells in Male White Rats (&lt;i&gt;Rattus norvegicus&lt;/i&gt;)

Stress induced by sleep deprivation can increase inflammation and oxidative stress, destroying the pyramidal and neuroglia cells in the prefrontal cerebral cortex and interrupting cognitive and behavioral functions. This study aims to observe the difference in the number of pyramidal and neuroglia cells in the prefrontal cortex of male white rats (Rattus norvegicus) after stress induction by paradoxical sleep deprivation (PSD) and total sleep deprivation (TSD). This study was conducted in the Anatomy Laboratory of the Faculty of Medicine, Universitas Jenderal Soedirman, from November 2019 to February 2020. The method of this study was a posttest-only design with a control group approach using ten rats for each group; that was control (K.I.), PSD (KII), and TSD (K.I.). PSD and TSD groups received sleep deprivation treatment for eight days for 20 hours/day and 24 hours/day, respectively. The mean pyramidal cell number decreased in the PSD (66.67±24.55) and TSD (65.90±34.91) compared to the control (77.10±26.11) group, but no significant differences were found between all groups (p&gt;0.05). The mean neuroglial cell number was lower in the PSD (97.78±28.17) and TSD (75.80±22.39) compared to the control (126.00±48.81). Post-hoc Bonferroni test showed a significant difference between control and TSD (p&lt;0.05) but not between control and PSD or PSD and TSD (p&gt;0.05). In conclusion, there was a significant difference in the number of neuroglial cells but not pyramidal cells in the prefrontal cortex of male white rats (Rattus norvegicus) after stress induction with total sleep deprivation (TSD).

Reduced Resting-State EEG Power Spectra and Functional Connectivity after 24 and 36 Hours of Sleep Deprivation.

Total sleep deprivation (TSD) leads to cognitive decline; however, the neurophysiological mechanisms underlying resting-state electroencephalogram (EEG) changes after TSD remain unclear. In this study, 42 healthy adult participants were subjected to 36 h of sleep deprivation (36 h TSD), and resting-state EEG data were recorded at baseline, after 24 h of sleep deprivation (24 h TSD), and after 36 h TSD. The analysis of resting-state EEG at baseline, after 24 h TSD, and after 36 h TSD using source localization analysis, power spectrum analysis, and functional connectivity analysis revealed a decrease in alpha-band power and a significant increase in delta-band power after TSD and impaired functional connectivity in the default mode network, precuneus, and inferior parietal lobule. The cortical activities of the precuneus, inferior parietal lobule, and superior parietal lobule were significantly reduced, but no difference was found between the 24 h and 36 h TSD groups. This may indicate that TSD caused some damage to the participants, but this damage temporarily slowed during the 24 h to 36 h TSD period.

Effects of total sleep deprivation on sensorimotor gating in humans

Sensorimotor gating is a measure of pre-attentional information processing and can be measured by prepulse inhibition (PPI) of the startle reflex. Sleep deprivation has been shown to disrupt PPI in animals and humans, and has been proposed as an early phase 2 model to probe antipsychotic efficacy in heathy humans. To further investigate the reliability and efficacy of sleep deprivation to produce PPI deficits we tested the effects of total sleep deprivation (TSD) on PPI in healthy controls in a highly controlled sleep laboratory environment. Participants spent 4 days and nights in a controlled laboratory environment with their sleep monitored with polysomnography. Participants were randomly assigned to either normal sleep on all 4 nights (N = 17) or 36 h of TSD on the 3rd or 4th night (N = 40). Participants were assessed for sleepiness using the Karolinska Sleepiness Scale (KSS) and underwent a daily PPI task (interstimlulus intervals 30–2000 ms) in the evening. Both within-subject effects (TSD vs. normal sleep in TSD group alone) and between-subject effects (TSD vs. no TSD group) of TSD on PPI were assessed. TSD increased subjective sleepiness measured with the KSS, but did not significantly alter overall startle, habituation or PPI. Sleep measures including duration, rapid eye movement and slow wave sleep duration were also not associated with PPI performance. The current results show that human sensorimotor gating may not be reliably sensitive to sleep deprivation. Further research is required for TSD to be considered a dependable model of PPI disruption for drug discovery in humans.

Disturbance of REM sleep exacerbates microglial activation in APP/PS1 mice

Although both nonrapid eye movement (NREM) sleep loss and rapid eye movement (REM) sleep loss exacerbate Alzheimer’s disease (AD) progression, they exert different effects. Microglial activation can be beneficial or detrimental to AD patients under different conditions. However, few studies have investigated which sleep stage is the main regulator of microglial activation or the downstream effects of this activation. We aimed to explore the roles of different sleep phases in microglial activation and to investigate the possible effect of microglial activation on AD pathology. In this study, thirty-six 6-month-old APP/PS1 mice were equally divided into 3 groups: the stress control (SC), total sleep deprivation (TSD), and REM deprivation (RD) groups. All mice underwent a 48-hour intervention before their spatial memory was assessed using a Morris water maze (MWM). Then, microglial morphology, activation- and synapse-related protein expression, and inflammatory cytokine and amyloid β (Aβ) levels in hippocampal tissues were measured. We found that the RD and TSD groups exhibited worse spatial memory in the MWM tests. In addition, the RD and TSD groups showed greater microglial activation, higher inflammatory cytokine levels, lower synapse-related protein expression and more severe Aβ accumulation than the SC group, but there were no significant differences between the RD and TSD groups. This study demonstrates that disturbance of REM sleep may activate microglia in APP/PS1 mice. These activated microglia may promote neuroinflammation and engulf synapses but show a weakened ability to clear plaques.

Paradoxical effects from stimulus density manipulation provide new insight into the impact of sleep deprivation on PVT performance.

The psychomotor vigilance test (PVT), a 10-min one-choice reaction time task with random response-stimulus intervals (RSIs) between 2 and 10 s, is highly sensitive to behavioral alertness deficits due to sleep loss. To investigate what drives the performance deficits, we conducted an in-laboratory total sleep deprivation (TSD) study and compared performance on the PVT to performance on a 10-min high-density PVT (HD-PVT) with increased stimulus density and truncated RSI range between 2 and 5 s. We hypothesized that the HD-PVT would show greater impairments from TSD than the standard PVT. n = 86 healthy adults were randomized (2:1 ratio) to 38 h of TSD (n = 56) or corresponding well-rested control (n = 30). The HD-PVT was administered when subjects had been awake for 34 h (TSD group) or 10 h (control group). Performance on the HD-PVT was compared to performance on the standard PVTs administered 1 h earlier and 1 h later. The HD-PVT yielded approximately 60% more trials than the standard PVT. The HD-PVT had faster mean response times (RTs) and equivalent lapses (RTs > 500 ms) compared to the standard PVT, with no differences between the TSD effects on mean RT and lapses between tasks. Further, the HD-PVT had a dampened time-on-task effect in both the TSD and control conditions. Contrary to expectation, the HD-PVT did not show greater performance impairment during TSD, indicating that stimulus density and RSI range are not primary drivers of the PVT's responsiveness to sleep loss.

Effects of dopamine transporter in the ventral tegmental area on sleep recovery after propofol anesthesia in sleep-deprived rats

ObjectivePrevious studies indicate that propofol can help with recovery from sleep deprivation and has anti-anxiety effects. However, the underlying neurochemical mechanism remains unclear. This study aimed to investigate the effects of dopamine transporter (DAT) in the ventral tegmental area (VTA) on sleep and anxiety recovery after propofol anesthesia in rats with 24 h total sleep deprivation (TSD). MethodsAdult male Sprague-Dawley rats were in natural sleep or sleep deprived for 24 h in a sleep deprivation rat system. The rats received propofol anesthesia (75 mg/kg, i.p.) or natural sleep. Dopamine transporter knockdown was performed by microinjection of AAV-DAT-RNAi vector. EEG was measured in each group to evaluate the subsequent sleep. The elevated plus maze test (EPMT) and open field test (OFT) were used to evaluate locomotion and anxiety level in rats. Immunofluorescence was used to verify virus location and transfection efficiency. ResultsCompared with NC group, the anxiety level of Propofol group showed no significant difference, but REM sleep decreased. Compared with the TSD group, the anxiety level of the TSD + Propofol group was reduced and the sleep recovery was closer to baseline. Compared with TSD + AAV-NC group, anxiety level and sleep time increased in TSD + AAVi group, REM increased within 24 h after sleep deprivation. The sleep time of TSD + AAVi + Propofol group was between those of TSD + AAV-NC group and TSD + AAVi group. TSD + AAV-NC + Propofol group had the least sleep time and the lowest anxiety level. Conclusion1. Propofol did not change anxiety level in normal rats, but reduced REM sleep, while it could accelerate sleep recovery and reduce anxiety level in sleep-deprived rats. 2. In sleep deprived rats with DAT knockdown, propofol improved sleep and anxiety levels more slowly, especially producing more REM rebound, suggesting that the improvement of sleep and anxiety levels in sleep-deprived rats with propofol may be related to DAT in VTA region.

0119 Effects of Total Sleep Deprivation on Performance on a Continuous Performance Matching Task

Abstract Introduction Tasks requiring individuals to identify specific stimuli may create response/non-response conflict, which may impair performance depending on stimulus feature overlap. Whether sleep deprivation interacts with such impairment is unknown. We investigated the effects of total sleep deprivation (TSD) on stimulus identification in a continuous performance matching task (CPMT). Methods N=85 adults (ages 21–40; 50f) completed a 4-day laboratory study with 10h baseline sleep (22:00–08:00), a 38h acute TSD or 10h sleep opportunity (control condition), and 10h recovery sleep. The ~6min CPMT was administered every 2–4h during wakefulness. Participants completed 300 trials where a 3-digit number was flashed on the screen for 100ms. They were instructed to respond (mouse-click) within 900ms, but only if the number was the same as the preceding number (i.e., a repeat); for all other trials a response was to be withheld. The 5 daytime testing sessions (09:00–21:00) at baseline (day 2) and after TSD/control (day 3) were used for analysis. Trials were classified based on number of digits matching the preceding trial (stimulus feature overlap): none (180 trials), one (30 trials), two (near-repeat; 30 trials), or all (repeat; 60 trials). Hit and false alarm (FA) rates were analyzed with mixed-effects ANOVA for day, condition, trial type, and their interactions. Mean response time (MRT) was analyzed equivalently for repeat trials only. Results Hit rate declined from day 2 to day 3 in the TSD group (F[1,83]=0.15, p&amp;lt;0.001), but not the control group (F[1,83]=0.018, p=0.335). Though FA rate was low overall (&amp;lt;0.06), FA frequency was higher on trials with greater stimulus feature overlap. FA rate increased on day 3 for the TSD group (all p&amp;lt;0.004), especially for near-repeats (F[1,415]=-0.014, p&amp;lt;0.001). Changes in MRT were statistically significant, but negligible (&amp;lt;20ms). Conclusion Our results suggest that greater stimulus feature overlap on the CPMT was associated with greater costs required to resolve conflict. Sleep deprivation exacerbated these costs. Interpretation is limited however, because a response was not required for non-repeat trials. Implementing a two-alternative forced choice version of the task in future TSD studies would address this limitation. Support (If Any) PRMRP W81XWH-16-1-0319 and W81XWH-20-1-0442

0118 Performance on a Computerized Threat Elimination Task in an Animated Environment during Total Sleep Deprivation

Abstract Introduction Military and law enforcement operators must make split-second decisions on whether to shoot during confrontations. Quick responses are crucial when force is necessary, but accurate decision-making is also imperative. Often, decisions are made while fatigued, which could impair speed and/or accuracy. Furthermore, the reliability of background information may impact performance. We investigated performance on a computerized shooting task during a total sleep deprivation (TSD) study. Methods N=86 healthy adults (39 males, age 21-38) completed a 4-day/3-night in-laboratory study, randomly assigned to a TSD (n=56) or control (n=28) condition. A custom task was administered after 32h or 8h of wakefulness (TSD and control groups). Participants were to shoot enemy robots (press spacebar) and not shoot friendly robots (no response) within 500ms of each robot being revealed inside shipping crates (1-5s inter-trial-interval). The task introduction described which crates would contain enemies, but the intel’s accuracy varied across four phases: 100% (20 trials), 80% (120 trials), and 20% (40 trials), then irrelevant in a new environment (60 trials). Reaction time (RT) and accuracy (hits and false alarms (FAs)) were analyzed using 2x4 mixed-effects ANOVAs to determine the effects of condition, phase, and their interaction. Results There was a significant effect of phase on RT (p&amp;lt;0.001); in both conditions, participants reacted faster in phase 1 than all other phases. However, there was no effect of condition (p=0.20) or phase-condition interaction (p=0.080) on RT. There were significant effects of condition on hits (p&amp;lt;0.001) and FAs (p=0.004); TSD had fewer hits and more FAs than the control group. There was an effect of phase on hits (p=0.045), with fewer hits in phase 1, and a condition-phase interaction (p=0.026) showing that the TSD group experienced less improvement in hits. For FAs, there was no effect of phase (p=0.86) or phase-condition interaction (p=0.86). Conclusion The results suggest a speed/accuracy tradeoff during TSD, where relative to the control group, RTs remained equivalent, but accuracy was worse. In both groups, the RT slowing from phase 1 to subsequent phases, suggests that participants initially used the intel to facilitate quicker decision-making, but disregarded it once it was not completely reliable. Support (If Any) CDMRP grants W81XWH-16-1-0319 and W81XWH-20-1-0442

0125 Fluid Intelligence Does Not Mediate Cognitive Throughput Deficits during Total Sleep Deprivation

Abstract Introduction The Digit Symbol Substitution Test (DSST) has been used in sleep research to measure slowing of cognitive throughput. The task shows large aptitude differences in baseline performance and substantial inter-individual differences in vulnerability to performance deficits during total sleep deprivation (TSD). Fluid intelligence (Gf) is generally positively related to processing speed. However, DSST performance is typically found to be independent of Gf. The possible interaction of sleep loss with Gf on performance remains to be examined. Methods N=56 healthy adults (ages 22–37, 29 females) completed a 4-day/3-night in-laboratory study and were randomly assigned (2:1 ratio) to a TSD (n=37) or control (n=19) condition. Sleep opportunities were from 22:00–08:00 on the first (baseline) and last (recovery) night for the TSD group and on all three nights for the control group. Subjects completed a 4min, computerized DSST twice on day 2 (baseline) and twice on day 3 (TSD or control). At baseline, subjects also completed the Shipley Institute of Living Scale (SILS). The abstraction score was used to categorize fluid intelligence (Gf) as relatively high (≥34, n=36) or low (&amp;lt;34, n=20). Mean DSST throughput (number of correct responses in the 4min task) was analyzed using mixed-effects ANOVA with fixed effects for day (2, 3), condition (TSD, control), and their interaction, with and without Gf category (high, low) as a covariate. Results As expected, DSST throughput was significantly reduced by TSD (day by condition interaction: F[1,166]=27.99, p&amp;lt;0.001). Adding Gf had no effect on the day by condition interaction, and Gf category was not significant as a covariate (F[1,166]=1.67, p=0.20). Conclusion Our results indicate that the Gf measure from the SILS does not capture the aspects of cognition that are influenced by TSD and that lead to a decline in DSST throughput. This is consistent with findings that while the DSST has high sensitivity for cognitive dysfunction in clinical settings, it has low specificity in identifying components of cognition responsible for dysfunction. Support (If Any) ONR N00014-13-1-0302 and PRMRP W81XWH-20-1-0442.

The beneficial effects of green tea on sleep deprivation-induced cognitive deficits in rats: the involvement of hippocampal antioxidant defense

BackgroundThe weight of evidence suggests that sleep is essential for the processes of memory consolidation and sleep deprivation (SD) impairs the retention of long-term memory in both humans and experimental animals, which is associated with oxidative stress damage within the brain. Green tea polyphenols have revealed carcinogenic, antioxidant, anti-, and anti-mutagenic properties. We aimed to investigate the possible protective effect of green tea extract (GTE) and its main active catechin, epigallocatechin-3-gallate (EGCG), on post-training total sleep deprivation (TSD) -induced spatial memory deficits and oxidative stress profile in the hippocampus of the rat. MethodsMale rats were treated with saline, GTE (100 and 200 mg/kg/day), and EGCG (50 mg/kg/day) intraperitoneally for 21 days and then trained in Morris water maze (MWM) in a single day protocol. Immediately after the end of MWM training, animals were sleep deprived for 6 h by the gentle handling method, and then evaluated for spatial memory. Hippocampal levels of malondialdehyde, (MDA), and thiol was assessed as oxidant and antioxidant markers. ResultsSpatial memory was impaired in the TSD group and GTE at the dose of 200 mg/kg/day as well as EGCG at the dose of 50 mg/kg/day could reverse the impairment to the saline-treated levels. Despite the unchanged MDA levels, hippocampal total thiol was significantly decreased after TSD and EGCG increased it to the basal levels. ConclusionIn conclusion, green tea and its main catechin, EGCG, could prevent memory impairments during 6 h of TSD; probably through normalizing the antioxidant thiol defense system which was impaired during TSD.

The decrease of histomorphometry and function of pancreas in male albino rats after induced by sleep deprivation

Background: Sleep disturbance accelerates type 2 diabetes mellitus by reducing insulin secretion and by the occurrence of difficulty in controlling sleep behaviour in humans so that it is necessary conduct a study by using experimental animals.Objective: This study aims to determine histophotometric differences of pancreas and differences of glucose tolerance in male albino rats (Rattus norvegicus) after induced by stress paradoxical sleep deprivation (PSD) and total sleep deprivation (TSD). Methods: This study applied a post-test only with control groups consisting of 30 male albino rats (Wistar strain) divided randomly into 3 groups: control group, PSD group and TSD group. The mean number and diameter of islets of Langerhans were calculated per slide and were averaged for each group at a magnification of 400 X. The percentage of beta cells in one islet of Langerhans was (ß-p) that was a number of normal beta cells (Bn) divided for the total beta cells (Bt) (normal and damaged) x 100%. The glucose level based on the sampling time was made a curve shape, and the area under the 0-to-120-minute curves (AUC0-120) was calculated by using a trapezoidal formula.Results: The lowest AUC0-120 level of glucose was the control group (14,082 ± 955mg/dL) and the highest was the TSD group (16,293 ± 2,195 mg/dL); the Post-Hoc LSD test showed a significant difference (p&lt;0.05) between the control-PSD group and the TSD-control group. The mean result of pancreatic ß cells mass with the lowest number was in the TSD group (76.3 ± 4.8), and the highest result was in the control group (94.3 ± 2.7); Post-Hoc LSD showed a significant difference (p &lt;0.05) in the control-PSD group and the TSD-control group. The lowest mean in cell diameter of islets of Langerhans was in the TSD group (0.132 ± 0.031 mm), and the highest mean was in the control group (0.213 ± 0.019 mm). Conclusion: Sleep deprivation could reduce pancreatic ß cell mass and cell diameter of islets of Langerhans and increase glucose tolerance levels.

The Beneficial Effects of Green Tea on Sleep Deprivation-Induced Cognitive Deficits in Rats: The Involvement of Hippocampal Antioxidant Defense

Background: The weight of evidence suggests that sleep is essential for the processes of memory consolidation and sleep deprivation (SD) impairs the long-term memory in both humans and animals, which is related to oxidative stress damage within the brain. Green tea polyphenols have demonstrated antioxidant, anti-carcinogenic, and anti-mutagenic properties. We aimed to investigate the possible protective effect of green tea extract (GTE) and its main active catechin, epigallocatechin-3-gallate (EGCG), on post-training total sleep deprivation (TSD) -induced spatial memory deficits and oxidative stress profile in the hippocampus of the rat. Methods: Male rats were treated with saline, GTE ( 100 and 200 mg/kg/day), and EGCG (50 mg/kg/day) intraperitoneally for 21 days and then trained in Morris water maze in a single day protocol. Immediately after the end of MWM training, animals were sleep deprived for 6 h by the gentle handling method, and then evaluated for spatial memory. Hippocampal levels of malondialdehyde, (MDA), and thiol was assessed as oxidant and antioxidant markers. Results: Spatial memory was impaired in the TSD group and GTE at the dose of 200 mg/kg/day as well as EGCG at the dose of 50 mg/kg/day could reverse the impairment to the saline-treated levels. Despite the unchanged MDA levels, hippocampal total thiol was significantly decreased after TSD and EGCG increased it to the basal levels. Conclusion: In conclusion, green tea and its main catechin, EGCG, could prevent memory impairments during 6 h of TSD; probably through normalizing the antioxidant thiol defense system which was impaired during TSD.

Morphology and DNA fragmentation spermatozoa in animal models with sleep deprivation-induced stress

Background: A stress, sleep deprivation, can cause imbalance of reactive oxygen species (ROS) that can damage DNA, lipids and proteins of spermatozoa, consequently leading to infertility.Objective: The aim of this study is to investigate differences of morphology and DNA fragmentation with some models of sleep deprivation in spermatozoa of white male Wistar rat strain (Rattus novergicus).Methods: This study was an experimental study with post-test-only with control group design. There were 30 male Wistar rats which were randomly divided into 5 groups: control group, paradoxical sleep deprivation (PSD) group, total sleep deprivation (TSD) group, sleep recovery (SR) group, PSD group + SR group, and TSD group + SR group. Stress induction was conducted for 5 days. Morphological abnormality of spermatozoa was observed by creating sperm removal tinged by eosin and nigrosine. DNA fragmentation was performed by determining DNA fragmentation index (DFI). Morphological data of spermatozoa were analysed by One-Way Annova and Post-Hoc Turkey test, and DNA fragmentation of spermatozoa was analysed by Kruskal Wallis and Mann Whitney test to determine differences among the groups.Results: The highest mean of the abnormal morphology was in PSD Group (89.5 %, p=0.004). The normal mean of DNA fragmentation was found in control group, PSD+SR group and TSD+SR group, PSD and TSD groups. Bad DNA fragmentation index was found in PSD and TSD groups (30.16% and 31.4%, p=0.023).Conclusion: There were differences of morphology and DNA fragmentation of the spermatozoa in the male Wistar rat strain induced by various models of sleep deprivation.

Sleep differentially impacts involuntary intrusions and voluntary recognitions of lab-analogue traumatic memories.

Despite the critical role of sleep in memory and emotion processing, large remains unknown regarding how sleep influences trauma-related symptoms arising from maladaptive memory/emotional processes, such as those among patients with post-traumatic stress disorder. Employing a trauma film paradigm, we investigated how post-trauma sleep versus sleep deprivation influenced involuntary intrusions and voluntary recognition of traumatic memories. Sixty participants were randomly assigned to sleep or total sleep deprivation group following experimental trauma induction. Participants were assessed with: (a) lab-based and 7-day diary-based involuntary intrusions; (b) voluntary recognitions of traumatic memories 12-hr and 7-day post-trauma induction; and (c) post-traumatic stress disorder-like symptoms measured by the Impact of Event Scale-Revised. We found that compared with sleep deprivation, slept participants experienced fewer traumatic intrusions across 7 days, reported lower emotional hyperarousal, and showed more accurate recognition of trauma-related stimuli. Moreover, higher subjective sleep quality was associated with fewer intrusions only in the sleep group, while a reversed pattern emerged in the sleep deprivation group. These results provide novel evidence supporting the therapeutic benefits of sleep in protecting mental well-being from trauma exposure. To the extent that sleep modulates trauma-related symptoms, sleep can be conceived as the potential target for early interventions among trauma victims.

The role of sleep disturbances in depressive-like behavior with emphasis on α-ketoglutarate dehydrogenase activity in rats.

Sleep disorders may induce anxiety- and depressive-like behaviors. Furthermore, sleep disorders can alter the function of α-KGDH (α-ketoglutarate dehydrogenase), which is involved in the citric acid cycle. In this study, we evaluated the effect of two models of sleep deprivation (SD) including total SD (TSD) and partial SD (PSD), and two models of napping combined with each models of SD on rats’ performance in Forced Swim Test (FST) and α-KGDH activity in both hemispheres of the amygdala. 64 male Wistar rats were used in this study. A modified water box was also used to induce SD. The results showed that, immobility was increased in 48-hour PSD group, indicating a possible depressive-like behavior. Swimming time was also increased following 48-hour TSD. However, climbing time was decreased in 48-hour PSD/TSD groups. Additionally, α-KGDH activity was increased in the left amygdala in 48-hour TSD and PSD groups. In conclusion, PSD may increase depressive-like behavior. TSD and PSD can decrease swimming time but increase climbing time, and these effects may be related to serotonergic and noradrenergic transmissions, respectively. Increase in α-KGDH activity in the left amygdala may be related to the brain's need for more energy during prolonged wakefulness. α-KGDH activity in the right amygdala was unaffected probably due to a decrease in alertness following SD.

0294 Baseline Response Speed Predicts Locus Coeruleus Integrity Change After Sleep Deprivation

Abstract Introduction Locus coeruleus (LC) is the major source of norepinephrine (NE) in the brain, which plays a key role in maintaining arousal and alertness. Sleep loss significantly impairs arousal and alertness. However, it is unknown whether sleep loss disrupts LC integrity, which can be measured non-invasively by diffusion tensor imaging (DTI). In the current study, we used DTI to examine the effects of one night of acute total sleep deprivation (TSD) on fractional anisotropy (FA), an index reflecting fiber density, axonal diameter and myelination. Methods We analyzed DTI and psychomotor vigilance test (PVT) data from N=54 health adults (23 females, age range 21–50 years) from a well controlled in-laboratory sleep deprivation study. Participants were randomized to either a TSD condition (n=40) without sleep on night 2, or a control condition (n=14) with no sleep loss. Standard DTI scans were conducted on the morning of day 2 and day 3 between 0700h-1000h. The PVT reciprocal response time (RRT) was used to measure individual’s response speed at baseline without sleep loss. LC regions-of-interest (ROI) were defined by standard templates from Keren et al. (2009). Imaging data were analyzed using FSL toolbox. Results For the whole TSD group, no differences were found in the LC FA values before and after sleep deprivation (p &amp;gt; .2). However, when dividing the TSD group to a slow group and a fast group based on their baseline PVT response speed, significantly increased LC FA were found in the slow group (p = .007) but not in the fast group (p &amp;gt; .4). The PVT RRT negatively correlated with LC FA value changes after TSD (r = -.44, p = .004). No correlations were found between the PVT RRT and LC FA changes in the control group. Conclusion Our results showed that baseline vigilance response speed correlated with LC integrity change after sleep deprivation, with slower response exhibiting greater changes in LC integrity. These findings support the key role of LC-NE system in the regulation of alertness and arousal. Support Supported in part by NIH grants R01-HL102119, R01-MH107571, R21-AG051981. CTRC UL1RR024134, and P30-NS045839.

0125 Sleep Deprivation Impairs the Ability to Overcome Pre-Existing Framing Bias

Abstract Introduction When presented with a choice between sure gains or losses versus gambles, people tend to select sure gains over gambles, but gambles over sure losses. This pre-existing framing bias is embedded in the Framed Gambling Task (FGT), in which subjects choose between a sure option (gain or loss) and a gamble (card from one of two decks). For optimal performance, subjects need to recognize that one deck (‘good deck’) results in better average outcomes than the other deck (‘bad deck’) and select the gamble or sure option depending on the deck (good/bad) rather than the frame (sure loss/gain). A speeded version of the FGT, with 2s response deadlines to induce time pressure, was used in a laboratory total sleep deprivation (TSD) study to determine the impact of sleep loss on the ability to overcome pre-existing framing bias. Methods Eight-six subjects (ages 21–38; 47 females) were randomized (2:1 ratio) to a TSD condition (n=56) or control condition (n=30). They completed the speeded FGT at 11:00 on the baseline day (session 1), and again the following day (session 2) after 27h of wakefulness (TSD group) or 3h of wakefulness (control group). Performance accuracy was defined in terms of optimal task performance, i.e., gambling when the good deck was presented and not gambling when the bad deck was presented. Each test bout had 72 trials across three trial blocks. Results Accuracy improved across trial blocks (F1,84=20.44, p&amp;lt;0.001). In session 2, the TSD group showed lower accuracy (condition by session interaction: F2,84=4.15, p=0.045) and less improvement across trial blocks (condition by session by trial block interaction: F2,168=3.97, p=0.021) than the control group. Even under TSD, the frequency of response timeouts (RT&amp;gt;2s) was low (&amp;lt;3.5% of trials). Conclusion Sleep deprivation degraded FGT performance under time pressure, indicating reduced ability to overcome pre-existing framing bias. Support PRMRP award W81XWH-16-1-0319

The effect of crocin on total sleep-deprivation induced amnesia in male Wistar rats

Introduction: In recent years, Crocin has been used for its pharmacological functions, such as memory and learning enhancement. The aim of the present study was to assess the effect of Crocin on total sleep deprivation (TSD)-induced amnesia in male Wistar rats. Materials and Methods: The water box apparatus was used to induce sleep deprivation followed by Y- maze task as an index of learning and memory (the percentage of time in the novel arm during the retention phase was reported as an index of memory performances). The rats were divided into 12 groups, 8 rats in each group, including four control groups, four sham groups, and four TSD groups. Each group received saline and Crocin at doses of 1, 5 or 15 mg/kg twice a day. Results: The findings revealed that TSD for 24 h impaired memory function. In addition, the intra-peritoneal injection of Crocin at all doses (1, 5 and 15 mg/kg) did not change the percentage of time spent in the novel arm of Y-maze in sham of TSD, whereas it abolished the responses induced by the TSD groups. Conclusion: The findings showed a close interaction between the Crocin and SD. Based on the findings, Crocin seems to possess a modulatory effect on SD-induced amnesia.