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Experimental sleep fragmentation (SF) is characterized by frequent brief arousals without reduced total sleep time and causes daytime sleepiness and impaired neurocognitive processes. This study explored the impact of SF on error monitoring. Thirteen adults underwent auditory stimuli-induced high-level (H) and low-level (L) SF nights. Flanker task performance and electroencephalogram data were collected in the morning following SF nights. Compared to LSF, HSF induced more arousals and stage N1 sleep, decreased slow wave sleep and rapid-eye-movement sleep (REMS), decreased subjective sleep quality, increased daytime sleepiness, and decreased amplitudes of P300 and error-related positivity (Pe). SF effects on N1 sleep were negatively correlated with SF effects on the Pe amplitude. Furthermore, as REMS was reduced by SF, post-error accuracy compensations were greatly reduced. In conclusion, attentional processes and error monitoring were impaired following one night of frequent sleep disruptions, even when total sleep time was not reduced.

This study characterizes the different response patterns of sleep and wakefulness (W) to short light-dark (LD) cycles in albino mice and examines whether retinal degeneration resulting from prolonged bright light treatment and/or rd/rd mutation alters such response patterns. Eight young male Institute for Cancer Research (ICR) mice with normal eyes, seven young male rd/rd Friend Virus B type (FVB) mice, six young ICR and five young rd/rd FVB mice receiving 48-h bright light treatment, and five older rd/rd FVB mice were implanted with skull and muscle electrodes to record sleep and W. All the mice were maintained in 12-h-12-h LD cycles at baseline and received 2 days of short LD cycle treatment, which included 5-min-5-min LD cycles for a total of 24 cycles presented 4h after lights-on and again 4h after lights-off. All the five mouse groups maintained photo-entrainment of sleep and W rhythms at the baseline and showed a preference for paradoxical sleep (PS) occurrence in the 5-min dark period and non-rapid eye movement sleep (NREMS) in the 5-min light period and a brief alerting effect of light onset on experimental days. Retinal degeneration rising from bright light treatment and/or genetic mutation failed to eliminate or reduce the response of PS and NREMS to short LD cycles, although it enhanced the LD contrast of W, i.e., bright light treatment prolonged the alerting effect of light and the rd mutation increased the suppressing effect of the dark on W. These results suggest that sleep responses to short LD cycles and the brief alerting effect of light were independent of the photoreceptors in the outer retina. Furthermore, the residual photoreceptors in the outer retina and/or the photosensitive cells in the inner retina may actively modulate the effect of light and dark signals on W.

Chronic circadian desynchronization induced by repeated 12 h light-dark cycle shifts conducted twice weekly resulted in elevated food intake, body weight gain, and retroperitoneal fat mass in male F344 rats. Using a proteomic approach, we found that repeated light-dark shifts caused changes in expression levels of five hypothalamic (four upregulated) and 22 retroperitoneal fat (13 upregulated) 2-DE protein spots. Proteins involved in carbohydrate metabolism and in the citric acid cycle were upregulated, indicating a positive energy balance status. In addition, the hypothalamic gamma-amino butyric acid (GABA) aminotransferase was upregulated, thus suggesting a connection between the brain GABAeric system and the modulation of food intake. Furthermore, the upregulation of fatty acid-binding protein 4 and the downregulation of 78 kDa glucose-regulated protein in the fat implicated the development of insulin resistance. We observed the upregulation of two antioxidant enzymes that might serve as protection against insulin dysfunction associated with oxidative stress. Finally, the downregulation of hypothalamic voltage-dependent anion-selective channel protein 1 and fat ATP synthase suggested a reduction in synthesis of mitochondrial ATP. These findings are in partial agreement with those of studies of obesity induced by genotype and a high-fat diet.

In this study, we investigated the feasibility of applying manual muscle testing (MMT) for bedding selection and examined the bedding effect on sleep. Four lay testers with limited training in MMT performed muscle tests for the selection of the bedding systems from five different mattresses and eight different pillows for 14 participants with mild sleep-related respiratory disturbances. For each participant individually, two bedding systems-one inducing stronger muscle forces and the other inducing weaker forces-were selected. The tester-participant pairs showed 85% and 100% agreement, respectively, for the selection of mattresses and pillows that induced the strongest muscle forces. The firmness of the mattress and the height of the pillow were significantly correlated with the body weight and body mass index of the participants for the selected strong bedding system but not for the weak bedding system. Finally, differences were observed between the strong and the weak bedding systems with regard to sleep-related respiratory disturbances and the percentage of slow-wave sleep. It was concluded that MMT can be performed by inexperienced testers for the selection of bedding systems.

To examine whether scheduled forced wheel activity counteracts the increased body weight gain in rats undergoing chronic circadian desynchronization induced by repeated 12-h shifts in the light–dark cycle. Four age- and body weight-matched groups of adult male F344 rats were subjected to 12-h intermittent forced wheel activity daily (2.2 km/day). Each group had the following schedule for 13 weeks: a fixed schedule of a daily 12:12-h light–dark cycle and activity training (WF); a fixed light–dark cycle and 12-h shifts twice a week in activity training (WS); 12-h shifts twice a week in the light–dark cycle and a fixed schedule of activity training (LSWF); and 12-h shifts twice a week in both the light–dark cycle and activity training (LSWS). Two additional age- and body weight-matched sedentary rat groups were selected from our database: one was maintained on a fixed light–dark cycle (LC) and the other was subjected to 12-h shifts twice a week in the light–dark cycle (LS). The four rat groups that were exercised showed different response patterns of the daily body temperature rhythm to different combinations of forced activity and lighting schedules. Their food intake was more than that of the two sedentary rat groups, but their body weight was comparable with that of the LC rats and less than that of the LS rats during the forced activity period. The LSWS rats were heavier than the WF and WS rats in the first and second months of the experimental treatment, but their body weight was comparable with that of the WS and WF rats in the third month. Forced activity was effective in reducing the body weight gain in chronic circadian desynchronization that was induced by repeated shifts in the light–dark cycle, although such an effect might become significant only after some time.

STUDY OBJECTIVES: To verify if error monitoring, involving detection and remedial actions, is affected by sleep deprivation. DESIGN: Event-related brain potentials (ERPs) and electroencephalogram spectrum during performance of Flanker task were obtained in a within-subject, counter-balanced, repeated-measures design. SETTING: Sleep deprivation and data collection were conducted in a laboratory setting. PARTICIPANTS: Sixteen young healthy adults (7 women, 18-23 years old) INTERVENTIONS: Performance and electroencephalogram data were collected after normal sleep and sleep deprivation. MEASUREMENTS AND RESULTS: Compared to normal sleep, 1 night of sleep deprivation resulted in slower and more varied reaction times, more response errors and omissions, and impaired posterror adjustments to response accuracy. Concomitantly, 2 error-related ERPs, error-related negativity and Pe, showed reduced amplitude measurements after sleep deprivation. Conversely, conflict monitoring as expressed behaviorally and by the N2 component of the ERP was not attenuated by sleep deprivation. Ten of the sixteen participants maintained similar accuracy levels under both sleep conditions, although they still showed reduced error-related negativity and error positivity amplitude measurements and impaired error remedial actions for accuracy. Electroencephalogram spectral activity at beta and theta frequency bands was related to response correctness on subsequent trials but not related to that of preceding trials under both sleep conditions. CONCLUSIONS: One night of sleep deprivation impaired both the error detection and error remedial actions and highlighted the inability to avoid making errors again after erroneous responses were already made. The results showed that a vicious cycle occurred between performance deterioration and impairment of error-remedial mechanisms that inevitably led to making more successive errors. Language: en

This study was aimed at clarifying whether the lights-off stimulation effect on paradoxical sleep (PS) enhancement in albino rats depends on sleep and wakefulness states. Male Sprague-Dawley rat pairs were subjected to lights-off stimulation for 320 s when one of the two rats was in non-rapid-eye movement sleep (NREM) continuously for at least 64 s (NREM-off condition). Simultaneously, the other rat received the same lights-off stimulation during any sleep and wakefulness state (random-off condition). Each rat underwent both lights-off conditions. The sequence of the two lights-off conditions was counter-balanced. PS was enhanced during the lights-off period in both the NREM-off and random-off conditions. However, the increased amount of PS was greater in the NREM-off condition than the random-off condition. In the random-off condition, rats had more PS in the lights-off period than in the preceding and succeeding lights-on periods only if they were in high EEG amplitude NREM (HS) at lights-off. Thus, this study verified that the lights-off stimulation effect on PS enhancement in the albino rat depended on the sleep states. However, the lights-off treatment did not alter the relationship between PS and preceding NREM, or the hippocampal theta activity or the PS latency in the lights-off period.

SLEEP LOSS DUE TO SLEEP DEPRIVATION OR FRAGMENTATION AND ITS CONSEQUENCE, I.E., SLEEPINESS, ARE COMMON IN MODERN SOCIETY. SLEEP loss and sleepiness contribute significantly to performance decrements and accidents, such as motor vehicle crashes and work error-related damages.1 Performance decrements after sleep loss are generally attributed to attention deficit, and this proposition is supported by several behavior,2,3 electrophysiologic,4,5 and functional brain imaging studies.6 Attention is a multidimensional cognitive process, and the results of several studies have suggested that sleep loss induces selective impairment of attention processes, particularly the top-down attention control processes that rely on the frontal lobe.2,3,6 This corresponds with the view of Horne7 that frontal lobe functions are sensitive to total sleep loss. The frontal lobe is critically involved in executive function, including the ability to plan or set goals, supervisory attention processes, response inhibition, and action monitoring, such as error detection and conflict processing. A series of recent studies conducted by us8–10 and others11,12 have shown that all components of error monitoring, including error detection, error correction, and posterror speed and accuracy adjustments, are impaired following sleep deprivation. Thus, sleep deprivation-related performance decrements and accidents appear to result from deficits in both attention processes and performance monitoring, particularly error monitoring in the latter. The results of previous studies have suggested that the decline in vigilance task performance during sleep deprivation is in part related to reduced motivation.13–15 The feedback of the knowledge of results14,15 and monetary rewards13 reduce some negative effects of sleep loss on vigilance task performance. Vigilance is commonly defined as sustained attention or tonic alertness.1 Given that the reduction of vigilance related to a low arousal level gives rise to performance decrements following sleep deprivation, monetary incentives are thought to have general effects on the performance of vigilance tasks, such as effects related to arousal, alertness, or mental effort.14–16 Additionally, monetary incentives have recently been proposed to selectively influence the top-down attention mechanisms in the performance of tasks that require a high degree of top-down attention control processes.17–20 A previous study used a cued attention task in which subjects responded to targets preceded by spatially valid, invalid, or neutral (noninformative) cues and illustrated that monetary incentives enhanced the response speed in the case of the trials with the valid and invalid cues but not those with the neutral cues.19 Furthermore, a recent study has shown that a continuous 2-hour performance of a task that requires a high degree of cognitive control results in performance reduction in terms of the response speed, accuracy, and stability.21 Performance decrements due to prolonged task performance are accompanied by a decrease in the brain activity, including the amplitude of the contingent negative variation component of the event-related potential (ERP) that indexes the preparatory attention22,23 and the amplitude of the P300 component that is related to the deployment of attention resources.24 Increasing the motivation level by financial rewards attenuates the changes in behavior performance and brain activity during prolonged task performance.21 However, whether motivation incentives attenuate the negative effects of sleep deprivation on the performance of tasks that require a high degree of cognitive control needs to be studied, despite the many studies that have used vigilance tasks to investigate this.13–15 Thus, the first objective of this study was to examine whether motivation incentives reduce the effects of sleep deprivation while subjects perform tasks that require higher cognitive control processes. We used a flanker task,25 which requires a high degree of top-down attention control processing and action monitoring, with concurrent electroencephalographic (EEG) recordings for behavior and electrophysiologic examination of the effects of monetary incentives on attention processes and action monitoring after 1 night of total sleep deprivation, which was similarly applied in our previous studies.8–10 A previous study26 has shown that financial penalties for errors not only increase the performance accuracy, but also enhance error detection, as reflected by the increase in the amplitude of event-related negativity (ERN), which is a negative component of the response-locked ERPs and is frontocentrally maximized.27 As mentioned above, continuous 2-hour task performance also results in a reduction in error monitoring, such as in error detection (as reflected by the reduced ERN amplitude), error correction, and posterror slowing.21 In addition, monetary rewards lead to attenuation of the changes in error monitoring during prolonged task performance. It is proposed that the anterior cingulate cortex, located in the medial frontal cortex, is the generator of ERN (reviewed in28,29). Considering that monetary incentives can facilitate the activation of the medial frontal cortex in putatively well-rested subjects17,19 and can improve the reductions in error monitoring (ERN amplitude, error correction, and posterror slowing) during prolonged task performance,21 it is likely that monetary incentives can also reduce, if not completely block, the effect of sleep deprivation on error monitoring. Since the flanker task has been frequently used to study error monitoring and was used in this study, we also examined whether motivation incentives interacted with sleep deprivation to influence error monitoring.

Previous behavioral and electrophysiologic evidence indicates that one night of total sleep deprivation (TSD) impairs error monitoring, including error detection, error correction, and posterror adjustments (PEAs). This study examined the hypothesis that error correction, manifesting as an overtly expressed self-generated performance feedback to errors, can effectively prevent TSD-induced impairment in the PEAs. Sixteen healthy right-handed adults (seven women and nine men) aged 19-23 years were instructed to respond to a target arrow flanked by four distracted arrows and to correct their errors immediately after committing errors. Task performance and electroencephalogram (EEG) data were collected after normal sleep (NS) and after one night of TSD in a counterbalanced repeated-measures design. With the demand of error correction, the participants maintained the same level of PEAs in reducing the error rate for trial N + 1 after TSD as after NS. Corrective behavior further affected the PEAs for trial N + 1 in the omission rate and response speed, which decreased and speeded up following corrected errors, particularly after TSD. These results show that error correction effectively maintains posterror reduction in both committed and omitted errors after TSD. A cerebral mechanism might be involved in the effect of error correction as EEG beta (17-24 Hz) activity was increased after erroneous responses compared to after correct responses. The practical application of error correction to increasing work safety, which can be jeopardized by repeated errors, is suggested for workers who are involved in monotonous but attention-demanding monitoring tasks.

Light-to-dark transitions have been found to enhance paradoxical sleep (PS) in albino rats but not pigmented rats. Furthermore, PS inducing effect of dark pulses in albino rats depends on sleep states. This study examined whether the relationship between PS and preceding non-rapid-eye-movement sleep (NREMS) in pigmented Brown Norway rats was different from that in albino F344 rats and whether such a difference was associated with different responses to dark pulses in the two rat strains. Both rat strains showed a positive relationship between PS and preceding NREMS. However, only the albino F344 rats exhibited the PS inducing effect of dark pulses. Dark pulses did not alter the relationship between PS and preceding NREMS in either rat strain, and, reciprocally, nor did duration of preceding NREMS affect dark pulse-induced PS enhancement. Furthermore, this study verified that dark pulses given during NREMS in albino F344 rats specifically induced the suppression of NREMS concomitant with the enhancement of PS. This study proposed that dark pulses might inhibit NREMS and facilitate PS regulating areas concurrently in albino rats.

This study is aimed at verifying the causal relationship of chronic circadian desynchronization and changes in body weight control. Eight male albino F344 rats aged between 12–15 wk were subjected to twice weekly 12-h shifts of the daily light-dark (LD) cycle for 13 wk (3 mo). Continuous circadian phase shifts consisting of intermittent phase delay and advance and reduced circadian amplitudes were consistently displayed in all five experimental rats implanted intraperitoneally with heart rate, body temperature, and activity transponders. The experimental rat maintained a greater body weight during LD shifts and even after 10 days of recovery than that of the age-matched control rat, which was maintained on a regular LD cycle. Body weight gain was greater in the first 2 mo of LD shifts in the experimental rat than in the control rat. Relative to the baseline, food intake and activity percentages were increased and reduced, respectively, for the experimental rats. Features of these results, such as increased body weight gain and food intake, and reduced activity, suggest a causal relationship of chronic circadian desynchronization and changes in body weight control in male albino F344 rats.

In this study we evaluated the effect of a two-credit (100 min./week) “Sleep Management” course on the sleep patterns of college students as the course progressed over an 18-wk. semester. Curricular activity included lectures, group discussions, and practice of self-evaluation of sleep. Instead of giving the students the whole list of sleep hygiene at the outset of the course, each concept of sleep hygiene was introduced and discussed under related lecture topics. A total of 241 students (131 men and 110 women) took the course and kept 7-day sleep logs three times. Concurrently, sleep-log data were collected from 65 students (32 men and 33 women) who were not taking the course. Both groups showed similar varieties of academic backgrounds and characteristics of sleep patterns at the beginning. Similarly, their sleep patterns, namely, rise time, nighttime awakenings, time asleep, time in bed, sleep efficiency, and rise time regularity, changed over the semester. Women in both groups had more nighttime awakenings. In contrast, sleep quality was progressively better for the group in the course but not for the control group. Only women in the course decreased their nap time in the second and third months. Thus, the course of “Sleep Management” only had a mild and limited effect on sleep patterns. The course content needs refinement to maximize influence on students' sleep patterns and habits, particularly, on reduction of insufficient sleep and daytime sleepiness which are the highest ranking sleep problems among college students.

Since gender effect is inconsistent and grade effect has not been addressed in previous studies, we investigated both effects on the daily sleep patterns in a group of young college students.The sample consisted of 237 students aged 18-24 years. Each subject completed a 7-day sleep log.Gender differences were found in several sleep variables and those were mostly not dependent on weekday/weekend difference. The female students went to bed and rose earlier and had longer sleep latency, more awakenings, and poorer sleep quality than the male. Gender differences were also shown in the relationship between sleep quality and other sleep variables. The correlation between sleep quality and rise time, time in bed, and sleep efficiency was stronger in men than in women. In contrast, grade differences were mostly dependent on weekday/weekend difference. The freshmen rose earlier and had shorter sleep time than did the other students on weekdays only. Sleep latency was the longest in seniors on weekdays only.This study showed that gender differences in sleep patterns and sleep difficulties were remarkable in the group of young college students. Alarmed by the high prevalence of sleep difficulties among general college students, it is recommended that the students should be informed of their sleep problems and the consequences.

Rats subjected to chronic total sleep deprivation (TSD) by the disk-over-water method have shown very large, sustained rebounds in paradoxical sleep (PS) (also known as REM sleep). Other studies have indicated that cholinergic mechanisms are involved in the instigation and maintenance of PS. Hypothetically, the large PS rebounds could be mediated by an upregulation of cholinergic receptors during TSD. To evaluate this hypothesis, regional brain cholinergic receptors were compared in rats subjected to 10-day TSD by the disk-over-water method (TSD rats), yoked control (TSC) rats which received the same physical stimulation but with much smaller reductions in sleep, and home cage control (HCC) rats. L-[3H]nicotine and [3H]quinuclidinyl benzilate were used as specific cholinergic radioligands for nicotinic and muscarinic receptor binding assays, respectively. Nicotinic receptor binding was not significantly different among groups for any of the brain regions assayed, including frontal cortex, parietal cortex, thalamus, amygdala, hippocampus, anterior hypothalamus, posterior hypothalamus, caudate, limbic system (including septal area, olfactory tubercle, and nucleus accumbens), midbrain, pons, and medulla. Thus, there was no evidence that changes in nicotinic receptors mediate the PS rebounds. For muscarinic receptor binding, TSD rats differed significantly from control rats only in showing a higher binding affinity than TSC rats in the limbic system and a lower binding density than HCC rats in the hippocampus. On the other hand, significant differences in muscarinic receptor binding sites between rats selectively deprived of PS and their yoked controls were found only for the septal area.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of chronic total sleep deprivation (TSD) on the regulation of central noradrenergic receptors was evaluated. Rats were subjected to 10 days of TSD by the disk-over-water method. As in previous TSD studies, these rats showed greater increases in food intake and energy expenditure and greater eventual declines in waking body temperature than their yoked-control (TSC) rats. After sacrifice, alpha 1-, alpha 2-, and beta-adrenoceptors were determined in 11 brain regions using radioligand binding assays with [3H]prazosin, [3H]rauwolscine, and 125I-iodocyanopindolol, respectively. Adrenoceptor density and affinity values were significantly different among TSD, TSC, and normally caged control rat groups only for the cerebellum, which showed higher alpha 2-binding density concomitant with lower affinity and lower beta-binding density than cage control rats. Such changes are attributable to apparatus or stimulus effects common to TSD and TSC rats. Given the absence of firm evidence for a TSD-induced downregulation of central noradrenergic receptors, the present results offer no support for the hypothesis of Siegel and Rogawski that a major function of paradoxical sleep is to upregulate these receptors.

To avoid a possible confound between the effects of sleep loss and disturbed circadian rhythms in previous studies of total sleep deprivation (TSD) by the disk-over-water method, TSD rats and their yoked control (TSC) rats had been maintained in constant light both before and during the experiment. With circadian rhythms of both groups flattened by constant light, group differences in outcome measures could be attributed to sleep loss. However, the constant light control entailed the possibility that the sleep loss effects might obtain only in constant light. To evaluate this possibility, three TSD-TSC rat pairs maintained on a 12 hour light: 12 hour dark (LD) schedule were studied. TSC rats showed only minor changes during the deprivation period. As in previous studies, TSD rats showed increased food intake; decreased weight; increased energy expenditure; debilitated appearance; lesions on the tail and paws; an initial increase followed by a large decrease in body temperature; impending death; and recovery sleep, which featured large, selective, sustained rebounds of paradoxical sleep and a reversal of all observed TSD-induced changes. Thus, TSD produced the same changes during an LD schedule as during constant light. The amplitude of the diurnal body temperature rhythm declined over the course of TSD and then almost completely recovered during the first day of recovery sleep. The decline was interpreted as the result of deprivation-induced thermoregulatory changes.