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PubMed1992

[Effects of paradoxical sleep deprivation on the activity of opiate receptors isolated from synaptic membranes of the rat brain].

The specific binding of 3H-naloxone with opiate receptors isolated from brain synaptic membranes of control and paradoxical sleep deprived rats were studied. This extreme state was shown to reduce the naloxone-binding activity of synaptic membranes by 35% and isolated receptors by 25-28%. The values of Kd and Bmax were calculated for isolated opiate receptors at different stages of purification. Considerable decrease of 3H-naloxone binding sites density (2 times) in the isolated opiate receptors with simultaneous increase of their affinity (3-4,5 times) was found following 24 hours paradoxical sleep deprivation. These findings suggest development of fixed alterations in the structure and functions of integral receptor proteins under extreme influences.

Animals↗
PubMed2004

The effects of acute sleep deprivation on performance of medical residents in a regional hospital: prospective study.

OBJECTIVE: To evaluate the effects of acute sleep deprivation on the level of perceived occupational stress and cognitive functioning in a group of medical residents. DESIGN: Prospective study. SETTING: Regional hospital, Hong Kong. PARTICIPANTS: Twenty-one residents who had regular in-hospital on-call duties. MAIN OUTCOME MEASURES: From January to April 2002, participants were asked to complete the Raven Advanced Progressive Matrices (sets I and II) and Occupational Stress Inventory-Revised tests at the beginning of an on-call day. They then repeated the tests towards the end of their on-call duties on their next on-call day, at a mean (standard deviation) interval of 8.9 (2.3) days. Occupational Stress Inventory-Revised test scores were transformed into T-scores to provide information about an individual's scores relative to the scores of participants in a normative sample. RESULTS: The group slept for a mean (standard deviation) of 2.9 (1.0) hours during 29.3 (3.8) hours of on-call duties. Before the on-call duties, participants' mean T-scores for the Occupational Stress Inventory-Revised test ranged from 50.6 to 54.5 for the Occupational Role Questionnaire, 52.0 to 57.0 for the Personal Strain Questionnaire, and 37.3 to 52.3 for the Personal Resources Questionnaire. After on-call duties, apart from a slight increase in Role Insufficiency T-scores (50.6 [5.9] versus 52.1 [6.0]; P=0.044), there was no significant change in all other scales of the Occupational Stress Inventory-Revised test. The scores of the Raven Advanced Progressive Matrices test remained stable after the on-call duties (11.3 [1.2] versus 11.5 [0.8], P=0.129 for set I; 29.9 [5.5] versus 30.2 [6.3], P=0.2 for set II). CONCLUSION: Acute sleep deprivation among medical residents was not associated with any significant changes in both cognitive functioning and level of stress perceived.

Adult↗
PubMed1986

Sleep deprivation of rats by punitive and non punitive procedures.

A series of experiments compared sleep deprivation of rats by sleep contingent shock and by non punitive procedures. Sleep overrode shock in approximately 24 hours. Animals were kept awake by non punitive procedures for 12 and 15 days. Recovery measures were higher for the non punitive procedures.

Animals↗
PubMed1999

Regional differences in the dynamics of the cortical EEG in the rat after sleep deprivation.

OBJECTIVE: To investigate regional changes of the cortical sleep EEG in the rat, recordings were obtained from a frontal and an occipital derivation, on a baseline day (n = 14 male rats, Sprague-Dawley strain) and after 24 h sleep deprivation (SD, n = 7). METHODS: Spectral analysis of the vigilance states revealed state and frequency specific differences in EEG power by two-way ANOVA and post-hoc t tests. RESULTS: In the theta band (6.25-9.0 Hz) occipital power was larger than frontal power in waking and REM sleep, whereas frontal power was larger in the frequency range between 10.25-16.0 Hz in non-REM sleep and REM sleep. After SD frontal power in the 2-4 Hz band in non-REM sleep was increased more than occipital power and frontal power in the 10.25-16.0 Hz range was more attenuated. In REM sleep frontal power in the theta band and in the 10.25-16.0 Hz range was more increased than occipital power. Power in the waking EEG did not differ between the two derivations after SD. CONCLUSIONS: The differential responses to SD may reflect regional use-dependent aspects of sleep regulation. These observations support the notion that sleep is not only a global phenomenon but has also local, use-dependent features.

Animals↗
PubMed2005

Performance and alertness effects of caffeine, dextroamphetamine, and modafinil during sleep deprivation.

Stimulants may provide short-term performance and alertness enhancement during sleep loss. Caffeine 600 mg, d-amphetamine 20 mg, and modafinil 400 mg were compared during 85 h of total sleep deprivation to determine the extent to which the three agents restored performance on simple psychomotor tasks, objective alertness and tasks of executive functions. Forty-eight healthy young adults remained awake for 85 h. Performance and alertness tests were administered bi-hourly from 8:00 hours day 2 to 19:00 hours day 5. At 23:50 hours on day 4 (after 64 h awake), subjects ingested placebo, caffeine 600 mg, dextroamphetamine 20 mg, or modafinil 400 mg (n=12 per group). Performance and alertness testing continued, and probe tasks of executive function were administered intermittently until the recovery sleep period (20:00 hours day 5 to 8:00 hours day 5). Bi-hourly postrecovery sleep testing occurred from 10:00 hours to 16:00 hours day 6. All three agents improved psychomotor vigilance speed and objectively measured alertness relative to placebo. Drugs did not affect recovery sleep, and postrecovery sleep performance for all drug groups was at presleep deprivation levels. Effects on executive function tasks were mixed, with improvement on some tasks with caffeine and modafinil, and apparent decrements with dextroamphetamine on others. At the doses tested, caffeine, dextroamphetamine, and modafinil are equally effective for approximately 2-4 h in restoring simple psychomotor performance and objective alertness. The duration of these benefits vary in accordance with the different elimination rates of the drugs. Whether caffeine, dextroamphetamine, and modafinil differentially restore executive functions during sleep deprivation remains unclear.

Adult↗
PubMed2002

Sleep deprivation, disorganization and fragmentation during opiate withdrawal in newborns.

OBJECTIVE: To determine specific sleep characteristics in neonatal opiate withdrawal, referred to as the Neonatal Abstinence Syndrome (NAS), by measuring sleep efficiency, deprivation, disorganization and fragmentation in three groups: (i) healthy term neonates; (ii) opiate-exposed neonates who were treated for opiate withdrawal; and (iii) a group of opiate-exposed neonates who did not require treatment. METHODS: A cohort study recording sleep patterns of neonates at 2-10 days of age (after 36 or more weeks of gestation) was carried out. Twenty-one neonates were exposed to opiates during pregnancy and 15 neonates were healthy controls. Sleep characteristics were predefined, and treated newborns were divided into early and stabilized treatment groups. Polygraphic recordings of sleep, movement and breathing were made continuously after a daytime feed. RESULTS: Sleep deprivation, disorganization and fragmentation were found in newborns with NAS and were associated with the severity of the withdrawal. Neonates treated for NAS displayed increased wakefulness during early treatment (deprivation), but were similar to controls once stabilized. Both treated and non-treated groups had reduced amounts of quiet sleep (deprivation). Treated newborns showed an increase in indeterminate sleep (disorganization) and arousals-to-wakefulness (fragmentation). CONCLUSION: This study determined the exact nature and degree of sleep disturbances in newborns during acute opiate withdrawal. The findings contribute to a further understanding of the physiology underlying neonatal opiate withdrawal and suggest that some changes in sleep are due to opiate withdrawal but others may reflect opiate dependency in utero.

Electroencephalography↗
PubMed1983

Recovery sleep following sleep deprivation in intact and suprachiasmatic nuclei-lesioned rats.

Recovery sleep was studied for 3-5 days following 24 h of sleep deprivation (TSD) in normal rats and in rats lacking circadian rhythms (CRs) of sleep because of prior lesioning of the suprachiasmatic nuclei (SCN). One group of lesioned rats was run in constant dim light. Another lesioned group and an intact group were run on a 12:12 dark-light schedule with TSD and recovery beginning at lights-off. All groups showed immediate rebounds of high-amplitude NREM sleep and paradoxical sleep, confined mostly to the first 12-18 h of recovery, and decreases in moderate and low-amplitude NREM sleep during the first 6-12 h of recovery. Thus, sleep stage rebound priorities were little affected by CRs. Total sleep rebound was initially greatest in intact rats, but limited mostly to the first 12 h of recovery. Total sleep rebound was distributed over a longer period in SCN rats, but total accumulated rebound was similar in all groups. Thus, CRs appear to modulate the timing but not the amount of accumulated total sleep rebound. Results were interpreted in terms of ceiling effects on total sleep, delayed rebounds, and competition between CRs and homeostatic recovery processes. Recovery sleep of lesioned rats on the dark-light schedule was marked by a transient diurnal rhythm.

Animals↗
PubMed1993

The effects of sleep deprivation and incentives on human performance.

This study explores whether KR (knowledge of results) and reward compensate for the negative joint effects of sleep deprivation and signal degradation in a choice-reaction task. The negative effect of signal degradation on performance was aggravated by sleep loss and time-on-task, whereas KR improved performance, especially when signals were degraded. Reward changed the effects of time-on-task owing to lack of sleep. Performance was also improved by a brief task interruption after 30 minutes' work, with 5 more minutes to go. These results can be interpreted in terms of the performance model of Sanders (1983), which links energetic mechanisms to stages of information processing. A lack of energetic supply from the arousal mechanism to perceptual processing, induced by signal degradation, sleep deprivation, and time-on-task, was effectively counteracted by KR:KR enables the mobilization of effort to compensate for this lack of arousal. The relation between reward and KR is not yet clear. The interruption effect suggests that the influence of time-on-task is not due to loss of arousal, but causes a reallocation of resources by effort.

Adult↗
PubMed2003

Seizure associated with sleep deprivation and sustained-release bupropion.

This case report describes a generalized seizure associated with sustained-release bupropion use and sleep deprivation. The subject, a 31-year-old female smoker, was participating in a clinical trial evaluating an investigational medication for smoking cessation that used sustained-release bupropion as an active control. After 5 weeks of bupropion use, the subject experienced a generalized tonic clonic seizure after staying up nearly all night packing and moving to a new residence. The patient had no other risk factors for seizures. We suggest that sleep deprivation may add to the risk of bupropion-associated seizures.

Adult↗
PubMed1998

Effects of short-term sleep deprivation on murine immunity to influenza virus in young adult and senescent mice.

Sleep has been proposed as an innate host defense, exerting effects on both specific and nonspecific immunity. In one of the more striking papers dealing with the effects of sleep on specific immunity, Brown et al (Reg. Immunol. 1989; 2: 321-325) reported that depriving influenza virus-immune mice of sleep for 7 hours following total respiratory tract viral challenge abrogated anti-viral immunity within the lungs and lowered the level of anti-influenza antibody in lung homogenates. In the solidly-immune convalescent mouse, nasobronchial immunity to influenza virus has been shown to be due to secretory IgA (S-IgA) within the mucosal mucocilliary blanket, while serum IgG has been shown to mediate protection within the lung parenchyma. In this study we attempted to duplicate the work of Brown et al in solidly immune mice. We were unable to abrogate mucosal anti-influenza viral immunity with a single post-viral-challenge sleep-deprivation episode, nor were we able to depress this immunity with one pre- and two post-challenge sleep-deprivation episodes in young adult or old mice, or with two pre-challenge sleep-deprivation episodes in old mice. Sleep deprivation did not depress the level of serum influenza-specific IgG antibodies, and resulted in increased influenza-specific serum IgG compared with normally sleeping mice in aged immune mice boosted 3 weeks before challenge and sleep deprived once before and twice after challenge (p = 0.005). No differences in anti-viral respiratory immunity were apparent between young and old mice. We conclude that short-term sleep deprivation has minimal effects on pre-existing mucosal and humoral immunity in either the young adult or the senescent mouse.

Aging↗
PubMed2005

Does amygdalar perfusion correlate with antidepressant response to partial sleep deprivation in major depression?

This study used functional MRI (fMRI) to clarify the sites of brain activity associated with the antidepressant effects of sleep deprivation (SD). We hypothesized: (1) baseline perfusion in right and left amygdalae will be greater in responders than in nonresponders; (2) following partial sleep deprivation (PSD), perfusion in responders' right and left amygdalae would decrease. Seventeen unmedicated outpatients with current major depression and eight controls received perfusion-weighted fMRI and structural MRI at baseline and following 1 night of late-night PSD. Baseline bilateral amygdalar perfusion was greater in responders than nonresponders. Clusters involving both amygdalae decreased from baseline to PSD specifically in responders. Right amygdalar perfusion diverged with PSD, increasing in nonresponders and decreasing in responders. These novel amygdalar findings are consistent with the overarousal hypothesis of SD as well as other functional imaging studies showing increased baseline amygdalar activity in depression and decreased amygdalar activity with remission or antidepressant medications.

Adolescent↗
PubMed1994

[Effect of REM sleep deprivation on the each seizure stage in feline amygdaloid kindling].

The effect of REM sleep deprivation (RD) on the each seizure stage in feline amygdaloid kindling (AM-K) was studied. RD for 12 hours (12-h RD) was performed by applying the platform procedure at stages 2 and 4, and immediately after RD the triggering threshold of each seizure stage and the duration of after discharge was measured. At stage 6, 12-h and 72-h RD were performed, and the generalized seizure triggering threshold (GST), the duration of after discharge, and the latency to generalized convulsive seizure (LGS) were measured. For the controls, a platform sufficiently large to allow a cat to lie down and sleep was used under the same conditions as those for RD (Non-RD). With the platform procedure employed in this study, the %REM decreased significantly to 2% of what it was before 12-h RD (p < 0.01). After the 12-h RD, the %REM and %S-2 increased significantly compared with those during the RD (p < 0.05-0.01), revealing a rebound phenomenon. After the 12-h RD, the %W-2 also showed a significant decrease (p < 0.05). The results were as follows: (1) The triggering seizure threshold of stage 2 after the 12-h RD showed a significant decrease (p < 0.01). Though the AD duration after RD prolonged than those after Non-RD, significant differences was not noted. (2) The triggering threshold and AD duration of stage 4 after 12-h RD showed no significant change. (3) GST, AD duration, LGS showed no significant change by 12-and 72-h RD. The results of present study led to the following conclusions: At stage 2 of AM-K, REM sleep increased temporarily, and consequently the REM pressure is elevated after RD so much that it lowers the triggering threshold at stage 2 of AM-K. On the other hand, at stages 4 and 6 of AM-K, REM sleep is temporarily decreased, and consequently the REM pressure is not elevated by RD so that the triggering threshold at stages 4 and 6 of AM-K were not lowered.

Amygdala↗
PubMedDate not supplied

Four hours of paradoxical sleep deprivation impairs alternation performance in a water maze in the rat.

Sixteen rats were deprived of paradoxical sleep (PS) for 4 h using the "flower pot" technique and 16 other served as yoked controls. PS-deprived and control rats then had to learn a water maze using either a standard allocentric configuration (i.e., finding the submerged platform using external cues; n = 6/group) or an alternation version (goal platform alternating between two locations; n 10/group). Rats were submitted to six trials with a cutoff time of 60 s and an intertrial interval of 5 min. Criterion was set as two consecutive successful completions. PS-deprived rats made more quadrant entries and took more time to reach criterion on the alternation task than control rats while both groups were equal on the allocentric task. Based on lesion studies (Ethier et al., this issue) we propose that tasks that require an intact medial prefrontal cortex are particularly sensitive to PS deprivation.

Animals↗
PubMed1999

Sleep deprivation in depression: what do we know, where do we go?

Manipulations of the sleep-wake cycle, whether of duration (total or partial sleep deprivation [SD]) or timing (partial SD, phase advance), have profound and rapid effects on depressed mood in 60% of all diagnostic subgroups of affective disorders. Relapse after recovery sleep is less when patients are receiving medication; it may be prevented by co-administration of lithium, pindolol, serotonergic antidepressants, bright light, or a subsequent phase advance procedure. Diurnal and day-to-day mood variability predict both short-term response to SD and long-term response to antidepressant drug treatment. These mood patterns can be understood in terms of a "two-process model of mood regulation" based on the model well established for sleep regulation: the interaction of circadian and homeostatic processes. The therapeutic effect of SD is postulated to be linked to changes in disturbed circadian- and sleep-wake-dependent phase relationships and concomitant increase of slow-wave-sleep pressure; additionally, SD-induced sleepiness may counteract the hyperarousal state in depression. This model has the advantage of providing a comprehensive theoretical framework and stringent protocols ("constant routine," "forced desynchrony") to dissect out specific disturbances. Many aspects tie in with current serotonergic receptor hypotheses of SD action. A treatment inducing euthymia in severely depressed patients within hours is an important therapeutic option that has come of age for clinical use.

Antidepressive Agents↗
PubMed1994

[Studies on the isolation of endogenous sleep factors from Tupaia Belangeri Chinensis (TBC) after sleep deprivation].

The present study was undertaken to explore endogenous sleep factors isolated from 48-72 h sleep deprived (SD) male Tupaia belangeri chinensis (TBC). Only drink ad libitum (10% glucose) was available within 24 h before collection of urine. Controlled "clean" urinary samples were pooled and stored at 20 C. Fraction I-V from the urine were determined after ultrafiltration and Sephadex-G15. Amino-acid analysis of each fraction was automatically done by a 835 Amino-acid Analyzer, respectively. Bioassay was performed in 40 adult rabbits weighing 2.5-3.5 kg of either sex. Experiments were undertaken via the mesodiencephalic intraventricular infusion. Results show that S2C (Fraction-III) (50 micrograms/rabbit, i.c.v.) exhibited significant delta-enhancing effect compared to the controls. Further purification was done with Sephadex G-25 and Sephadex LH-20. The more purified S4B (50 micrograms/rabbit, i.c.v.) also exhibited significant delta-enhancing effect compared to the controls. The amino-acid analysis of Fraction-III revealed that the compositional contents of S2C and S4B are different from what have been known with Factor S, DSIP and SPS.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed2005

Increased sympathetic and decreased parasympathetic cardiovascular modulation in normal humans with acute sleep deprivation.

Cardiovascular autonomic modulation during 36 h of total sleep deprivation (SD) was assessed in 18 normal subjects (16 men, 2 women, 26.0 +/- 4.6 yr old). ECG and continuous blood pressure (BP) from radial artery tonometry were obtained at 2100 on the first study night (baseline) and every subsequent 12 h of SD. Each measurement period included resting supine, seated, and seated performing computerized tasks and measured vigilance and executive function. Subjects were not supine in the periods between measurements. Spectral analysis of heart rate variability (HRV) and BP variability (BPV) was computed for cardiac parasympathetic modulation [high-frequency power (HF)], sympathetic modulation [low-frequency power (LF)], sympathovagal balance (LF/HF power of R-R variability), and BPV sympathetic modulation (at LF). All spectral data were expressed in normalized units [(total power of the components/total power-very LF) x 100]. Spontaneous baroreflex sensitivity (BRS), based on systolic BP and pulse interval powers, was also measured. Supine and sitting, BPV LF was significantly increased from baseline at 12, 24, and 36 h of SD. Sitting, HRV LF was increased at 12 and 24 h of SD, HRV HF was decreased at 12 h SD, and HRV LF/HF power of R-R variability was increased at 12 h of SD. BRS was decreased at 24 h of SD supine and seated. During the simple reaction time task (vigilance testing), the significantly increased sympathetic and decreased parasympathetic cardiac modulation and BRS extended through 36 h of SD. In summary, acute SD was associated with increased sympathetic and decreased parasympathetic cardiovascular modulation and decreased BRS, most consistently in the seated position and during simple reaction-time testing.

Adolescent↗
PubMed1988

[ATPase activity in neurons and glial cells of the brain of the rat after REM-sleep deprivation (cytophotometric study)].

Modified Washstein and Meisel's techniques were used for quantitative estimation of ATPases activity in the rat brain. The specific activity of Na+,K+-ATPase and Mg2+-ATPase was higher in glial cells than in the neurons. The 24-hr REM-sleep deprivation resulted in an enhancement of the activity of ATPases in neurons of the hippocampus whereas the activity of the above enzymes lowered in the gliocytes. The findings can be due to the changes in excitability of the neurons and depolarization of glia during the sleep deprivation.

Adenosine Triphosphatases↗
PubMed1995

Sleep deprivation in rats with preoptic/anterior hypothalamic lesions.

Chronic total sleep deprivation (TSD) of rats by the disk-over-water method reliably produces initial increases and subsequent decreases in waking intraperitoneal (Tip) and hypothalamic (Thy) temperatures, progressive increases in energy expenditure, skin lesions on the tail and plantar surfaces, debilitated appearance, and eventual death. We investigated the possible role of the preoptic/anterior hypothalamus (POAH) in the mediation of the TSD effects by comparing these effects in POAH-lesioned and unlesioned rats. Bilateral POAH lesions sufficient in size to impair homeothermic responses to changes in ambient temperature did not produce TSD-like temperature changes under baseline ambient temperatures of 28-29 degrees C, implying that the thermoregulatory changes produced by TSD do not result from impairment of the lesioned area. However, the possibility remains that the TSD effects are mediated by damage to POAH areas that were not lesioned. During TSD, lesioned and unlesioned rats showed similar progressive increases in energy expenditure, but the lesioned rats showed earlier, steeper, and eventually greater declines in Tip and Thy. This result suggests that in unlesioned rats the POAH may counter-regulate against, and thereby attenuate, the reduction in heat retention caused by TSD. This failure of regulation in lesioned rats is consistent with their impaired response to ambient temperature change and implies that, in unlesioned rats, some POAH thermoregulatory mechanisms continue to function normally during TSD. Lesioned rats did not show the characteristic TSD-induced early increases in Tip and Thy. This result could imply either that heat retention was so compromised that body temperatures did not rise in spite of a TSD-induced increases in thermoregulatory setpoint, or that the setpoint increase in unlesioned rats is POAH-mediated. Notwithstanding the greater Tip and Thy declines in lesioned rats, they survived the TSD procedure longer than the unlesioned rats, thus supporting previous indications that death did not result from hypothermia.

Analysis of Variance↗