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PubMedDate not supplied

Repeated sleep deprivation as a therapeutic Zeitgeber for circular type manic depressive disturbance.

A post-menopausal woman suffering from a circular type manic depressive psychosis who had been treated by drugs was followed for 8 months on a self-reporting mood rating scale. The drug regimen was continued over a further 8 months but with the addition of 5 nights of sleep deprivation at the depth of her recurrent depressed moods. Time series analyses of the subject's longitudinal mood scores revealed a persistent cycle of 32 days. After 5 sleep deprivation treatments this cycle shortened to 28 days which endured at least for the ensuing 8 months. After sleep deprivation and decrease of the amplitude, an improvement of mood was obtained. It is suggested that the increased LD ratio obtained in sleep deprivation may be as therapeutic as the actual loss of sleep itself.

Bipolar Disorder↗

PubMed1995

Somnogenic effects of sleep deprivation and Escherichia coli inoculation in rabbits.

To evaluate the impact of sleep deprivation (SD) on microbially induced alterations in sleep, we used gentle handling to deprive rabbits of sleep for 4 h before or after intravenous inoculation with Escherichia coli (EC). Sleep was monitored for the next 20 h. EC inoculation alone increased slow-wave sleep (SWS) time, delta-wave amplitude (DWA) during sleep and SWS bout length during the initial 2-4 h after inoculation. During the following 8-20 h, DWA during SWS was reduced relative to control values. SD alone increased SWS time and SWS bout length for 2 h after the end of the SD period. Rabbits subjected to SD for 4 h prior to EC inoculation demonstrated increases in SWS time, DWA during SWS and SWS bout length 2-4 h postinoculation. At some time points, these effects were greater in magnitude than those induced by either manipulation alone, but they were generally equivalent to the additive effects of the individual treatments. Rabbits subjected to SD after EC inoculation (i.e. during the period in which EC increases sleep) demonstrated increases in SWS time and DWA during SWS for only 2 h after the end of the SD period, suggesting that these animals maintained a sleep deficit as compared to rabbits inoculated with EC alone. SD alone elicited hyperthermia in rabbits, and EC-inoculated rabbits subjected to SD developed fevers greater than those induced by either treatment alone. Other clinical indices were not significantly affected by the combined treatments. These data indicate that the sleep changes that occur subsequent to bacterial inoculation are altered in sleep-deprived rabbits, but that SD does not exacerbate clinical illness in this model.

Journal Article↗

PubMed1985

Sleep deprivation, physical fatigue, and the perception of exercise intensity.

This paper presents the results of three experiments to determine the effect of sleep deprivation and physical fatigue on ratings of perceived exertion (RPE) for exercise of short (30 s) and long (15-50 min) duration. In the first, 12 male subjects walked on a treadmill, 50 min every 3 h, at 28% of their VO2max for 60 h without sleep. The RPE, recorded at the mid-point of each exercise bout, increased progressively with sleep loss. In the second experiment, when 12 female subjects performed ten 30-s bicycle exercise bouts before and after 54 h without sleep, there was no significant increase in RPE. In the third experiment, which examined the effect of physical fatigue on RPE, seven males performed two sets of ten 30-s bouts of cycle exercise before and after treadmill exercise at 70% of their VO2max to voluntary exhaustion. In one set, RPE was recorded; in the other, power output was measured. During the treadmill running, increases in RPE were observed and attributed to fatigue. This same fatigue caused only small changes in RPE and power output for the cycle exercise. The combined data suggest that where the exercise is of several minutes' duration, RPE is increased by sleep deprivation and by physical fatigue. Where the exercise period is as short as 30 s, sleep deprivation has no effect and physical fatigue causes only a small change in the perception of exercise intensity.

Adult↗

PubMed2005

Effect of rapid-eye-movement sleep deprivation on rat hypothalamic prostaglandins.

In this study, we investigated thyroid hormones, thyroid stimulating hormone (TSH), prostaglandin D(2) (PGD(2)) and prostaglandin E(2) (PGE(2)) levels in rapid-eye-movement (REM) sleep-deprived rats compared with controls. The aim of the present study was to detect the effect of REM sleep deprivation (RSD) especially on hypothalamic prostaglandin levels. Twenty-seven male rats were randomly assigned in three groups as dry cage control, yoked control, and RSD. RSD rats were sleep deprived for 10 consecutive days. At the end of 10th day all rats were sacrificed for measurement. Our results indicated that total triiodothyronine (T(3)) and thyroxine (T(4)) decreased in the RSD group while there was no change in TSH. We also measured hypothalamic PGD(2) and PGE(2) levels, but we could not find any significant change between groups.

Animals↗

PubMed2005

Orexin and MCH neurons express c-Fos differently after sleep deprivation vs. recovery and bear different adrenergic receptors.

Though overlapping in distribution within the posterior hypothalamus, neurons containing orexin (Orx) and melanin concentrating hormone (MCH) may play different roles in the regulation of behavioural state. In the present study in rats, we tested whether they express c-Fos differently after total sleep deprivation (SD) vs. sleep recovery (SR). Whereas c-Fos expression was increased in Orx neurons after SD, it was increased in MCH neurons after SR. We reasoned that Orx and MCH neurons could be differently modulated by noradrenaline (NA) and accordingly bear different adrenergic receptors (ARs). Of all Orx neurons (estimated at approximately 6700), substantial numbers were immunostained for the alpha1A-AR, including cells expressing c-Fos after SD. Yet, substantial numbers were also immunostained for the alpha2A-AR, also including cells expressing c-Fos after SD. Of all MCH neurons (estimated at approximately 12,300), rare neurons were immunostained for the alpha1A-AR, whereas significant numbers were immunostained for the alpha2A-AR, including cells expressing c-Fos after SR. We conclude that Orx neurons may act to sustain waking during sleep deprivation, whereas MCH neurons may act to promote sleep following sustained waking. Some Orx neurons would participate in the maintenance of waking during deprivation when excited by NA through alpha1-ARs, whereas MCH neurons would participate in sleep recovery after deprivation when released from inhibition by NA through alpha2-ARs. On the other hand, under certain conditions, Orx neurons may also be submitted to an inhibitory influence by NA through alpha2-ARs.

Animals↗

PubMed1984

Enkephalinase inhibition antagonizes the increased susceptibility to seizure induced by REM sleep deprivation.

In order to elucidate the relationship between REM sleep and the enkephalinergic system, the effects of REM sleep deprivation (REMSD), stress and the enkephalinase inhibitor phosphoramidon on handling-induced convulsions were studied in mice. REMSD, stress and phosphoramidon (25-500 micrograms icv) increased the frequency of handling-induced convulsions (HIC) in normal mice. However, only in the last two groups were HIC antagonized by naloxone (1 mg/kg IP). In REMSD mice, phosphoramidon decreased the frequency of HIC, this effect being abolished by naloxone. The increase of neuronal excitability during REMSD is suggested to be associated with an insufficiency of the enkephalinergic system.

Animals↗

PubMedDate not supplied

REM sleep deprivation and food intake.

The effect of REM-sleep deprivation (REM-SD) on diet preference was studied in rats. REM-SD for a period of 72 hrs produced an increase in day, night and 24 hrs (day plus night) intakes of Carbohydrate Rich diet (CRD) and Total diet (TD). Body weight (BWt) was also increased. The maximum increase in the above parameters were recorded on the 2nd day of REM-SD. During recovery period the intakes of TD fully recovered, but the BWt and consumption of CRD remained high. Intakes of Balanced diet (BD) remained significantly on the lower side when compared to the pre REM-SD mean values. During REM-SD, the rats preferred CRD than BD. The body temperature did not show any change. The increase in TD intake and BWt could be the result of an increase in insulin level and the change appears to be mediated by the activation of hypothalamic feeding centre.

Animals↗

PubMed2004

Functional imaging of working memory after 24 hr of total sleep deprivation.

The neurobehavioral effects of 24 hr of total sleep deprivation (SD) on working memory in young healthy adults was studied using functional magnetic resonance imaging. Two tasks, one testing maintenance and the other manipulation and maintenance, were used. After SD, response times for both tasks were significantly slower. Performance was better preserved in the more complex task. Both tasks activated a bilateral, left hemisphere-dominant frontal-parietal network of brain regions reflecting the engagement of verbal working memory. In both states, manipulation elicited more extensive and bilateral (L>R) frontal, parietal, and thalamic activation. After SD, there was reduced blood oxygenation level-dependent signal response in the medial parietal region with both tasks. Reduced deactivation of the anterior medial frontal and posterior cingulate regions was observed with both tasks. Finally, there was disproportionately greater activation of the left dorsolateral prefrontal cortex and bilateral thalamus when manipulation was required. This pattern of changes in activation and deactivation bears similarity to that observed when healthy elderly adults perform similar tasks. Our data suggest that reduced activation and reduced deactivation could underlie cognitive impairment after SD and that increased prefrontal and thalamic activation may represent compensatory adaptations. The additional left frontal activation elicited after SD is postulated to be task dependent and contingent on task complexity. Our findings provide neural correlates to explain why task performance in relatively more complex tasks is better preserved relative to simpler ones after SD.

Adult↗

PubMed2002

REM sleep deprivation suppresses acquisition of classical eyeblink conditioning.

STUDY OBJECTIVES: The aim of this study was to investigate the issue of whether REM sleep is involved in implicit learning through the cerebellum-related neural circuit via the use of classical eyeblink conditioning (CEC). DESIGN: Subjects were divided into three groups: control (sleep without interruption), REM sleep deprivation (RD), and slow wave sleep (stage 3+4) deprivation (SD). The CEC was performed after 8 hours of ordinary nocturnal sleep or sleep disrupted at a selected sleep stage. SETTING: A university-based sleep laboratory. PATIENTS OR PARTICIPANTS: Twenty-seven healthy volunteers (all men, aged 23.2+/-0.6 years). INTERVENTIONS: The CEC was measured after selective sleep deprivation or ordinary nocturnal sleep. MEASUREMENTS AND RESULTS: The eyeblink reflex was conditioned using a classical delay conditioning paradigm. The conditioned response (CR) was determined by electromyography measurements of the orbicularis oculi muscles. The rate of appearance of the CR was compared among the three groups. Compared with the control subjects, RD subjects were significantly deficient in their capacity to acquire conditioned eyeblinks, while no difference was found among the SD subjects. CONCLUSIONS: This study suggests that RD suppresses the cerebellar function in CEC and that REM sleep is closely linked with the learning function in the cerebellum.

Adult↗

PubMedDate not supplied

Aging does not affect the sleep endocrine response to total sleep deprivation in humans.

Aging is associated with decreased sleep continuity, slow wave sleep (SWS), growth hormone (GH) release and an increased hypothalamo-pituitary-adrenocortical (HPA) system activity. Total sleep deprivation (TSD) is a strong stimulus for sleep. To determine if aging affects the response to TSD, for the first time the combined effects of TSD on conventional and spectral sleep electroencephalographic (EEG) parameters and GH, cortisol and prolactin secretion were compared in elderly (60-80 years; n = 7) vs. younger subjects (20-30 years; n = 7). MANOVA revealed a reduction of SWS in the elderly. TSD led to an increase in SWS, a decrease in sleep onset latency, rapid eye movement (REM) density and by trend REM-latency without a global group difference. GH was reduced, whereas prolactin was enhanced in the elderly. After TSD GH was unchanged and prolactin secretion was enhanced without group difference. Thus, the plasticity of the sleep-endocrine system in response to TSD is sustained during aging. The possible involvement of the GABAergic system, that seems not to be severely impaired with age, is proposed.

Adult↗

PubMed2003

Time estimation during prolonged sleep deprivation and its relation to activation measures.

This is the first study to analyze variations in time estimation during 60 h of sleep deprivation and the relation between time estimation performance and the activation measures of skin resistance level, body temperature, and Stanford Sleepiness Scale (SSS) scores. Among 30 healthy participants 18 to 24 years of age, for a 10-s interval using the production method, we found a lengthening in time estimations that was modulated by circadian oscillations. No differences in gender were found in the time estimation task during sleep deprivation. The variations in time estimation correlated significantly with body temperature, skin resistance level, and SSS throughout the sleep deprivation period. When body temperature is elevated, indicating a high level of activation, the interval tends to be underestimated, and vice versa. When the skin resistance level or SSS is elevated (low activation), time estimation is lengthened, and vice versa. This lengthening is important because many everyday situations involve duration estimation under moderate to severe sleep loss. Actual or potential applications of this research include transportation systems, emergency response work, sporting activities, and industrial settings in which accuracy in anticipation or coincidence timing is important for safety or efficiency.

Adolescent↗

PubMedDate not supplied

Increased voluntary alcohol drinking concurrent with REM-sleep deprivation.

The alcohol intake of twenty adult Long-Evans male rats was recorded before, during and after rapid eye movement sleep (REM) deprivation produced with the flowerpot technique modified by using a cuff pedestal and an electrified grid floor instead of water. The alcohol intake reached a steady level of 2.8 g/kg/day in the 3 weeks before REM deprivation. During seven REM-sleep deprivation days the alcohol intake was significantly elevated, finally increasing to 3.7 g/kg/day. A rebound decrease in alcohol drinking was then observed during the "REM-rebound" phase immediately after the termination of REM-sleep deprivation. The results suggest a possible vicious circle of REM-sleep deprivation increasing alcohol drinking and alcohol intake causing REM-sleep deprivation.

Alcohol Drinking↗

PubMed2000

Systemic injection of a nitric oxide synthase inhibitor suppresses sleep responses to sleep deprivation in rats.

We hypothesized that nitric oxide (NO) may play a role in homeostatic sleep regulation. To test this hypothesis, we studied the sleep deprivation (SD)-induced homeostatic sleep responses after intraperitoneal administration of an NO synthase inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME, a cumulative dose of 100 mg/kg). Amounts and intensity of sleep were increased in response to 8 h of SD in control rats (n = 8). Sleep amounts remained above baseline for 16 h after SD followed by a negative rebound. Rapid eye movement sleep (REMS) and non-REMS (NREMS) intensities were elevated for 16 and 4 h, respectively. L-NAME treatment (n = 8) suppressed the rebound increases in NREMS amount and intensity. REMS rebound was attenuated by L-NAME in the first dark period after SD; however, a second rebound appeared in the subsequent dark period. REMS intensity did not increase after SD in L-NAME-injected rats. The finding that the NO synthase inhibitor suppressed rebound increases in NREMS suggests that NO may play a role as a signaling molecule in homeostatic regulation of NREMS.

Animals↗

PubMed2006

Serotonin and 5-hydroxy-indole-acetic acid contents in dorsal raphe and suprachiasmatic nuclei in normal, malnourished and rehabilitated rats under 24 h of sleep deprivation.

It has been discussed that serotonin (5-HT) could be involved in the effects of sleep deprivation (SD) and/or malnutrition (M) on the sleep-wake cycle. The aim of this work was to study the effects of the M, SD and its interaction on 5-HT and 5-hydroxy-indole-acetic acid (5-HIAA) contents in the dorsal raphe (DR) and the suprachiasmatic nuclei (SCN), two sleep-wake cycle regulators. Forty-eight puppets rats were obtained from mothers fed with low or normal casein diet. They were allocated in 3 groups (n=16 each): prenatal/postnatal casein malnutrition (6/6%), prenatal casein malnutrition/nutritional casein rehabilitation (6/25%) and prenatal/postnatal casein well-nourished state (25/25%). When rats were 60 days old, 24 animals were exposed to sleep deprivation by means of forced locomotion during 24 h. The remaining 24 were kept under normal conditions of sleep-wake cycle. Then, all animals were sacrificed by decapitation. DR and SCN were dissected and processed to determine the 5-HT and 5-HIAA contents by means of HPLC. It was observed that 6/6% rats showed a 5-HT increase (DR p<0.011; SCN p<0.019) as well as in SD (DR p<0.0008; SCN p<0.0009) with respect to 25/25% rats. No differences were found in 6/25% rats. Therefore, 5-HIAA decreased significantly in both nuclei in all the groups, notably in M+SD animals (DR p<0.001; SCN p<0.001). We conclude that the sleep-wake cycle disruptions produced by chronic M and SD are mediated in part by a synergistic effect on 5-HT in the DR-SCN pathway, perhaps due to a delay in the development of such brain structures.

Animals↗

PubMed1996

Sleep deprivation does not induce sister chromatid exchange in humans.

In a preliminary study Bamezai and Kumar (1992) reported that a 24-h period of sleep deprivation may raise sister chromatid exchange (SCE) frequencies up to 193% in peripheral blood lymphocytes. This was reinvestigated to clarify the role of sleep duration as a confounder for SCE, which is a well-established parameter for biomonitoring in occupational medicine. In our study, the SCE baseline and the influence of a 24-h period of sleep deprivation (test period) on SCE were investigated for 20 non-smoking volunteers (10 females and 10 males; 20-29 years of age). There was no significant difference (Pall = 0.094) between the deviations of the two SCE rates of the control period (mean: -0.21 +/- 0.90 SCE) and the differences between SCE rates before and after sleep deprivation (mean: 0.42 +/- 0.94 SCE) of each proband. No significant difference was detected between females and males, and SCE did not correlate with age or sleep duration. Therefore we conclude that the influence of sleep deficit on SCE is in the range of a normal day-to-day variance, and has not to be taken into account when SCE is used for a genotoxic monitoring at the workplaces.

Adult↗

PubMed1977

A method for sleep depriving rats.

A method is described for sleep depriving up to 12 rats at a time by placing them in two large rotating cylinders. EEG data, previously unavailable for rats treated in this manner, show that total sleep time was significantly reduced from 47.0% to 3.8% of a 24-hr period. There was no selective reduction of REM or non-REM sleep.

Animals↗

PubMed2000

Moderate sleep deprivation produces impairments in cognitive and motor performance equivalent to legally prescribed levels of alcohol intoxication.

OBJECTIVES: To compare the relative effects on performance of sleep deprivation and alcohol. METHODS: Performance effects were studied in the same subjects over a period of 28 hours of sleep deprivation and after measured doses of alcohol up to about 0.1% blood alcohol concentration (BAC). There were 39 subjects, 30 employees from the transport industry and nine from the army. RESULTS: After 17-19 hours without sleep, corresponding to 2230 and 0100, performance on some tests was equivalent or worse than that at a BAC of 0.05%. Response speeds were up to 50% slower for some tests and accuracy measures were significantly poorer than at this level of alcohol. After longer periods without sleep, performance reached levels equivalent to the maximum alcohol dose given to subjects (BAC of 0. 1%). CONCLUSIONS: These findings reinforce the evidence that the fatigue of sleep deprivation is an important factor likely to compromise performance of speed and accuracy of the kind needed for safety on the road and in other industrial settings.

Adult↗

PubMed1990

Effects of REM sleep deprivation of ACTH-induced yawning.

Central administration of ACTH in rats induces yawning and stretching. In order to study the effects of REM sleep deprivation on ACTH-induced yawning, the peptide was injected immediately after the REM sleep deprivation period or 24 h later. REM sleep deprivation impaired ACTH-induced yawning, but after a 24-hour recovery period, rats displayed a number of yawns similar to those in control animals. Implications for an involvement of dopaminergic and mainly cholinergic systems are discussed.

Adrenocorticotropic Hormone↗