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Results for “SLEEP DEPRIVATION”

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PubMed1989

[A world record in marathon tennis: sleep deprivation and performance].

We studied the effects of marked sleep deprivation on the EEG patterns and performance of a physically fit man (age 26) on the occasion of the world record continuous marathon tennis play (147 hours, 20 minutes). Before and immediately after the marathon, the sleep patterns of the player were recorded in our laboratory. After playing for 40 and 80 hours and within 24 hours, the performance changes were evaluated each hour. Amounts of the different sleep stages during the first recovery night compared with those of the baseline indicate an increase of 56% for total sleep time, 54% for stages 1 and 2, 154% for stages 3 and 4 and 20% for REM sleep. During the second recovery night, only REM sleep showed an increase. Activity index showed a marked decrease after 80 hours of sleep deprivation compared with that after 40 hours and was dramatically worsened during nighttime. The number of faults and pauses was also increased after 80 hours, suggesting a clear performance deterioration. Our results confirmed the effects of sleep deprivation on the recovery and performance deterioration.

Adult↗

PubMed1991

The levels of urinary epinephrine during daytime REM sleep deprivation.

Urinary excretion of epinephrine during REM sleep deprivation in the daytime was examined in an attempt to determine whether epinephrine excretion during sleep is related to the structure of disturbed sleep. Six healthy males were subjected to two experimental conditions: 1) day sleep without interruption, as a control condition, and 2) day sleep with REM sleep deprivation. Under both conditions, epinephrine excretion levels of five of the subjects were found to be distributed along a basal regression line, expressing the relationship of epinephrine excretion and percent of waking time, as calculated in a previous study. The epinephrine levels of the one remaining subject exceeded the values predicted by the regression line. His sleep structure was not only distorted under REM deprivation conditions but also under control conditions as well. These results suggest that the basal regression line is useful for observing the existence of sleep disturbance; indeed, a subject with epinephrine excretion levels much higher than those predicted by the regression line was found to have spontaneously disturbed sleep. More study is needed to clarify the relationship between high epinephrine levels and disturbed sleep.

Adult↗

PubMed1998

Effects of sleep deprivation in neonatal rats.

This investigation represents the first systematic study of sleep homeostasis in developing mammals that spans the preweaning and postweaning periods. Neonatal rats from 12 to 24 days of postnatal life (P12-P24) were anesthetized with Metofane (methoxyflurane) and implanted with miniaturized electroencephalographic (EEG) and electromyographic electrodes. After 48 h of recovery, neonatal rats were sleep deprived for 3 h by either gentle handling or forced locomotion. We find that 3-h sleep deprivation produces dramatically different compensatory responses at different stages of postnatal development. In striking contrast to adult rats, sleep deprivation does not increase slow-wave sleep EEG delta (0.5-4.0 Hz) activity in rats younger than P24. However, P12-P20 rats do show evidence of sleep regulation because they show compensatory increases in sleep time and sleep continuity during recovery. In P12 rats, approximately 90% of total slow wave sleep time lost during the sleep-deprivation period was recovered during subsequent sleep. A similar recovery of active sleep time was observed in P20-P24 rats. These findings suggest not only that sleep is regulated in neonatal rats but that the accumulation and/or discharge of sleep need changes dramatically between the third and fourth postnatal weeks.

Activity Cycles↗

PubMed1979

Lymphocyte and granulocyte reactions during sleep deprivation.

The possible influence of 48 hr of sleep deprivation on in vitro DNA synthesis of blood lymphocytes and on the adhesiveness and intracellular, stainable activity of alkaline phosphatase in blood granulocytes was studied in twelve young male volunteers. Following the sleep deprivation, all 12 subjects showed marked reductions of DNA synthesis after stimulation with phytohemagglutinin. Pre-exposure levels were regained 5 days after terminating the vigil. No changes were noted in granulocyte adherence or alkaline phosphatase activity. The results suggest that sleep deprivation may decrease cell-mediated immune reactions and thereby impair some aspects of host defense.

Adult↗

PubMed2006

Effects of sleep and sleep deprivation on immunoglobulins and complement in humans.

Evidence from preclinical and clinical studies indicates that concentrations of cytokines are altered in sleep deprivation. However, data on the impact of sleep deprivation on concentrations of immunoglobulin and complement have received little scientific examination. The purpose of this study was to investigate the effects of 24h sleep deprivation on parameters of humoral immunity. Ten healthy volunteers (5 men and 5 women, 21-25 years old) stayed awake from 07:00 on day 1 until 07:00 on day 2 (sleep deprivation group), while another eight (4 men and 4 women, 21-23 years old) slept normally during the night (control group). Blood samples were drawn from the antecubital vein each day at 07.00. Parameters of humoral immunity, including serum IgG, IgA, IgM and C3, C4, were measured using an automatic analysis system. Experimental data showed that the levels of IgG, IgA, IgM and C3, C4 were all higher in the sleep-deprived group than in the control group (P<0.05). These findings indicate that sleep deprivation enhances changes in the parameters of serum humoral immunity.

Adult↗

PubMed1997

Assessing vigilance through a brief pencil and paper letter cancellation task (LCT): effects of one night of sleep deprivation and of the time of day.

Behavioural effects of the lack of sleep in normal subjects have been investigated mostly by experimenter-paced choice reaction times in prolonged stimulus detection tasks. However, length and procedure complexity of these tasks limit their use in research on larger numbers of subjects. The aim of the present study was to assess the effectiveness of a brief subject-paced pencil and paper performance task, i.e. letter cancellation task (LCT) in revealing the effects of one night of sleep deprivation. In addition, the authors evaluated sleep loss and time of day effects on six Visual Analogue Scales (VAS) measuring subjective activation-deactivation. Results show that a LCT is sensitive in revealing the effects of time of day and of 24 h of sleep deprivation. Effects of sleep deprivation were also revealed by VAS data. Sleepiness, tiredness and energy scales on the VAS were also affected by time of day. Despite the sensitivity of both the LCT and VAS, there was little correspondence between performance and subjective measures.

Adult↗

PubMed1988

Effects of lithium on dopamine behavioural supersensitivity induced by rapid eye movement sleep deprivation.

The effects of lithium on the potentiation of d-amphetamine-induced hyperlocomotion were evaluated in rapid eye movement (REM) sleep deprived rats. Under control conditions, pretreatment with lithium during 7 days did not modify the hyperlocomotion produced by d-amphetamine. REM sleep deprivation induced a pronounced potentiation of the locomotor response to d-amphetamine. In a stress control group this potentiation also occurred, but to a lesser degree than in the REM sleep deprived group. Lithium pretreatment prevented the increased response to d-amphetamine in both REM sleep deprived and stress control animals. The effects of lithium in REM sleep deprived rats are in accordance with reports that lithium is able to prevent the development of dopamine receptor supersensitivity. However, it cannot be excluded that in both REM sleep deprived and stress control groups the increased response to d-amphetamine is related to noradrenergic changes and/or noradrenergic-dopaminergic interactions. REM sleep deprivation seems to be an interesting model to study the underlying mechanisms of manic-depressive illness.

Animals↗

PubMed1981

A comparative study of the diagnosis value of drug-induced sleep EEGs and sleep EEGs following sleep deprivation in patients with complex partial seizures.

The purpose of the study was to investigate whether the sleep EEG after sleep deprivation has a stronger provocative effect than the drug-induced sleep EEG. For this purpose a sleep EEG, induced by 2 mg/kg body weight of promazine hydrochloride, was recorded. On the following day a sleep EEG of the same patient was recorded after sleep deprivation of 24--26 h. If only patients whose wake EEGs were free from epileptic activity are considered, the rate of provocation was 58%. As epileptic activity could be recorded even in the sleep EEG without sleep deprivation in 45%, the advantage gained by recording a sleep EEG after sleep deprivation (52%) is only relatively small. The occurrence of epileptic activity was shown to be significantly more frequent amongst women and those who developed epilepsy at a younger age. For practical purposes it is recommended that for those patients whose wake EEGs are free from epileptic activity, a sleep EEG--possibly drug-induced--should be recorded. Only in instances where epileptic activity can not then be recorded should a wake EEG after sleep deprivation be carried out, and followed immediately, if necessary, by a sleep EEG.

Adolescent↗

PubMed1975

Rapid eye movement (rem) sleep deprivation: effect on acid mucopolysaccharides in rat brain.

The effect of rapid eye movement (REM) sleep deprivation on the total content and proportion of different mucopolysaccharides (AMPS) containing uronic acid in rat brain was studied. REM sleep deprivation was induced by the water tank methods. Five experimental groups of animals were used: control, stressed, REM sleep deprived, post-stress sleeping and post-deprivation sleeping rats. No changes of AMPS were observed in any of the experimental groups when the whole brain was analysed. A significant increase of AMPS was found in the cerebral hemispheres of stressed and REM deprived rats. A significant decrease of AMPS was observed in the cerebellum and brain stem. A further increase of AMPS was found in the cerebral hemispheres after the rebound of REM sleep following its deprivation, and after the recovery sleep following the stress. A significant increase of AMPS was found in the brain stem of rats allowed to recuperate after REM deprivation or stress as compared with the stressed and REM deprived animals. Recovery sleep induced a significant increase of AMPS in the cerebellum in previously stressed rats, while previously REM deprived rats exhibited a further decrease of AMPS from control values. The possible functional meaning of these results is discussed in relation to the role of REM sleep in protein synthesis and learning and memory processes. Intriguing, well-controlled positive findings and the fact that no experimental design is known where stress is minimal while REM deprivation is 100 per cent, justify and encourage continued efforts in studying the biochemical state of the brain during sleep and/or its alterations.

Adrenal Glands↗

PubMed1998

Involvement of stress in the sleep rebound mechanism induced by sleep deprivation in the rat: use of alpha-helical CRH (9-41).

A previous study demonstrated the efficacy of the corticotropin-releasing hormone (CRH) receptor antagonist, alpha-helical CRH (9-41), in blocking the paradoxical sleep increase induced by stress. In the present study, this peptide was used to evaluate the involvement of the stress component of the sleep deprivation, in the paradoxical sleep rebound. Rats were subjected for 10 h to the classical water-tank sleep-deprivation technique and were given, every 2 h throughout the sleep deprivation period, intracerebroventricular injections of either 100 microg/5 microl of alpha-helical CRH (9-41) or vehicle alone. Continuous recordings showed that antagonist treatment decreased the PS rebound, but not the SWS rebound, following sleep deprivation. These findings suggest that, in the water-tank sleep deprivation method, stress, acting via CRH activation, is the main factor inducing the paradoxical sleep rebound.

Animals↗

PubMed2003

Palatable solutions during paradoxical sleep deprivation: reduction of hypothalamic-pituitary-adrenal axis activity and lack of effect on energy imbalance.

Paradoxical sleep deprivation (PSD) induces increased energy expenditure in rats, insofar as rats eat more but loose weight throughout the deprivation period. In the present study, rats were offered water, saccharin or sucrose to drink during the deprivation period, since it has been proposed that carbohydrates reduce the hypothalamic-pituitary-adrenal (HPA) axis response to stress. Rats were submitted to the flower pot technique for 96 h. During the PSD period, they were weighed daily and food and fluid intake was assessed twice a day. At the end of the PSD period, rats were killed and plasma concentrations of glucose, adrenocorticotropic hormone (ACTH) and corticosterone were assayed. Compared to their control counterparts, all paradoxical sleep-deprived rats consumed more food, but lost weight. Paradoxical sleep-deprived rats given sucrose drank more than their control counterparts (especially in the light phase of the light/dark cycle). Paradoxical sleep-deprived rats showed increased food intake during all periods throughout the experiment, with peak intake during the dark phase and nadir during the light phase of the light/dark cycle. All paradoxical sleep-deprived rats showed lower glucose plasma levels than control rats and increased relative adrenal weight. However, when given saccharin or sucrose, paradoxical sleep-deprived rats showed lower concentrations of ACTH and corticosterone than their water-provided counterparts, indicating that palatable fluids were capable of lowering HPA axis activation produced by PSD. The fact that PSD induced energy imbalance regardless of the relative attenuation of the HPA axis activity produced by saccharin or sucrose suggests that the HPA axis may play only a secondary role in this phenomenon, and that other mechanisms may account for this effect. The data also suggest that supply of palatable fluids can be an additional modification to reduce the stress of the flower pot method.

Adrenal Glands↗

PubMed2002

Influence of 24-hour sleep deprivation on respiration in lambs.

The aim of this study was first to examine the effects of 24-h sleep deprivation on apnea index and duration in lambs. The effects on sleep architecture and sigh and swallowing indices were also studied. The impact of postnatal maturation on all measured variables was assessed by studying two different age groups. Twelve lambs (six aged 1-2 d and six aged 23-24 d on the day of surgery) were chronically instrumented for polysomnographic recordings including sleep state assessment, nasal flow, diaphragm electromyogram, and glottal constrictor muscle electromyogram. Two recordings, one control and one after 24-h sleep deprivation, were performed in all lambs. Results show that the effects of sleep deprivation predominate in rapid eye movement sleep in the younger group, with increased rapid eye movement sleep proportion and apnea, sigh, and swallowing index. Our results in lambs suggest that the consequences of sleep deprivation upon respiration are predominant early after birth. Although the potential relationship of these observations to neonatal apneas and sudden infant death syndrome has yet to be defined, awareness of the effects of sleep deprivation is important for neonatal care.

Animals↗

PubMed1983

The effect of sleep deprivation on the EEG in epilepsy.

Many published studies report an increased incidence of epileptiform EEG activity following sleep deprivation in persons with epilepsy in whom a previous routine EEG was normal or inconclusive. Few such studies, however, permit a clear distinction to be made between the effects of sleep deprivation per se, sleep induction following deprivation, or simply repeated EEG recording. Sixty-nine patients have been investigated in whom a routine waking record, a secobarbital-induced sleep recording and an EEG following 24 h sleep deprivation were obtained in random order irrespective of whether or not the initial EEG contained epileptiform activity. For each record the incidence of epileptiform activity if any, was quantified in terms of discharges per minute for wake, drowsiness and each sleep stage. The findings confirmed the marked activating effect of light sleep on the EEG but there was no evidence of an overall increase in discharge rate after sleep deprivation either in the waking state or in the various sleep stages when these were compared with secobarbital-induced or spontaneous sleep. There was a significant increase of generalized discharges in the waking state only, after sleep deprivation, but a decrease in incidence of focal epileptiform activity. It is concluded that although specific indications may exist for the use of sleep deprivation, as a general method of EEG activation in epilepsy it has no advantages over barbiturate-induced sleep to offset the greater inconvenience to patients.

Adult↗

PubMed2004

Involvement of dopamine receptors in cocaine-induced genital reflexes after paradoxical sleep deprivation.

Previous work has demonstrated that paradoxical sleep deprivation (PSD) potentiates cocaine-induced genital reflexes in male rats. To examine the possibility that this effect might involve alterations in binding to the DA transporter (DAT), we examined [3H] WIN 35,248 binding in brain after 96 h of PSD. No changes were found in any of the 11 brain regions examined. Since we had previously identified changes in D2 receptor binding after PSD, we next examined the effects of DA receptor subtype antagonists on cocaine-induced reflexes in sleep-deprived rats. Separate groups of PSD rats received saline, haloperidol (0.4, 0.8 or 1.6 mg/kg), SCH 23390 (0.25, 0.5, 1 mg/kg) or sulpiride (50, 100, 200 mg/kg) 60 min prior to acute cocaine (7 mg/kg). In saline pretreated rats, cocaine-induced penile erection (PE) in 100% of SD rats. This percentage was not significantly reduced by haloperidol at any dose, but was significantly reduced in rats pretreated with SCH 23390 (1 mg/kg) or sulpiride (100 or 200 mg/kg). In addition, acute cocaine-induced ejaculation in 80% of SD rats. This effect was not affected by haloperidol at any dose, but was significantly reduced by all doses of SCH 23390 and by the 200 mg/kg dose of sulpiride. These results suggest that the potentiating effects of cocaine on penile erection and ejaculation are likely due to PSD-induced changes in DA postsynaptic receptor sensitivity rather than alterations in DA transporter. They further suggest that both D1 and D2 receptors may play a role in these effects.

Analysis of Variance↗

PubMed2002

Sleep deprivation impairs long-term potentiation in rat hippocampal slices.

To determine if 12-h sleep deprivation disrupts neural plasticity, we compared long-term potentiation (LTP) in five sleep-deprived and five control rats. Thirty minutes after tetanus population spike amplitude increased 101 +/- 15% in 16 slices from sleep deprived rats and 139 +/- 14% in 14 slices from control rats. This significant (P < 0.05) reduction of LTP, the first demonstration that the sleep deprivation protocol impairs plasticity in adult rats, may be due to several factors. Reduced LTP may indicate that sleep provides a period of recuperation for cellular processes underlying neural plasticity. Alternatively, the stress of sleep deprivation, as indicated by elevated blood corticosterone levels, or other non-sleep-specific factors of deprivation may contribute to the LTP reduction.

Animals↗

PubMed1997

EEG delta power and auditory arousal in rested and sleep-deprived rabbits.

Slow-wave activity in the electroencephalogram is thought to reflect the depth or intensity of sleep. This hypothesis is primarily derived from studies of rats or humans. However, some characteristics of sleep of rabbits differ from those of rats or humans. To determine whether slow-wave activity (power density in the delta frequency band of 0.5-5.0 Hz) correlates with arousability in rabbits, we presented auditory stimuli (72-90 dB) to control or sleep-deprived animals during slow-wave sleep. The resulting behavioral responses, defined by changes in eye state and body posture, and the latency to return to sleep were used as measures of arousability. Behavioral responsiveness to auditory stimuli increased with increasing stimulus intensity in both control and sleep-deprived animals. Overall, however, sleep-deprived animals exhibited fewer postural changes and eye openings than did control rabbits. Sleep-deprived rabbits also more rapidly returned to sleep after the stimulus presentation than did control animals. Latency to return to sleep was correlated with delta power before stimulus presentation, but behavioral responsiveness was not. These data suggest that, in this rabbit model, delta power may not be predictive of behavioral arousability but may reflect sleep propensity.

Acoustic Stimulation↗

PubMed2001

Influence of sleep deprivation coupled with administration of melatonin on the ultrastructure of rat pineal gland.

The effects of sleep deprivation with or without melatonin treatment on the pineal morphology in rats were studied. Five days after sleep deprivation and using electron microscopy, many of the pinealocytes exhibited structural alterations including dilation of the cisternae of the rough/smooth endoplasmic reticulum, Golgi saccules and mitochondria, and an increase in the numbers of lipid droplets, vacuoles and dense-core vesicles. These features were considered as morphological evidence of increased synthesis or secretion by the pineal gland. In addition, numerous membranous profiles, considered to be degraded cellular organelles, were observed in some pinealocytes and sympathetic nerve terminals. It is suggested that the occurrence of degenerating organelles had resulted from the deleterious effect of sleep deprivation. This may be attributed to an overload of secretory activity of the pineal gland during stress elicited by the long-term sleep deprivation, leading to functional exhaustion and irreversible damage of the oxidation-related organelles. In sleep-deprived rats receiving a single injection of melatonin (10 mg/kg) for 5 consecutive days, the above features indicative of pinealocytic activation were attenuated. In fact, all signs of degeneration of cellular organelles were rarely found. These results suggest that the pineal gland is itself a target for exogenously administered melatonin. Thus, melatonin when administered systemically may be used as a potential neuroprotective drug against neuronal damage induced by sleep deprivation.

Animals↗

PubMed1998

Sleep deprivation increases rat hypothalamic growth hormone-releasing hormone mRNA.

Much evidence indicates that growth hormone-releasing hormone (GHRH) is involved in sleep regulation. We hypothesized that GHRH mRNA would increase and somatostatin (SRIH) mRNA would decrease during sleep deprivation. With the use of RT-PCR and truncated internal standards, rat hypothalamic GHRH mRNA and SRIH mRNA levels were evaluated after sleep deprivation. After 8 or 12 h of sleep deprivation there was a significant increase in rat hypothalamic GHRH mRNA expression compared with time-matched control samples. Hypothalamic GHRH mRNA levels were not significantly different from control values after 1 or 2 h of recovery after 8 h of sleep deprivation or after 2 h of recovery after 12 h of sleep deprivation. In control animals, variations in hypothalamic GHRH mRNA levels were observed. GHRH mRNA expression was significantly higher in the afternoon than at dark onset or during the dark period. SRIH mRNA levels were significantly suppressed at the termination of an 8-h sleep deprivation period and were significantly higher after dark onset than in the morning. The alterations in GHRH and SRIH mRNA expressions after sleep deprivation and recovery support the notion that GHRH plays an important role in sleep homeostasis and suggest that these neuropeptides may interact reciprocally in modulating sleep as they do in the control of growth hormone secretion.

Animals↗