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PubMed1982

Quipazine has a biphasic effect on slow wave sleep and reduces REM sleep rebound in REM sleep deprived rats.

Rats implanted with electrodes for polygraphic recording were deprived of REM sleep for 24 hr. Following REM sleep deprivation animals were injected with quipazine maleate (7.5 mg/kg IP) and were polygraphically recorded for 48 hr. The results show that quipazine reduces REM sleep rebound and that it has a biphasic effect on slow-wave sleep: initial 6 hr suppression is followed by a delayed increase in the second 24 hr recording period. The initial suppression of slow-wave sleep we attribute to the stimulation of central serotonergic receptors while the effect on REM sleep rebound may result from quipazine's action on central catecholamines.

Animals↗

PubMed2003

Cardiac changes during sleep in sleep-deprived infants.

OBJECTIVE: To evaluate the influence of a brief period of sleep deprivation on cardiac autonomic controls during sleep in healthy infants. DESIGN: Twelve healthy infants with a median age of 8 weeks (range, 7 to 18 weeks) were recorded polygraphically during a morning and an afternoon nap in a sleep laboratory. They were sleep deprived for approximately 2 hours, either in the morning or in the afternoon, before being allowed to fall asleep. Six infants were sleep deprived before the morning nap, and 6 before the afternoon nap. During both naps, their sleep, breathing, and heart-rate characteristics were continuously recorded. Spectral analysis of heart rate was evaluated as a function of sleep stages. Two major peaks were recognizable: a low-frequency component related to sympathetic and parasympathetic activities and a high-frequency component reflecting parasympathetic tonus. The ratio of low-frequency to high-frequency powers was calculated as an index of sympathovagal interaction. RESULTS: When sleep deprived, the infants had an increase in basal heart rate during non-rapid eye movement sleep (P=.021). With sleep deprivation, the ratio of low-frequency to high-frequency powers increased in non-rapid eye movement sleep (P=.005). These findings were consistent with an increase in sympathetic tone. CONCLUSION: Infants exposed to short-term sleep deprivation manifest changes in cardiac autonomic controls during sleep. These findings could be relevant to mechanisms associated with the sudden infant death syndrome.

Female↗

PubMed1994

Sleep deprivation in the rat at different ambient temperatures: effect on sleep, EEG spectra and brain temperature.

To investigate the relationship between thermoregulation and sleep regulation, rats were sleep-deprived for 3 hours at two different ambient temperatures. Sleep deprivations (SD) were performed at 23 degrees C (SD-23) and at 32 degrees C (SD-32) in the beginning of the 12-h light period in animals chronically implanted with ECoG and EMG electrodes, and with epidural and hypothalamic thermistors. SD-32 enhanced cerebral temperature more than SD-23 at both brain sites. The SD-induced hyperthermia was followed by a fall of brain temperature below baseline. During recovery from either SD procedure, waking was reduced and sleep continuity increased. REM sleep was increased after SD-32. EEG slow-wave activity (spectral power density in the 0.75-4.0 Hz band) exceeded the baseline level in the first 3-h interval of recovery; however, the effects of SD-23 and SD-32 did not differ. In the same time interval, power density in the 1.25-1.5 Hz bin as well as in some bins in the theta and alpha band was higher after SD-32 than after SD-23. The increase in hypothalamic temperature during SD did not correlate with the increase in SWA during recovery. It is concluded that even a brief SD has major repercussions on recovery sleep whereas the extent of cerebral hyperthermia during SD is only a minor factor.

Animals↗

PubMed1993

Sleep deprivation in depressed adolescents and psychiatric controls.

Up to 70% of depressed adults have an antidepressant response to sleep deprivation. To study the effects of sleep deprivation on depression severity and level of arousal in psychiatrically disturbed adolescents, we deprived 17 patients of sleep for 36 hours. Severity of depression and subjective arousal were assessed at baseline, during sleep deprivation, and after 1 night's recovery sleep. We found that severely depressed adolescents showed a significant decrease in depression severity, whereas depressed patients in remission and psychiatric controls worsened after sleep deprivation. Patients with depression in remission showed a significant decrease in subjective arousal after sleep deprivation. In contrast to findings in depressed adults, the effects of sleep deprivation persisted after 1 night of recovery sleep, and diurnal variation of mood did not predict response to sleep deprivation. These findings are consistent with those reported in the adult literature, and suggest a common psychophysiology between adult and adolescent depression.

Adolescent↗

PubMed2004

Sleep deprivation and cellular responses to oxidative stress.

STUDY OBJECTIVES: It has been hypothesized that sleep deprivation represents an oxidative challenge for the brain and that sleep may have a protective role against oxidative damage. This study was designed to test this hypothesis by measuring in rats the effects of sleep loss on markers of oxidative stress (oxidant production and antioxidant enzyme activities) as well as on markers of cellular oxidative damage (lipid peroxidation and protein oxidation). DESIGN: The analyses were performed in the brain and in peripheral tissues (liver and skeletal muscle), after short-term sleep deprivation (8 hours), after long-term sleep deprivation (3-14 days), and during recovery sleep after 1 week of sleep loss. Short-term sleep deprivation was performed by gentle handling; long-term sleep deprivation was performed using the disk-over-water method. SETTING: Sleep research laboratory at University of Wisconsin-Madison. PARTICIPANTS AND INTERVENTIONS: Adult male Wistar Kyoto rats (n = 69) implanted for polygraphic (electroencephalogram, electromyogram) recording. MEASUREMENTS AND RESULTS: Aliquots of brain, liver, or skeletal muscle homogenate were used to assess oxidant production, superoxide dismutase activity, lipid peroxidation, and protein oxidation. No evidence of oxidative damage was observed at the lipid and/or at the protein level in long-term sleep-deprived animals relative to their yoked controls, nor in the cerebral cortex or in peripheral tissues. Also, no consistent change in antioxidant enzymatic activities was found after prolonged sleep deprivation, nor was any evidence of increased oxidant production in the brain or in peripheral tissues. CONCLUSION: The available data do not support the assumption that prolonged wakefulness may cause oxidative damage, nor that it can represent an oxidative stress for the brain or for peripheral tissue such as liver and skeletal muscle.

Animals↗

PubMed2005

Clinical assessment of blood leukocytes, serum cytokines, and serum immunoglobulins as responses to sleep deprivation in laboratory rats.

The specific systems and mechanisms affected by sleep deprivation that may perpetuate disease processes in humans still are speculative. In laboratory rats, prolonged sleep deprivation induces a state marked by abnormal control over indigenous bacteria that results in transient infections of internal tissues and eventual lethal septicemia. The present studies investigated changes in blood, serum, and bone marrow parameters that may provide diagnostic clues to immunopathology. Prolonged sleep deprivation was produced in rats by the disk-over-water method, a well-established and selective means that does not interfere with normal waking behaviors. Measurements included bone and blood differential white blood cell counts, multiple serum cytokines and chemokines, several major Ig classes and subclasses, and serum endotoxin concentrations. The results indicated mild, regenerative neutrophilia in sleep-deprived rats, initially accompanied by immature neutrophils and later by monocytosis. The corresponding serum cytokine profile revealed an evolving proinflammatory state, particularly by high incidence of interleukin-1beta, implicating mononuclear phagocytes and resident tissue cells as main intermediary sources. In addition, multiple serum Ig classes were increased by sleep deprivation without experimental administration of an exogenous antigen. Despite this immune activation, there was failure to eradicate invading bacteria and toxins, suggesting competing anti-inflammatory processes or interference with immune effector functions during sleep deprivation. Nearly all of the immune-related events that emerged as responses to sleep deprivation have been implicated as etiological or provocative factors in other disease processes and may provide means by which sleep deprivation as a risk factor in disease may become understood.

Adaptation, Physiological↗

PubMed1999

Impairment of driving performance caused by sleep deprivation or alcohol: a comparative study.

A study was conducted to assess the relative impact of partial sleep deprivation (restriction to 4 h sleep before testing) and full sleep deprivation (no sleep on the night before testing) on 2 h of simulated driving, compared with an alcohol treatment (mean blood alcohol content = 0.07%). Data were collected from the 64 male participants on the primary driving task, psychophysiology (0.1 Hz heart rate variability), and subjective self-assessment. The results revealed that the full sleep deprivation and alcohol group exhibited a safety-critical decline in lane-keeping performance. The partial sleep deprivation group exhibited only noncritical alterations in primary task performance. Both sleep-deprived groups were characterized by subjective discomfort and an awareness of reduced performance capability. These subjective symptoms were not perceived by the alcohol group. The findings are discussed with reference to the development of systems for the online diagnosis of driver fatigue. Potential applications of this research include the formulation of performance criteria to be encompassed within a driver impairment monitoring system.

Adult↗

PubMed2005

Facilitation of task performance and removal of the effects of sleep deprivation by an ampakine (CX717) in nonhuman primates.

The deleterious effects of prolonged sleep deprivation on behavior and cognition are a concern in modern society. Persons at risk for impaired performance and health-related issues resulting from prolonged sleep loss would benefit from agents capable of reducing these detrimental effects at the time they are sleep deprived. Agents capable of improving cognition by enhancing brain activity under normal circumstances may also have the potential to reduce the harmful or unwanted effects of sleep deprivation. The significant prevalence of excitatory alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamatergic receptors in the brain provides a basis for implementing a class of drugs that could act to alter or remove the effects of sleep deprivation. The ampakine CX717 (Cortex Pharmaceuticals), a positive allosteric modulator of AMPA receptors, was tested for its ability to enhance performance of a cognitive, delayed match-to-sample task under normal circumstances in well-trained monkeys, as well as alleviate the detrimental effects of 30-36 h of sleep deprivation. CX717 produced a dose-dependent enhancement of task performance under normal alert testing conditions. Concomitant measures of regional cerebral metabolic rates for glucose (CMRglc) during the task, utilizing positron emission tomography, revealed increased activity in prefrontal cortex, dorsal striatum, and medial temporal lobe (including hippocampus) that was significantly enhanced over normal alert conditions following administration of CX717. A single night of sleep deprivation produced severe impairments in performance in the same monkeys, accompanied by significant alterations in task-related CMRglc in these same brain regions. However, CX717 administered to sleep-deprived monkeys produced a striking removal of the behavioral impairment and returned performance to above-normal levels even though animals were sleep deprived. Consistent with this recovery, CMRglc in all but one brain region affected by sleep deprivation was also returned to the normal alert pattern by the drug. The ampakine CX717, in addition to enhancing cognitive performance under normal alert conditions, also proved effective in alleviating impairment of performance due to sleep deprivation. Therefore, the ability to activate specific brain regions under normal alert conditions and alter the deleterious effects of sleep deprivation on activity in those same regions indicate a potential role for ampakines in sustaining performance under these types of adverse conditions.

Animals↗

PubMed1989

Sleep deprivation in the rat: I. Conceptual issues.

Sleep deprivation is a potentially powerful strategy for discovering the function(s) of sleep, but the approach has had limited success. Few studies have described serious physiological consequences of sleep deprivation, perhaps because the deprivation has not been maintained long enough. However, prolonging deprivation usually requires sustained, frequently intense stimulation, which makes it difficult to determine whether subsequent impairment resulted from the sleep loss or from the stimulation per se. Accordingly, several older studies that showed severe impairment have been neglected or discounted, because the impairment could have resulted from the stimulation. To evaluate the effects of sleep deprivation independent of the stimulation used to enforce deprivation, we have used an apparatus that can awaken experimental rats while delivering the same gentle stimulation to control rats according to a schedule that only moderately shortens their sleep.

Animals↗

PubMed2002

Selective REM sleep deprivation during daytime. II. Muscle atonia in non-REM sleep.

One of the hallmarks of rapid eye movement (REM) sleep is muscle atonia. Here we report extended epochs of muscle atonia in non-REM sleep (MAN). Their extent and time course was studied in a protocol that included a baseline night, a daytime sleep episode with or without selective REM sleep deprivation, and a recovery night. The distribution of the latency to the first occurrence of MAN was bimodal with a first mode shortly after sleep onset and a second mode 40 min later. Within a non-REM sleep episode, MAN showed a U-shaped distribution with the highest values before and after REM sleep. Whereas MAN was at a constant level over consecutive 2-h intervals of nighttime sleep, MAN showed high initial values when sleep began in the morning. Selective daytime REM sleep deprivation caused an initial enhancement of MAN during recovery sleep. It is concluded that episodes of MAN may represent an REM sleep equivalent and that it may be a marker of homeostatic and circadian REM sleep regulating processes. MAN episodes may contribute to the compensation of an REM sleep deficit.

Adult↗

PubMed1998

Brief paradoxical sleep deprivation impairs reference, but not working, memory in the radial arm maze task.

Selective deprivation of paradoxical sleep after learning results in memory deficits in a variety of tasks. The present experiment was designed to examine the effects of paradoxical sleep deprivation (PSD) upon spatial working and reference memory. Adult male Sprague-Dawley rats were trained for 10 days in an eight-arm radial maze. Food rewards were available in four of the arms, while the other four arms were never baited. After each daily training session, different groups of rats were given 4 h of PSD, beginning either immediately, 4 h, or 8 h after the training experience. An additional group received PSD during the period 13-24 h following daily training. The group that received PSD for 4 h immediately following daily training showed significant impairment compared to the other groups, but the deficit was limited to the reference component of the task. This result suggests that PSD causes deficits only in long-term forms of spatial memory.

Animals↗

PubMedDate not supplied

[Delusion and sleep deprivation].

In this article, the authors report two observations of short delusion that occurred after taking Guronsan--a psychostimulant commercialized in France--for a few days, with the intention of maintaining a total deprivation of sleep for three days in both cases. The ensuing clinical picture included a state of depersonalization, a loss of the sense of reality, illusions and even visual hallucinations as well as a delirious feeling of persecution. These disorders altered with the state of vigilance and the patients remembered them clearly. The authors discussed the etiopathogenic role of this psychotrope, as its components--acid ascorbic, glucuronamide and caffein--are not mentioned in literature as causing factors of a psychotic state. Then they compared this psychotrope with other molecules: amphetamines in particular may start a delirium of persecution, but normally they just reveal an underlying psychotic structure, which doesn't seem to be the case here, where the two young adults were only found a little immature. Chloroquine has sometimes been incriminated for disorders similar to those mentioned above, with a difference lying in a greater stability in the duration of these disorders that would persist several days after the end of the treatment. The clinical picture of the two cases was more labile and sedation was complete as soon as the absorption of the psychotrope was interrupted and sleep was restored at the same time. That is why the authors emphasize the importance of the deprivation of sleep as a causing factor of those delusion disorders which have particularly been observed in the case of solitary navigators. The psychiatrist dealing with emergencies shouldn't overlook this clinical and etiological possibility, all the less so as the treatment is simple and the resort to neuroleptics unnecessary.

Adult↗

PubMed1994

Influence of sleep deprivation on learning among surgical house staff and medical students.

BACKGROUND: Sleep deprivation as a result of in-house night call may alter capacity to learn. Surgical residents and medical students, in both sleep-deprived and rested states, read surgical journal articles and later answered questions regarding their content as a measure of ability to learn while participating in scheduled night call. METHODS: Medical students (n = 35) and residents (n = 21) rotating on surgical services kept logs of hours slept during a 4-week study period. Subjects read six selected articles at separate early morning sittings during weeks 1 and 3. A multiple choice test was given 1 week after each session to assess short-term recall, and all tests were given again 3 months later to assess retention of information over the longer term. Scores were compared with the sleep data. Subjective measures of fatigue and motivation elicited from subjects also were evaluated. RESULTS: Sleep deprivation (4 hours or less uninterrupted sleep per night) resulted in increased fatigue and decreased motivation among medical students and residents (p < 0.05, t test). Objective scores on tests administered 1 week and 3 months after reading did not show an effect attributable to sleep deprivation (p > 0.05, t test). CONCLUSIONS: Sleep deprivation leads to subjective feelings of increased fatigue and decreased motivation. Residents and medical students, however, whether sleep deprived or not, obtain comparable scores on objective tests measuring both short-term and long-term retention of newly learned material. The ability to learn medically relevant information does not appear to be significantly altered by the degree of sleep deprivation associated with clinical rotations on surgical services.

Adult↗

PubMed1997

Sleep deprivation affects speech.

Historical accounts of sleep loss studies have described changes in the content and patterns of speech, although to date these claims have not been systematically studied. We examined the effects of sleep loss on the spontaneous generation of words during a verbal word fluency task and the articulation of speech during a vocalized reading task. Nine subjects underwent two counterbalanced 36-hour trials involving sleep deprivation (SD) and no sleep deprivation (NSD). After SD, there was a significant deterioration in word generation and a tendency for subjects to become fixated within a semantic category. There was a significant reduction in the subjects' use of appropriate intonation in the voice after SD, with subjects displaying more monotonic or flattened voices. These findings are discussed in light of neuropsychological evidence concerning the functions of sleep in relation to the frontal cortex and in light of the implications for interpersonal communication in the event of sleep loss.

Adult↗

PubMed1998

Postural control, attention and sleep deprivation.

We investigated the effect of sleep deprivation on postural control during a simple reaction time task (SRT), during a task requiring the intermittent inhibition of a reaction (IRT), and in the absence of a concurrent information processing task. Postural sway, i.e. changes in center of pressure on a force platform, was recorded in three increasingly difficult standing conditions (fixed platform, sway-referenced platform and sway-referenced platform with sway-referenced visual scene) during the three information-processing task conditions. Five healthy subjects performed the tasks either after normal sleep or following 24 h of sustained wakefulness. As hypothesized, sleep deprivation significantly increased postural sway only in the IRT condition. Within the IRT condition, sleep deprivation significantly increased sway across all postural conditions.

Adult↗

PubMed1980

Combined effects of alcohol and sleep deprivation in normal young adults.

The effect of combining sleep deprivation and moderate alcohol consumption in male college students differed from the effects of each treatment alone. Following either alcohol or sleep deprivation, there was mild performance impairment, decreased alertness and reduced amplitude and increased latency of cortical evoked potential (EP) components. Heart rate increased after alcohol and anxiety increased after sleep deprivation. When alcohol and sleep deprivation were combined, antagonistic effects were found for most measures (reaction time, heart rate, alertness, anxiety, latency of early EP components), but synergistic effects also occurred (performance accuracy, latency of late EP components). These effects were found in a double-blind experiment using 24 subjects. The experimental treatments were alcohol doses of 0, 0.45 and 0.90 ml/kg of 95% ethanol and 0 and 26 h of sleep deprivation.

Adult↗

PubMed2006

Odor identification accuracy declines following 24 h of sleep deprivation.

Brain imaging studies demonstrate that sleep deprivation reduces glucose metabolism and blood flow in the prefrontal cortex, and such reductions are associated with impairments in cognitive functioning. Although some of the greatest metabolic declines occur within the orbitofrontal cortex, little is known about the effects of sleep loss on the types of processes mediated by this region, including emotion, motivation, feeding, and olfaction. The present study tested odor identification accuracy when individuals were well rested and again following 24 h of wakefulness. Relative to rested baseline performance, sleep-deprived individuals demonstrated a significant decline in the ability to identify specific odors on the Smell Identification Test. This decrement in olfactory functioning occurred concomitantly with slowed psychomotor speed and increased ratings of self-reported sleepiness. Performance on a task that required complex mental set shifting did not change significantly following sleep deprivation, suggesting that the decrements in odor identification could not be attributed to task difficulty. Finally, while there was no relationship between subjective sleepiness and odor identification at rested baseline, greater subjective sleepiness was associated with better odor identification ability following 24 h of sleep loss. Possible implications of these findings are discussed.

Adolescent↗

PubMed2004

Loss of negative priming following sleep deprivation.

It has been argued that one night of sleep loss in young healthy adults produces changes similar to that associated with normal, healthy ageing--in particular, that young sleep-deprived adults perform similarly to 60-year-old sleep-satiated adults on some tasks of frontal lobe function. This proposition was examined using a protocol viewed by many to be a direct probe of nonvolitional attention mechanisms associated with frontal lobe function. A negative priming (NP) procedure was used to compare performance between non-sleep-deprived (NSD) and sleep-deprived (SD, 34 hr) young, healthy adults. This protocol allowed for exploration of two theories of the NP effect based on inhibitory or memorial processes. Under conditions believed to facilitate inhibitory processes a normal NP effect was found for NSD(16 ms) and SD (9 ms) participants. Under conditions believed to rely on memorial processes there was no NP effect following SD, compared with a normal NP effect for NSD participants (11 ms). Distractor interference was also greater following SD. These findings do not suggest a similar pattern of change following sleep loss in healthy young adults to that of normal, healthy, non-sleep-deprived aged groups.

Adolescent↗