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PubMed1983

Dopamine metabolism and receptor sensitivity in rat brain after REM sleep deprivation.

Different dopaminergic mechanisms that could explain behavioral supersensitivity to amphetamine or apomorphine in REM-deprived rats were examined. Four days of REM sleep deprivation induced a highly significant elevation in striatal DOPAC relative to normal controls, but not to stress controls. DOPAC levels in frontal cortex were not affected in any of the groups. Post synaptic D2 receptor number (Bmax) and affinity (Kd) were unchanged in both terminal regions. Similarly, no changes in pre-synaptic receptor sensitivity (apomorphine-induced inhibition of tyrosine hydroxylase) occurred in striatum. A stress control group exhibited no changes in any of the biochemical measures in comparison with either the REM deprived group or unstressed controls. Thus, the enhanced response to dopamine agonists reported previously is not due to altered dopamine receptor sensitivity. Alternative hypotheses to explain enhanced responses to direct and indirect acting dopamine agonists are discussed.

Animals↗
PubMed1988

The effect of total sleep deprivation on plasma melatonin and cortisol in healthy human volunteers.

Twelve healthy volunteers were included in this study. Baseline curves for melatonin and cortisol were obtained after one night of adaptation to laboratory conditions. From 10:00 p.m. to 6:00 a.m., blood samples were drawn every hour. On the third night, the subjects were kept awake at the sleep unit. Curves for the two hormones were then obtained after 36 h of total sleep deprivation (SD). The levels of these hormones were evaluated by calculating the area under the curve at each hour in both situations (basal and after sleep deprivation). It was found that the melatonin levels were increased after sleep deprivation, whereas the cortisol levels remained the same. These results suggest a mechanism by which a reset of abnormal rhythms can occur in depression.

Adolescent↗
PubMed1989

Interleukin-1 beta and muramyl dipeptide can prevent decreased antibody response associated with sleep deprivation.

A single, brief (8 h) period of sleep deprivation (DEP) was found to suppress secondary antibody response to sheep red blood cells in rats. This decrease could be totally prevented if either interleukin-1 beta (IL-1) or muramyl dipeptide (MDP) was administered at the beginning of the DEP vigil. Twenty-five units of IL-1 or 250 micrograms/kg MDP was found to be immunosuppressive in sleeping rats but, paradoxically, the combination of such doses with DEP alleviated this effect. Increased colonic temperatures associated with antigen and/or adjuvant administration were not related to the differences in antibody levels between sleeping and DEP animals. Activation of hypothalamic dopamine in IL-1-treated rats following DEP suggests that this monoamine transmitter system may participate in the observed protective activity of IL-1. The present findings extend the immune adjuvant effects of both IL-1 and MDP to protection of the host against behaviorally induced immunosuppression.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1999

Long distance driving and self-induced sleep deprivation among automobile drivers.

OBJECTIVE: To evaluate the sleep hygiene and prevalence of sleep deprivation among a large sample of automobile drivers. DESIGN: From the 15th of June to the 4th of August 1996, with the help of the French highway patrol, we randomly stopped automobile drivers at the toll booths of Bordeaux and Biarritz. All subjects completed a validated questionnaire on sleep/wake habits during the year. After answering the questionnaire, subjects completed a graphic travel and sleep log of the three days preceding the interview. PARTICIPANTS: We randomly stopped 2196 automobile drivers. Ninety-one percent of the sample (mean age 43 +/- 13 years) agreed to participate in the survey. RESULTS: Fifty percent of the drivers decreased their total sleep time in the 24 hours before the interview compared with their regular self-reported sleep time. 12.5% presented a sleep debt > 180 minutes, and 2.7% presented a sleep debt > 300 minutes. Being young, commuting to work, driving long distances, starting the trip at night, being an "evening" person, being a long sleeper during the week, and sleeping in on the week-end were risk factors significantly associated with sleep debt. CONCLUSION: The results of the study highlight variables (long-distance driving, youth, sleep restriction) that are frequently associated with sleep-related accidents.

Accidents, Traffic↗
PubMed1995

Functional analysis and treatment of escape-maintained aggression correlated with sleep deprivation.

Functional analysis identified the consequences that maintained aggressive behavior and the relationship between these consequences and sleep deprivation for an individual with severe mental retardation. Results showed that aggression was maintained by negative reinforcement contingencies (escape from demand) and that aggression was more severe when sleep deprivation was present. A multicomponent intervention resulted in reductions of aggression for up to 7 months.

Adult↗
PubMed2000

Slow-release caffeine: a new response to the effects of a limited sleep deprivation.

STUDY OBJECTIVES: The aim of this study is to assess the interest of the intake of a new galenic form of caffeine called "slow-release" caffeine (SR caffeine) during a decrease of vigilance due to a limited sleep deprivation. DESIGN: The controlled method used compared three doses of SR caffeine (150, 300 and 600 mg) with a placebo. Tests were performed 2, 9 and 13 hours after each treatment. Wakefulness level was assessed subjectively through questionnaires and analog visual scales, and objectively with the Multiple Sleep Latency Test. Performance level was also assessed regularly with an attention test, a grammatical reasoning test, a spatial recognition test, a mathematical processing test, a visual tracking test, a memory search test, and a dual task. The motor activity was evaluated by wrist actimeter and safety of treatment was observed by regular clinical examination. SETTING: NA. PARTICIPANTS: Twenty-four young and healthy volunteers (12 men and 12 women) participated in a 32-hour sleep deprivation. INTERVENTIONS: NA. RESULTS: The results show a significant effect of slow-release caffeine vs. placebo, and on vigilance and performance when subjects became tired. The effects of SR caffeine lasted 13 hours after treatment. SR caffeine 300 and 600 mg are efficacious doses but the optimal dose (maximum effect without any side effects) for both men and women is after all 300 mg. Globally, there is no difference between placebo and caffeine during the recovery night period. CONCLUSIONS: SR caffeine (300 mg) seems to be an efficient and safety substance to maintain a good level of vigilance and performance during limited sleep deprivation.

Adolescent↗
PubMed1997

Effects of sleep deprivation on serotonergic neuronal activity in the dorsal raphe nucleus of the freely moving cat.

Total sleep deprivation (TSD) for one or more nights produces a rapid antidepressant response in humans. Since most pharmacological treatments for depression increase brain serotonin neurotransmission, the purpose of the present study was to determine whether TSD increases the activity of serotonergic neurons in the dorsal raphe nucleus (DRN) in cats. Cats were prevented from sleeping by the experimenter, who monitored the behavioral state of each animal on a polygraph. Firing rates during quiet waking (QW) and active waking (AW) were obtained throughout a 24-h sleep deprivation period and subsequent 6-h recovery period. During the experiments, unit activity was also recorded during exposure to loud white noise, which elicited strong behavioral arousal. The inhibitory response of serotonergic DRN neurons to systemic administration of the selective 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) was determined before and after TSD to assess possible changes in 5-HT1A autoreceptor sensitivity. TSD increased mean firing rates by as much as 18% during both AW and white noise exposure. Maximal effects were observed after 15 h of TSD for AW, and after 18 h for white noise. QW firing rates also tended to be elevated throughout TSD. Firing rates for all conditions during the recovery period were not significantly different from baseline. The neuronal inhibition produced by 8-OH-DPAT was significantly diminished after TSD. Overall, these results indicate that TSD increases the firing rate of serotonergic DRN neurons during AW and arousal. This effect may be attributable to a decrease in the sensitivity of 5-HT1A autoreceptors. These findings are consistent with the hypothesis that TSD exerts its antidepressant action, at least in part, through an activation of brain serotonergic neurons.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2001

Is pre-attentive processing compromised by prolonged wakefulness? Effects of total sleep deprivation on the mismatch negativity.

We investigated the potential influence of sustained wakefulness on pre-attentive capacities by recording the mismatch negativity (MMN), an electrophysiological manifestation associated with nonintentional detection of auditory oddball stimuli. The MMN was elicited by pitch deviants presented to both ears via earphones, at the beginning of a total sleep deprivation session (baseline), after 24 hr, and after 36 hr of continuous controlled wakefulness. A conspicuous MMN response was elicited at all three sessions. With time, however, a small yet significant gradual reduction in the MMN amplitude was evident. Whereas previous research suggested that controlled attention-demanding tasks are hampered by sleep deprivation, the balance of the present results suggests that passive (total) sleep deprivation may also bring about some degradation in the pre-attentive detection of environmental irregularities and as a consequence may disrupt the reflexive shift of attention induced by such events.

Acoustic Stimulation↗
PubMed1998

Effects of sleep deprivation and other stressors on the immune and inflammatory responses of influenza-infected mice.

Many stressors have well-documented effects on host immune competence. However, two important stressors that have not been extensively characterized in terms of their immune-modulatory properties are sleep deprivation and alterations in light:dark cycles. We therefore evaluated the effects of these stressors on the immune and inflammatory responses of mice inoculated intranasally with influenza virus. In contrast to a previous report, sleep deprivation did not significantly alter viral clearance or antibody titers of either virus-naive or immunized mice. Exposure to constant light also failed to affect these variables. However, repeated overnight restraint, a well-characterized stressor, reduced the pulmonary inflammatory response elicited by influenza virus, as previously reported. The data indicate that sleep deprivation and altered light cycles do not markedly influence selected host defense responses to influenza infection under the conditions tested.

Amyloid↗
PubMed2001

Total sleep deprivation induces an acute and transient increase in NK cell activity in healthy young volunteers.

STUDY OBJECTIVES: To investigate the effects of one night's total sleep deprivation (TSD) on NK cell activity, with rigorous control of circadian phase of sampling points as well as physical exercise level in association with sleep deprivation. DESIGN: The mean sleep onset time of each subject before starting the study was defined as his 0000 h. This study was composed of a Sleep-Sleep session (sleep times, 00:00 h - 08:00 h and 24:00 h - 32:00 h) and a Sleep-Wake session (sleep time, 00:00 h - 08:00 h) with TSD (24:00 h - 32:00 h) placed in a cross-over design with 2-week interval between each session. In each session, the subjects were rested in the supine position under dim light from - 06:00 h to 36:00 h (for 42 hours). SETTING: University-based sleep and chronobiology laboratory PARTICIPANTS: 10 healthy adult men (mean age, 20.9 y; age range, 19-23 y) INTERVENTIONS: NA. MEASUREMENTS AND RESULTS: NK cell activity was measured every 4 hours from 12:00 h. NK cell activity during TSD (at 28:00 h) has been revealed to significantly increase (p=0.01) compared with the corresponding value in the Sleep-Sleep session. This effect was weaker at their usual waking time 32:00 h (p=0.07), and disappeared until 36:00 h (4 hours after awakening). The circadian rhythm phases (dim light melatonin onset time) were coincident between the 2 sessions. CONCLUSIONS: The present findings suggest that one night TSD induces an acute and transient increase in NK cell activity that is not influenced by the effects of circadian rhythm or the amount of physical exercise undertaken during TSD.

Adult↗
PubMed1999

Alpha activity in the human REM sleep EEG: topography and effect of REM sleep deprivation.

The topographical distribution of alpha activity (8.125-11.125 Hz) in the REM sleep EEG, its time course within and across REM sleep episodes, and the effects of selective REM sleep deprivation were investigated in 8 young males. Power spectra of bipolar derivations along the antero-posterior axis in the left (F3C3, C3P3, P301) and right (F4C4, C4P4, P402) hemisphere were calculated. Alpha activity increased along the antero-posterior axis in both hemispheres, and was dominant in the right hemisphere. It decreased within and across REM sleep episodes. Selective REM sleep deprivation resulted in a reduction of alpha activity in the REM sleep EEG. However, the topographical distribution and the time course were not affected. It is suggested that alpha activity in the REM sleep EEG is a marker of REM sleep homeostasis.

Brain↗
PubMed1988

Body core temperature and depression during total sleep deprivation in depressives.

Endogenously depressed patients were subjected to a total sleep deprivation (TSD) schedule of sleep-TSD-sleep-TSD. They were simultaneously treated with the antidepressant drug clomipramine. Self- and observer-rated depression was measured daily. Continuously measured rectal temperature (RT) data were available for the second TSD. It was found that a higher nocturnal minimum RT during this TSD was associated with a positive clinical response.

Body Temperature Regulation↗
PubMed1984

Effects of carbamazepine or imipramine alone or in association with amphetamine on the fighting time of REM sleep-deprived rats.

The fighting time of REM sleep-deprived rats was measured after both acute and long-term intraperitoneal treatment with carbamazepine (CBZ) or imipramine (IMI) alone or associated with amphetamine. Fighting time was increased by the lower doses of CBZ (5-20 mg/kg) or IMI (0.5-2 mg/kg) administered acutely. At the highest dose tested, CBZ (40 mg/kg) was not significantly different from the control value, and the fighting time observed after 4 mg/kg IMI was less than that observed with 2 mg/kg. Amphetamine (2 mg/kg) alone increased the fighting time and this effect was not modified by association with 5-40 mg/kg CBZ or 0.5-4 mg/kg IMI. Long-term treatment (14 days) with CBZ (20 mg kg-1 day-1) or IMI (2 mg kg-1 day-1) significantly reduced fighting time in contrast to the increase observed with a single acute treatment at the same dose. The fighting time of rats acutely treated with amphetamine (2 mg/kg) was significantly but not completely reduced by previous long-term pretreatment with CBZ, whereas IMI pretreatment had no effect. The differences between the effects of acute and long-term treatment with CBZ cannot be explained by the development of metabolic tolerance, since serum CBZ levels were the same in both situations.

Aggression↗
PubMed1992

Effects of biperiden on sleep at baseline and after 72 h of REM sleep deprivation in the cat.

We examined the effects of the muscarinic M1 antagonist biperiden in cats. In the first experiment a dose-response analysis was performed with intraventricular injection (IV ventricle) of biperiden. In the second experiment after REM sleep deprivation cats were injected with either biperiden (0.1 mg/kg) or saline. Biperiden produced a reduction in REM sleep percentage and an increase in REM sleep latency with these high doses. The 0.1 mg/kg biperiden dose, which did not suppress REM sleep at baseline, did reduce the REM sleep rebound. The present study suggests a modulatory role of biperiden on REM sleep regulatory processes. The fact that an effect of biperiden is noted only at the high doses suggests that at these doses the drug is influencing non-M1 receptors. Changes in the sensitivity of these receptors as a result of REM sleep deprivation might explain why a dose of biperiden will reduce REM sleep rebound, while being ineffective in suppressing REM sleep at baseline.

Animals↗
PubMed2000

Effect of sleep deprivation on overall 24 h growth-hormone secretion.

After sleep deprivation, the blunting of the normal sleep-related growth-hormone (GH) pulse is compensated during the day. Consequently, the amount of GH secreted during a 24 h period is similar whether or not a person has slept during the night. These results argue against the belief that sleep disorders in children can inhibit growth through a daily GH deficit.

Adult↗
PubMed1995

Induction of high SCEs in normal cells by 11-12 kDa plasma protein overexpressed in some sleep deprived volunteers.

The present study confirmed our earlier preliminary observation of induction of high SCEs in 1 day sleep-deprived healthy volunteers and showed that the property of induction of high SCE by after-sleep-deprived (ASD) plasma was retained both in 50% ammonium sulphate precipitates and in the dialysed plasma using a membrane of 12 kDa porocity. Further, nitrocellulose bound 11-12 kDa electrophoretically isolated plasma protein from ASD individuals was found responsible for the induction of high SCE in normal whole blood cultures. A short exposure of 3 h to 5% ASD plasma was enough to induce significantly high SCEs in normal lymphocytes which had undergone 2 replication cycles after the exposure to this factor.

Adult↗
PubMed2005

Effects of sleep deprivation on auditory and visual memory tasks.

Probe recognition tasks have shown the effects of sleep deprivation following a full night of sleep loss. The current study investigated shorter durations of deprivation by testing 11 subjects for accuracy and response time every 2 hr. from 10 p.m. through 8 a.m. We replicated Elkin and Murray's auditory single-probe recognition task using the number triplets and added two visual tasks with number and shape triplets. Series of six stimuli were each followed by a probe, which was presented after 2.5 sec. as a short delay or 20 sec. as a long delay. Accuracy performance showed a significant decrease for the long delay beginning after 4 a.m. for the two visual tasks. Response times were significantly slower for the visual shapes task using the short delay. Visual tasks, especially shapes, may be more prone to disruption by sleep deprivation, given the visual information load and the briefness of iconic memory.

Adolescent↗
PubMed1994

Clinical response to sleep deprivation and auditory-evoked potentials--preliminary results.

The biological substrate of the antidepressant effect of total sleep deprivation (TSD) has not yet been elucidated. Furthermore, electrophysiological predictors for the response to TSD have not been studied extensively. The aim of present study was to examine the changes in acoustically evoked potentials (N1, P2, N2, P300) after a night of sleep deprivation and to analyze differences between responders and nonresponders. 17 depressive inpatients were studied. The most prominent changes in auditory evoked potentials (responders and nonresponders) were found for the amplitude of the P300 component. Differences between responders and nonresponders could be established for the amplitude and latencies in the N1 component. Responders showed smaller N1 amplitudes before TSD but a higher increase after TSD than nonresponders.

Adult↗