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PubMed1996

Role of the locus coeruleus in the sleep rebound following two different sleep deprivation methods in the rat.

The aim of the present study was to assess the involvement of the locus coeruleus in the paradoxical sleep rebound following sleep deprivation in the rat. Animals were sleep-deprived for 10 h before, and after, specific N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) lesioning of the noradrenergic-locus coeruleus system. Sleep deprivation was produced using either an instrumental (water tank) or pharmacological (methylamphetamine) method. After lesioning, the rats submitted to the instrumental method showed a significant decrease in the paradoxical and slow-wave sleep rebounds (-54% and -78%, respectively), while animals receiving metamphetamine did not. Our results suggest that the noradrenergic system of the locus coeruleus is a relevant component of the sleep rebound mechanisms. However, the extent of involvement is dependent on the sleep deprivation method used.

Adrenergic Agents↗

PubMed2001

Sleep deprivation but not a whisker trim increases nerve growth factor within barrel cortical neurons.

Sleep is hypothesized to influence activity-driven changes in the brain microcircuitry. A change in the barrel cortex following the removal of the mystacial whiskers in rats is a model for synaptic plasticity. This model was combined with sleep deprivation and immunoreactivity for nerve growth factor (NGF) was determined. Sleep deprivation for 6 h after light onset significantly increased the number of NGF-immunoreactive pyramidal neurons in layer V of the barrel cortex. However, unilateral trimming of mystacial whiskers did not affect NGF immunoreactivity in the contralateral or ipsilateral barrel cortices when rats were allowed to sleep. If the rats received a unilateral whisker cut at light onset, and subsequently were deprived of sleep, increases in the NGF-immunoreactive neurons were only observed in the barrel cortex on the side that received input from the remaining intact whiskers. In contrast, NGF immunoreactivity on the side contralateral to the cut whiskers decreased in sleep-deprived animals to levels below those observed in the control animals that were allowed to sleep. These results suggest that NGF expression is influenced by the interaction of sleep, afferent input and the nature of ongoing synaptic reorganization. Further, results are consistent with the hypothesis that growth factors, such as NGF, form part of the mechanism responsible for sleep regulation and that they also form one facet of sleep-related synaptic plasticity.

Animals↗

PubMed1987

Effects of desipramine and total sleep deprivation on hormonal levels of healthy subjects.

Plasma prolactin (PRL) and growth hormone (GH) were serially measured over a 5-hour morning period in healthy subjects who twice received a single oral dose of 100 mg desipramine (DMI). The study was carried out both after a regular night of sleep and after 1 night of total sleep deprivation. Clinical studies have suggested that sleep deprivation could potentiate the therapeutic effects of antidepressants, and there were reports on DMI stimulation of GH. The basal PRL levels decreased after sleep deprivation, but subsequently increased after DMI, whereas the same dose of DMI did not affect PRL in the absence of after DMI, whereas the same dose of DMI did not affect PRL in the absence of sleep deprivation. The GH levels increased substantially (8- to 10-fold) after DMI in both experimental conditions. Sleep deprivation neither changed GH basal levels nor potentiated the DMI-induced GH increase.

Adult↗

PubMed2003

Rapid eye-movement sleep deprivation does not 'rescue' developmentally regulated long-term potentiation in visual cortex of mature rats.

The age at which it is possible to obtain a usually age-limited (developmental) form of long-term potentiation (LTP) in rat visual cortex slices can be extended by suppressing rapid eye movement (REM) sleep. In this study, we examined whether REM sleep deprivation can also 'rescue' this type of LTP in older rats. Rats, 42-59 days of age, were either REM sleep-deprived for 7-10 days (n=8), or not deprived of REM sleep (control group, n=8). Brain slices from visual cortex were tested for the developmental form- and a related, non-developmental form of LTP. Three of the eight REM sleep-deprived animals and four of the eight non-deprived animals met criteria for a valid attempt to induce the developmental form of LTP. Though the non-age-regulated form of LTP could be obtained in all seven of these animals, the developmental form could not be elicited in any, indicating that REM sleep deprivation does not uniformly affect all forms of LTP in adult rats. We conclude that extended periods of REM sleep deprivation do not facilitate induction of developmentally regulated LTP once the animal is beyond a certain age.

Age Factors↗

PubMed2005

[Combination therapy using sertraline with sleep deprivation and light therapy compared to sertraline monotherapy for major depressive disorder].

OBJECTIVE: Bright light therapy is effective and well tolerated in seasonal affective disorder and some studies reported an antidepressant effect of bright light also in non-seasonal depression. On the other hand, total sleep deprivation leads to a rapid and marked improvement of mood in 60% of depressed patients. Combinations of antidepressant medication with those somatic therapies are generally indicated. The aim of this study was to compare the efficacy of the combination of sertraline and partial sleep deprivation or light therapy with sertraline monotherapy in the treatment of major depression. METHOD: Thirty-seven patients with major depressive disorder were randomly allocated into 3 treatment groups. Thirteen were treated with sertraline and late partial sleep deprivation, 13 with sertraline and bright light therapy and 11 sertraline monotherapy as a control group. Outcome measures included daily (first 15 days) and weekly Hamilton Rating Scale for Depression and biweekly Hamilton Anxiety Rating Scale. RESULTS: Partial sleep deprivation group improved significantly and more rapidly. Accelerated treatment response was shown in sleep deprivation group that improvement was observed after the third day. Bright light and sleep deprivation combinations with sertraline were more effective than sertraline monotherapy for accompanied anxiety in depression. CONCLUSION: Late partial sleep deprivation in combination with sertraline can accelerate and increase the treatment response in non-seasonal major depressive disorder.

Adult↗

PubMed1991

Neuroendocrine and neurochemical consequences of long-term sleep deprivation in rats: similarities to some features of depression.

The paradigm of long-term sleep deprivation was used as a model of chronic inescapable stress in rats. Several basic metabolic parameters (body weight changes, food and water intake, rectal temperature, serum glucose and creatinine), adrenal and thyroid secretion, norepinephrine and dopamine content and turnover in discrete brain regions, and open field behaviour were examined in the course of the exposure to experimental stress. Sleep deprivation over 7-9 days caused complete physical exhaustion of the animals. It was accompanied by hypothermia and hyperphagia. Adrenal activity was characterized by significant hypercorticism, but also by a relative decrease of the responsiveness to ACTH. A gradual decrease in the thyroid secretion was observed. Sleep deprivation elicited a depletion of norepinephrine in the hypothalamus and decreased its turnover, whereas hippocampal norepinephrine content decreased without considerable turnover alterations. Striatal dopamine content and turnover remained unaffected. Behavioural depression and altered open field activity were also observed in exhausted animals. Long-term sleep deprivation, therefore, seems to reproduce some of the biological correlates of the depressive illness, and may be useful in studying the development of coping failure as a result of chronic stress exposure.

Adrenal Glands↗

PubMed1988

Sleep deprivation increases susceptibility to kindled and penicillin seizure events during all waking and sleep states in cats.

The timing of amygdala kindled and penicillin seizures was studied throughout the sleep-wake cycle in eight cats following near total sleep deprivation and a control procedure that did not affect sleep time. Sleep loss was induced by 24-h exposure to a modified "flower pot" procedure employing a small pedestal. The control procedure consisted of 24-h exposure to a larger pedestal. Sleep loss increased susceptibility to generalized kindled and penicillin seizures during all waking and sleep states but did not alter temporal patterns of seizure susceptibility. Both before and after sleep loss, kindled cats showed maximal seizure susceptibility, indexed by lowest seizure thresholds, during slow wave sleep (SWS) and transitions from SWS to REM sleep (REMS). The spike-wave discharges and motor seizures of systemic penicillin epilepsy were always most frequent during SWS and during drowsiness after awakening. Both models were invariably most resistant to seizures during stable REMS. To explain sleep- and sleep loss-activated seizures, we summarized previous work suggesting that sleep abnormalities dictate the timing of seizures and are exacerbated by sleep loss. Abnormal behavioral arousals and pathological somatomotor system excitability occur in both models and are particularly pronounced during seizure-prone intervals. Sleep loss may magnify somatomotor system hyperexcitability patterns in all states, thus allowing abnormal motor arousals and seizures to intrude during seizure-prone and seizure-resistant sleep and waking states.

Animals↗

PubMed2004

Acute cocaine effects in paradoxical sleep deprived male rats.

Cocaine is a psychomotor drug known to cause behavioural alterations. This study was conducted to characterize behavioural response to acute cocaine injection (7 mg/kg, ip) in paradoxical sleep deprived (PSD) male rats since sleep deprivation is also associated with several behavioural alterations. Cocaine or vehicle was administered to rats at the end of a 4-day period of sleep deprivation, and in home-cage control animals. Cocaine administration in control and PSD rats induced a significant increase in stereotyped behaviour in relation to saline-injected rats. PSD induced significant but heterogeneous effects in animals by increasing grooming while it had effect neither on stereotyped behaviours, locomotion nor on anxiety-like behaviours but significantly decreased rearing behaviour. PSD potentiates the action of cocaine on stereotyped behaviours suggesting supersensitivity of dopaminergic receptors. Thus, the present study indicated that the behavioural effects of cocaine could be modified by PSD. This in turn may have relevant implications in the cocaine effect in abusers under sleep deprived condition.

Analysis of Variance↗

PubMed1987

Quantitative analysis of the effects of slow wave sleep deprivation during the first 3 h of sleep on subsequent EEG power density.

The relation between EEG power density during slow wave sleep (SWS) deprivation and power density during subsequent sleep was investigated. Nine young male adults slept in the laboratory for 3 consecutive nights. Spectral analysis of the EEG on the 2nd (baseline) night revealed an exponential decline in mean EEG power density (0.25-15.0 Hz) over successive nonrapid eye movement--rapid eye movement sleep cycles. During the first 3 h of the 3rd night the subjects were deprived of SWS by means of acoustic stimuli, which did not induce wakefulness. During SWS deprivation an attenuation of EEG power densities was observed in the delta frequencies, as well as in the theta band. In the hours of sleep following SWS deprivation both the power densities in the frequency range from 1 to 7 Hz and the amount of SWS were enhanced, relative to the same period of the baseline night. Both the amount of EEG energy accumulating subsequent to SWS deprivation and its time course could be predicted accurately from the EEG energy deficit caused by SWS deprivation. The data show that the level of integral EEG power density during a certain period after sleep onset depends on the amount of EEG energy accumulated during the preceding sleep rather than on the time elapsed since sleep onset. In terms of the two-process model of sleep regulation (Borbély 1982; Daan et al. 1984) this finding indicates that EEG power density reflects the rate of decay of the regulating variable, S, rather than S itself, as was originally postulated.

Acoustic Stimulation↗

PubMed2000

Zolpidem and sleep deprivation: different effect on EEG power spectra.

To study the role of GABA-ergic mechanisms in sleep regulation, the combined action of 40 h sleep deprivation and either 20 mg zolpidem or placebo on the sleep electroencephalogram (EEG) were investigated by quantitative EEG analysis in eight young men who participated in a positron emission tomography study. Compared with baseline, sleep deprivation increased low-frequency (1.25-7.0 Hz) EEG power in non-rapid eye movement (NREM) sleep in the placebo night. After administration of zolpidem, power in the 3.75-10.0 Hz range and 14. 25-16.0 Hz band was reduced. The largest decrease was observed in the theta band. Comparison with placebo revealed that zolpidem attenuated power in the entire 1.75-11.0 Hz range. The plasma concentration of zolpidem at 4.5 h after intake showed a positive correlation with the drug-induced difference in power from placebo in the 14.25-16.0 Hz band. Regional EEG analysis based on bipolar derivations along the antero-posterior axis disclosed, for NREM sleep, a drug-induced posterior shift of power in the frequency range of 7.75-9.75 Hz. Zolpidem did not affect rapid eye movemnt sleep spectra. We conclude that sleep deprivation and agonistic modulation of GABAA receptors have separate and additive effects on power spectra and that their effects are mediated by different neurophysiological mechanisms.

Adult↗

PubMed2026

Clinical Performance in Critical Care Simulation under Sleep Deprivation: Effects of Power Napping in the Recovery Napping Protocol for Anesthesiologist Performance (R-NAP) Randomized Controlled Trial.

BACKGROUND: Sleep deprivation is common among anesthesia residents and impairs both technical and nontechnical skills such as leadership. Napping is recommended in fatigue management across healthcare and other safety-sensitive sectors, yet its effectiveness for healthcare providers remains underexplored. This study evaluated whether a 30-min nap opportunity improved simulated crisis performance after a 24-h shift. METHODS: Residents were tested twice: once rested and once using a 24-h shift to induce partial sleep deprivation. Between sessions, they were trained in fatigue management. In the sleep-deprived condition, they were randomized to a nap opportunity or a control condition. Actigraphy objectively assessed sleep and nap duration. The primary endpoint was overall simulated clinical performance (0 to 200; combined technical and nontechnical scores). Secondary endpoints were technical and nontechnical subscales. Group effects were primarily tested using intention-to-treat regression models adjusted for rested performance, previous sleep, and critical care experience. RESULTS: Thirty-five residents were enrolled (nap opportunity, n = 19; control, n = 16). In the primary analysis sample (n = 27), clinical performance was 14.8 points higher after the nap opportunity compared with controls (95% CI, 2.8 to 26.9; P = 0.018), corresponding to a 7.4% improvement. Technical skills did not differ significantly between groups, although more sleep was associated with better technical performance. Nontechnical skills were higher in the nap opportunity condition (+11.0 points; 95% CI, 2.2 to 19.8; P = 0.016), including significant effects of leadership and resource utilization. Exploratory analyses suggested associations between longer nap duration and multiple performance domains, strongest for technical skills ( P = 0.010). CONCLUSIONS: Napping appears to enhance clinical performance, while the nap opportunity, nap duration, and previous sleep deprivation each influenced technical and nontechnical performance in distinct ways. These findings support integrating napping and recovery into medical education and scheduling.

Adult↗

PubMedDate not supplied

[Effect of paradoxical sleep deprivation on elaboration and differentiation of alimentary conditioned reflexes].

Paradoxical sleep deprivation of cats by means of awakening them without any significant emotional stress does not affect the acquisition of sound discrimination. Paradoxical sleep deprivation by Jouvet's method producing emotional stress impairs the acquisition of sound discrimination. However, it fails to affect the reproduction of preliminary elaborated sound discrimination.

Animals↗

PubMed2006

Sleep deprivation increases cortical excitability in epilepsy: syndrome-specific effects.

OBJECTIVE: To use transcranial magnetic stimulation (TMS) to investigate the hypothesis that sleep deprivation increases cortical excitability in people with epilepsy. METHODS: We performed paired pulse TMS stimulation, using a number of interstimulus intervals (ISIs) on each hemisphere of 30 patients with untreated newly diagnosed epilepsy (15 idiopathic generalized epilepsy [IGE] and 15 focal epilepsy) and on the dominant hemisphere of 13 healthy control subjects, before and after sleep deprivation. RESULTS: Both hemispheres in patients with IGE and the hemisphere ipsilateral to the EEG seizure focus in those with focal epilepsy showed an increase in cortical excitability following sleep deprivation at a number of ISIs. This change in excitability was most prominent in the patients with IGE. Although there were minor changes after sleep deprivation in control subjects and the contralateral hemisphere in the focal epilepsy group seen at the 250-millisecond ISI, it was less than in the other groups. CONCLUSIONS: Sleep deprivation increases cortical excitability in epilepsy; the pattern of change is syndrome dependent.

Adolescent↗

PubMed2002

Selective sleep deprivation after daily torpor in the Djungarian hamster.

Sleep, daily torpor and hibernation are no longer considered homologous processes. Animals emerging from these states spend most of their time in sleep. After termination of the torpor-associated hypothermia, there is an initial high electroenecephalogram (EEG) slow-wave activity (SWA; 0.75-4.0 Hz) and a subsequent monotonic decline. Both of these features are similar to the effects elicited by prolonged waking. It was previously shown that when hamsters are not allowed to sleep immediately after emerging from torpor, an additional SWA increase above the level reached after sleep deprivation (SD) alone occurs during the delayed recovery. A similar manipulation in hibernating ground squirrels abolished the subsequent SWA increase, shedding doubt on the similarity of the regulatory aspects following torpor and hibernation. To further investigate the extent to which SWA is homeostatically regulated after torpor, Djungarian hamsters were subjected to 1.5 h partial non-rapid eye movement (NREM) sleep deprivation (NSD) that either immediately followed the emergence from torpor (T + NSD) or 4-h SD (SD + NSD). The NSD was attained by disturbing the animals when they exhibited NREM sleep with high amplitude slow-waves. To investigate whether regional aspects of sleep homeostasis are similar after torpor and SD, the EEG was recorded from a parietal and frontal derivation after 4-h SD. An increase in SWA in NREM sleep occurred after all conditions in both EEG derivations. There was no significant difference in SWA during the initial 1.5-h recovery when torpor, T + NSD and SD + NSD were compared. During recovery from torpor and SD, SWA was higher in the frontal than in the parietal derivation. Our results provide further evidence that torpor and SD have similar effects on sleep. The SWA increase did not disappear after the NSD; therefore, SWA is homeostatically regulated after daily torpor. The frontal predominance of slow waves encountered both after torpor and SD indicates that waking and torpor induce similar regional changes in EEG SWA.

Animals↗

PubMed2005

Sleep-wake behavior and responses of interleukin-6-deficient mice to sleep deprivation.

Interleukin (IL)-1 and tumor necrosis factor (TNF) are involved in the regulation of non-rapid eye movements sleep (NREMS). Accumulating evidence suggests IL-6 modulates sleep under some pathophysiologic conditions. We used mice lacking a functional IL-6 gene to investigate further a potential role for IL-6 in the regulation of sleep. IL-6 knockout mice (B6.129S6-Il6tm1Kopf; n=10) and C57BL/6J mice (n=10) were purchased from the Jackson Laboratory (Bar Harbor, ME). Twenty-four-hour baseline recordings were obtained from mice in the absence of any experimental manipulation. Mice were then subjected to 6-h sleep deprivation beginning at light onset. Recordings were obtained during the deprivation period and for 18 h thereafter. During baseline conditions there were no differences between mouse strains with respect to the duration, timing or intensity of NREMS. However, across the 24-h recording period IL-6 knockout mice spent approximately 30% more time in rapid eye movements sleep (REMS) than did C57BL/6J mice. Relative to C57BL/6J mice, core body temperatures of IL-6 knockout mice were higher during the light period of the light:dark cycle. Both strains responded to sleep deprivation by spending more time in NREMS and REMS. Although the total increase in the amount of NREMS after sleep deprivation was the same in both strains, IL-6 knockout mice took 6h longer to accumulate this additional sleep. Under the conditions of this study, IL-6 does not appear necessary for the full manifestation of NREMS, although this cytokine may influence the dynamics of responses to sleep deprivation. That mice lacking IL-6 spend more time in REMS suggests that interactions between IL-6 and REMS regulatory mechanisms may differ from those of IL-1 and/or TNF.

Animals↗

PubMed1992

Meta-analysis of the relationship between total sleep deprivation and performance.

Studies consistently show that total sleep deprivation (TSD) and measures of performance are negatively correlated. However, an accurate quantitative summary of the relationship between these variables has not yet been reported. After collection of the data from 27 relevant studies, meta-analytic techniques were used to test several hypotheses. The correlations were found to be highest for TSD of greater than or equal to 45 h, speed rather than accuracy measures of performance, and work-paced rather than self-paced tasks. These findings are consistent with the "lapse hypothesis" that posits microsleeps during long hours of sleep deprivation.

Chronobiology Phenomena↗

PubMed2005

Sleep homeostasis in rats assessed by a long-term intermittent paradoxical sleep deprivation protocol.

Numerous studies have evaluated the sleep homeostasis of rats after short- or long-periods of sleep deprivation, but none has assessed the effects of prolonged sleep restriction on the rat's sleep pattern. The purpose of the present study, therefore, was to evaluate the sleep homeostasis of rats under a protocol of chronic sleep restriction. Male Wistar rats were implanted with electrodes for EEG and EMG recordings. Using the single platform method, the animals were submitted to 18 h of sleep restriction, beginning at 16:00 h (lights on at 07:00 h), followed by a 6 h sleep window (from 10:00 h to 16:00 h) for 21 days. Immediately after this period, rats were allowed to sleep freely for 4 days (recovery period). The sleep-wake cycle was recorded throughout the entire experiment and the results showed that during the 6h sleep window there was an increase on the percentage of sleep time, reflected by augmented time in high amplitude slow wave sleep and in paradoxical sleep, when compared to baseline sleep, whereas bouts of awakening longer than 1.5 min were greatly reduced, with the animals exhibiting a monophasic-type sleep pattern. During the deprivation period, paradoxical sleep was abolished. High amplitude slow wave sleep was also greatly affected by the protocol. Nonetheless, one day of recovery was sufficient to restore the normal sleep pattern. These findings indicate that this protocol was capable to induce many changes in the rat's sleep patterns, suggesting that during the 6h sleep window there is a sleep adaptive homeostatic process.

Activity Cycles↗

PubMed2003

Effect of bright light on EEG activities and subjective sleepiness to mental task during nocturnal sleep deprivation.

The purpose of this study was to investigate the effect of the exposure to bright light on EEG activity and subjective sleepiness at rest and at the mental task during nocturnal sleep deprivation. Eight male subjects lay awake in semi-supine in a reclining seat from 21:00 to 04:30 under the bright (BL; >2500 lux) or the dim (DL; <150 lux) light conditions. During the sleep deprivation, the mental task (Stroop color-word conflict test: CWT) was performed each 15 min in one hour. EEG, subjective sleepiness, rectal and mean skin temperatures and urinary melatonin concentrations were measured. The subjective sleepiness increased with time of sleep deprivation during both rest and CWT under the DL condition. The exposure to bright light delayed for 2 hours the increase in subjective sleepiness at rest and suppressed the increase in that during CWT. The bright light exposure also delayed the increase in the theta and alpha wave activities in EEG at rest. In contrast, the effect of the bright light exposure on the theta and alpha wave activities disappeared by CWT. Additionally, under the BL condition, the entire theta activity during CWT throughout nocturnal sleep deprivation increased significantly from that in a rest condition. Our results suggest that the exposure to bright light throughout nocturnal sleep deprivation influences the subjective sleepiness during the mental task and the EEG activity, as well as the subjective sleepiness at rest. However, the effect of the bright light exposure on the EEG activity at the mental task diminishes throughout nocturnal sleep deprivation.

Adult↗