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PubMed2006

Serotonin turnover in different duration of sleep recovery in discrete regions of young rat brain after 24 h REM sleep deprivation.

Sleep plays an important role in restorative function and serotonin (5-hydroxytryptamine: 5HT) equally plays important roles in sleep. Though various studies have revealed the roles of 5HT in sleep/wake cycle, the mechanism involved is yet unclear. In the present study we investigated alteration of the 5HT turnover in various regions of the young rat brains after 24 hours (h) REM sleep (sREM) deprivation to elucidate the roles of 5HT in sleep restoration function in the these regions. The 5HT turnover was evaluated by the ratio of 5-hydroxyindole acetic acid against 5HT. The sREM deprivation was performed by the inverted flowerpot technique. The 5HT turnover showed significant alteration in the all regions of the brain examined after 24h sREM deprivation, particular depending on the brain region. These results revealed that sREM modulates the 5HT turnover in the brain with region specificity and this may be one of the restorative functions of sleep indicating that sREM is regionally generated.

Analysis of Variance↗
PubMed1991

Effects of circadian phase and duration of sleep deprivation on sleep and EEG power spectra in the cat.

The electroencephalogram (EEG) of cats was recorded under baseline conditions (LD 12:12) and after 4 and 8 h of sleep deprivation (SD). The EEG was analyzed by visual scoring and by spectral analysis. Under baseline conditions the 24-h distribution of sleep was bimodal: the smallest amounts of sleep occurred at the light-dark and dark-light transitions. EEG slow-wave activity (power density in the delta frequency range: 0.5-4.0 Hz) in non-rapid-eye-movement sleep (NREMS) showed a small variation over the 24-h period. When recovery sleep, following 4 h and 8 h of SD, started at the beginning of the dark period, no significant rebound of NREMS and REMS occurred during the 24-h recovery period. When recovery sleep, after 4 h of SD, started at the fifth hour of the light period, the amount of NREMS was increased. In all experiments the EEG power density in NREMS was enhanced after SD in the entire frequency range studied (0.5-31.5 Hz), but more prominently in the delta and theta (4.5-7.0 Hz) frequency bands. The effects dissipated in the course of the recovery period. The magnitude and duration of the enhancements of EEG power densities were dependent on the duration of SD and on the circadian phase at which SD was scheduled. It is concluded that in the cat sleep is a function of both circadian and homeostatic processes and that especially the EEG power density in NREMS is highly responsive to sleep loss.

Analysis of Variance↗
PubMed1990

The effect of 3-h and 6-h sleep deprivation on sleep and EEG spectra of the rat.

Vigilance states and EEG power density of the rat were determined after a 3- or 6-h sleep deprivation (SD) in the beginning of the 12-h light period. In comparison to baseline, non-rapid eye movement (REM) sleep showed a delayed and transitory increase after 3 h SD, and an immediate and persistent increase after 6 h SD. REM sleep was not affected. In non-REM sleep, EEG power density in the low-frequency range (0.75-6.0 Hz) was markedly enhanced after 6 h SD, but not significantly increased after 3 h SD. In REM sleep EEG activity in the 5-6 Hz band was increased after 6 h SD. We conclude that in the early part of the light period, 3 h waking prolongs non-REM sleep, whereas 6 h waking also enhances non-REM sleep intensity.

Animals↗
PubMed2000

Effects of sleep deprivation on sleep and sleep EEG in three mouse strains: empirical data and simulations.

Gene targeted mice can be used as models to investigate the mechanisms underlying sleep regulation. Three commonly used background strains for gene targeting (129/Ola, 129/SvJ and C57BL/6J) were subjected to 4-h and 6-h sleep deprivation (SD), and their sleep and sleep EEG were continuously recorded. The two-process model of sleep regulation has predicted the time course of slow-wave activity (SWA) in nonREM sleep after several sleep-wake manipulations in humans and the rat [3] [9]. We tested the capacity of the model to predict SWA in nonREM sleep on the basis of the temporal organization of sleep in mice. The strains differed in the amount and distribution of sleep and the time course of SWA. After spontaneous waking episodes of 10-30 min as well as after SD, SWA was invariably increased. Simulations of the time course of SWA were successful for 129/SvJ and C57BL/6J, but were not satisfactory for 129/Ola. Since the time constants are assumed to reflect the dynamics of the physiological processes involved in sleep regulation, the results provide a basis for the use of gene targeted mice to investigate the underlying mechanisms.

Animals↗
PubMedDate not supplied

Glucose metabolic response to total sleep deprivation, recovery sleep, and acute antidepressant treatment as functional neuroanatomic correlates of treatment outcome in geriatric depression.

OBJECTIVE: The variable speed and durability of response to antidepressant medications in geriatric depression is a significant clinical problem. The authors evaluated changes in cerebral glucose metabolism measured with positron emission tomography (PET) during a clinical trial designed to accelerate medication response by the use of one night of total sleep deprivation (TSD), and they asked whether changes would correlate with treatment outcome after 12 weeks of antidepressant treatment. METHODS: Twelve elderly, unipolar depressed patients underwent serial PET studies at baseline, post-TSD, post-recovery sleep (after an initial paroxetine dose), and after 2 weeks of paroxetine treatment. RESULTS: Decreased regional glucose metabolism after TSD, recovery sleep, and 2 weeks of treatment was associated with clinical improvement at 12 weeks. The right cingulate gyrus area was consistently correlated with clinical improvement across treatment conditions. CONCLUSION: These data indicate that the early metabolic alterations in the right cingulate gyrus and the persistence of these adaptive changes are associated with improvement in depressive symptoms.

Aged↗
PubMed1986

Effect of biologically active light and partial sleep deprivation on sleep, awakening and circadian rhythms in normals.

The effects of biologically active light (BL) on subjective and objective quality of sleep and awakening, as well as circadian rhythms in cortisol, temperature and well-being were studied in 10 hospitalized normal female volunteers as compared with partial sleep deprivation (PSD). After 2 adaption days, three 24-hour periods were recorded before (baseline), during (intervention) and after (recovery) treatment with BL (exposure between 5.00-9.00 p.m. and 6.00-9.00 a.m.; light sensitivity: 2,800 lx at eye level) and PSD (1.30-6.00 a.m.). Somnopolygraphic investigations demonstrated a significant improvement in sleep maintenance both after BL and PSD, while sleep induction improved only after PSD. Subjectively experienced sleep quality increased after both treatments. However, subjective and objective awakening quality (objectivated by means of psychometric test battery) was improved by BL only, while PSD produced no changes or even a deterioration. Cortisol levels tended to be lowered by BL, while the troughs increased after PSD; there was also an earlier rise in cortisol levels after PSD than BL. No significant differences were found in regard to temperature. Subjectively experienced well-being tended to improve after both interventions. Our findings concerning the beneficial effect of BL on objective and subjective quality of sleep and awakening in normals encourages us to initiate a single-dose study with BL in depressed patients.

Adult↗
PubMed1981

Sleep deprivation: effect on sleep stages and EEG power density in man.

Sleep was analysed in 8 young adults subjects during two baseline nights and two recovery nights following 40.5 h sleep deprivation. Sleep stages were scored from the polygraph records according to conventional criteria. In addition, the EEG records of the entire nights were subjected to spectral analysis to compute the frequency distribution of the power density in the 0.25-25 Hz range for 0.5 Hz or 1.0 Hz bins. In the first recovery night, the power density in the delta band was significantly higher than baseline for total sleep time as well as for sleep stages 2, 3 and 4, 4 and REM. These changes were not restricted to the delta band, but extended to higher frequency bands. Minor, but significant, effects of sleep deprivation were seen in the power density distribution of the second recovery night. In the baseline nights, a progressive reduction of power density in the delta/theta range was present for successive non-REM-REM sleep cycles for total sleep time and stages 2, 3 and 4, and 4. The results show that effects of sleep deprivation as well as trends within the sleep periods are readily apparent from spectral analysis, but are inadequately reflected by conventional sleep scoring. When the power density values were integrated over the entire frequency range (0.75-25 Hz) for each non-REM-REM sleep cycle, an exponential decline from cycle 1 to cycle 3 was suggested. The present findings support the hypothesis that the EEG power density in the low frequency range is an indicator of a progressively declining process during sleep whose initial value is determined by the duration of prior waking.

Adult↗
PubMed1975

Activation effects of sleep deprivation and sleep in seizure patients. An electroencephalographic study.

This paper reports on 294 patients with presumptive symptoms of epilepsy but no noteworthy, or only suspicious, EEG findings. With recording during sleep after 24-27 h of sleep deprivation, 138 persons showed definite epilepsy potentials. The remainder of the group showed no noteworthy findings. Nevertheless, on the basis of clinical observations and the course of the patient's illness, epilepsy was diagnosed in 27 patients of this second group. Neurophysiological aspects of the electroencephalographic provocation method are discussed.

Adolescent↗
PubMed2003

Direct comparison of total sleep deprivation and late partial sleep deprivation in the treatment of major depression.

BACKGROUND: There are clinical as well as experimental indications that--contrary to what is generally assumed--late partial sleep deprivation (LPSD) is not as effective as total sleep deprivation (TSD) in the treatment of depression. METHOD: We conducted a randomised balanced crossover study with 39 in-patients with major depression (mainly unipolar) in which both procedures LPSD and TSD were compared within a 1-week interval. Response was defined as a reduction of > or =30% in the 6-item Hamilton Depression Rating Scale and/or one of two self-rating scales (Adjective Mood Scale, Visual Analogue Scale). RESULTS: Overall response rate on the day after was low (0-53%, depending on the rating used). TSD proved slightly and in about half of the comparisons also significantly more effective than LPSD. In general, first treatments were more effective than second treatments; there were 10-20% second day responses; in up to 10% of the treatments patients worsened after sleep deprivation (using the same absolute criteria as for therapeutic response). LIMITATIONS: Non-blind rating, intentional and unintentional napping (microsleep) was not recorded, mainly unipolar depressives. CONCLUSIONS: Total sleep deprivation seems to be more effective than late partial sleep deprivation. We believe that there might be a dose-response relationship between hours of lost sleep and therapeutic effect within the range of 1 night.

Adult↗
PubMed1996

Paradoxical sleep deprivation and sleep recording following training in a brightness discrimination avoidance task in Sprague-Dawley rats: paradoxical effects.

Previously, we reported that posttraining paradoxical sleep deprivation (PSD) resulted in an enhancement of the subsequent avoidance performance for rats trained for 15 trials in a Y-maze brightness avoidance discrimination task. A series of experiments were conducted to try to further understand the reasons for results which were contrary to those of the bulk of the sleep-learning literature. Experiment 1 investigated the effectiveness of the PSD technique. Rats (N = 4) were sleep recorded while residing on a "swimming pool" apparatus for 24 h. Compared to their baseline values, all animals showed a very large reduction in paradoxical sleep and spent significantly more time awake. Slow-wave sleep was unchanged. In Experiment 2, proactive motor effects were tested. Rats were deprived of PS for 24 h and then tested in a hole board motor activity task. There was a slight effect of PS deprivation on the day following the PSD and no effect when the rats were retested 1 week later. Experiment 3 investigated possible proactive effects of PSD on avoidance performance. Rats exposed to PSD in the 24 h before training in the Y-maze task did not demonstrate any facilitative effect on the subsequent avoidance performance. Experiment 4 investigated the possibility that the PSD facilitative effect could be due to partial training. Rats were given 75 acquisition trials in the brightness discrimination Y-maze avoidance before being subjected to 24 h of PSD. PS-deprived animals showed superior avoidance scores compared to non-PSD controls when retested 24 h later. In Experiment 5, the same strain of rats (N = 11) were sleep recorded after exposure to a partial acquisition in a Y-maze brightness avoidance discrimination task. They were then continuously monitored for 4 consecutive days. The percent PS for the Trained rats was significantly lower than that for the Control animals. This drop in percent PS was not confined to any particular time period in the 24-h day. None of the other sleep parameters reached significance. Analyses of the present results suggest that PSD exerts its facilitative effects on posttraining consolidation processes. We present arguments suggesting that PSD can have effects opposite to those generally reported, in animals demonstrating poor avoidance abilities, in an avoidance task.

Animals↗
PubMedDate not supplied

Effect of 64 hours of sleep deprivation upon sleep in geriatric normals and insomniacs.

Fifty-eight geriatric normal and chronic insomniac sleepers were screened with sleep recordings to define groups of 12 Normal (Sleep Efficiency greater than 85%) and Insomniac (Sleep Efficiency less than 80%) sleepers. All subjects then had 4 baseline sleep nights, 64 hours of total sleep loss, and 4 recovery nights. Insomniacs, had lower sleep efficiencies and less REM than Normals during baseline. Sleep efficiency was high (97%) in both groups on the first recovery night but decreased toward baseline values in both groups between the second (Normal) and fourth (Insomniac) recovery night. The groups had relatively little slow wave sleep, but had a significant increase on the first recovery night. Five Normals and one Insomniac had REM latency of less than 15 min on their first recovery night. This REM latency was found to be significantly correlated with the amount of slow wave sleep on baseline. Decreased REM latency in initial recovery sleep was interpreted as evidence of decreased pressure for slow wave sleep in aging.

Aged↗
PubMed2000

What is causing excessive daytime sleepiness? Evaluation to distinguish sleep deprivation from sleep disorders.

Many people have a temporary spell, often in early afternoon, when they feel drowsy. This passing desire for a quick nap is completely different from excessive daytime sleepiness, which is a much more significant problem. Considering the potentially dire personal and economic consequences of falling asleep unintentionally or at inappropriate times, excessive daytime sleepiness must be taken very seriously. A thorough evaluation, as described by Dr. Mahowald, virtually always leads to a specific underlying cause, allowing effective treatment recommendations.

Diagnosis, Differential↗
PubMed2005

Gene expression in the rat brain during sleep deprivation and recovery sleep: an Affymetrix GeneChip study.

Previous studies have demonstrated that macromolecular synthesis in the brain is modulated in association with the occurrence of sleep and wakefulness. Similarly, the spectral composition of electroencephalographic activity that occurs during sleep is dependent on the duration of prior wakefulness. Since this homeostatic relationship between wake and sleep is highly conserved across mammalian species, genes that are truly involved in the electroencephalographic response to sleep deprivation might be expected to be conserved across mammalian species. Therefore, in the rat cerebral cortex, we have studied the effects of sleep deprivation on the expression of immediate early gene and heat shock protein mRNAs previously shown to be upregulated in the mouse brain in sleep deprivation and in recovery sleep after sleep deprivation. We find that the molecular response to sleep deprivation and recovery sleep in the brain is highly conserved between these two mammalian species, at least in terms of expression of immediate early gene and heat shock protein family members. Using Affymetrix Neurobiology U34 GeneChips , we also screened the rat cerebral cortex, basal forebrain, and hypothalamus for other genes whose expression may be modulated by sleep deprivation or recovery sleep. We find that the response of the basal forebrain to sleep deprivation is more similar to that of the cerebral cortex than to the hypothalamus. Together, these results suggest that sleep-dependent changes in gene expression in the cerebral cortex are similar across rodent species and therefore may underlie sleep history-dependent changes in sleep electroencephalographic activity.

Action Potentials↗
PubMed2005

Effects of sleep deprivation and recovery sleep upon cell proliferation in adult rat dentate gyrus.

Numerous behavioral and environmental factors modulate the production of new cells in the adult mammalian brain. Although sleep loss has previously been shown to dramatically suppress brain cell proliferation, the effect of recovery sleep after a period of sleep deprivation is not known. Using the disk-over-water paradigm, adult male Sprague-Dawley rats were sleep deprived for 48 h. Separate groups were then allowed either an 8 h period of recovery sleep or an additional 8 h of sleep deprivation. A third group of rats served as a control, and were not sleep deprived. At 54 h, all rats received an injection of 5-bromo-2'-deoxyuridine (200 mg/kg, i.p.) and were killed 2 h later. When compared with control rats, a 36% reduction in cell proliferation was observed in the dentate gyrus of rats subjected to 56 h of sleep deprivation. A similar reduction in proliferation (39%) was observed in rats allowed an 8 h period of recovery sleep. In both deprivation groups, the magnitude of suppression of cell proliferation was approximately twice as large in the posterior hippocampus as it was in the anterior hippocampus. These data confirm previous results that an extended period of sleep deprivation exerts a strong suppressant effect on cell proliferation in the rat dentate gyrus, and demonstrate that this suppression of cell proliferation shows no evidence of recovery for at least 8 h following a 48 h period of sleep deprivation.

Analysis of Variance↗
PubMed2004

Decreased arousals among healthy infants after short-term sleep deprivation.

OBJECTIVE: Sleep deprivation is a risk factor for sudden infant death syndrome (SIDS). Recent changes in normal life routines were more common among SIDS victims, compared with control infants. Sleep deprivation can result from handling conditions or from sleep fragmentation attributable to respiratory or digestive conditions, fever, or airway obstructions during sleep. Compared with matched control infants, future SIDS victims exhibited fewer complete arousals by the end of the night, when most SIDS cases occur. Arousal from sleep could be an important defense against potentially dangerous situations during sleep. Because the arousal thresholds of healthy infants were increased significantly under conditions known to favor SIDS, we evaluated the effects of a brief period of sleep deprivation on sleep and arousal characteristics of healthy infants. DESIGN: Fourteen healthy infants, with a median age of 8 weeks (range: 6-18 weeks), underwent polygraphic recording during a morning nap and an afternoon nap, in a sleep laboratory. The infants were sleep-deprived for 2 hours before being allowed to fall asleep. Sleep deprivation was achieved by keeping the infants awake, with playing, handling, and mild tactile or auditory stimulations, for as long as possible beyond their habitual bedtimes. To avoid any confounding effect attributable to differences in sleep tendencies throughout the day, sleep deprivation was induced before either the morning nap or the afternoon nap. Seven infants were sleep-deprived before the morning nap and 7 before the afternoon nap. The sleep and arousal characteristics of each infant were compared for the non-sleep-deprived condition (normal condition) and the sleep-deprived condition. During each nap, the infants were exposed, during rapid eye movement (REM) sleep, to white noise of increasing intensity, from 50 dB(A) to 100 dB(A), to determine their arousal thresholds. Arousal thresholds were defined on the basis of the lowest auditory stimuli needed to induce arousal. After the induced arousal, the infants were allowed to return to sleep to complete their naps. RESULTS: Sleep deprivation lasted a median of 120 minutes (range: 90-272 min). Most sleep characteristics were similar for the normal and sleep-deprived conditions, including sleep efficiency, time awake, percentages of REM sleep and non-REM sleep, frequency and duration of central apnea and of periodic breathing, duration of obstructive apnea, mean heart rate and variability, and mean breathing rates during REM sleep and non-REM sleep. After sleep deprivation, the duration of the naps increased, whereas there were decreases in the latency of REM sleep and in the density of body movements. More-intense auditory stimuli were needed for arousal when the infants were sleep-deprived, compared with normal nap sleep. Sleep deprivation was associated with a significant increase in the frequency of obstructive sleep apnea episodes, especially during REM sleep. No significant differences were noted when the effects of morning and afternoon sleep deprivation were compared. No correlation was found between the duration of sleep deprivation and either the frequency of obstructive apnea or the changes in arousal thresholds, although the infants who were more sleep-deprived exhibited tendencies toward higher auditory arousal thresholds and shorter REM sleep latencies, compared with less sleep-deprived infants. There were tendencies for a negative correlation between the auditory arousal thresholds and REM sleep latencies and for a positive correlation between the auditory arousal thresholds and the frequencies of obstructive apnea during REM sleep. CONCLUSIONS: Short-term sleep deprivation among infants is associated with the development of obstructive sleep apnea and significant increases in arousal thresholds. As already reported, sleep deprivation may induce effects on respiratory control mechanisms, leading to impairment of ventilatory and arousal responses to chemical stimulation and decreases in genioglossal electromyographic activity during REM sleep. These changes in respiratory control mechanisms could contribute to the development of obstructive apnea. The relationship between the development of obstructive apnea and increases in arousal thresholds remains to be evaluated. Adult subjects with obstructive sleep apnea exhibited both sleep fragmentation and increases in arousal thresholds. Conversely, sleep deprivation increased the frequency and severity of obstructive sleep apnea. In this study, the increases in arousal thresholds and the development of obstructive apnea seemed to result from the preceding sleep deprivation. The depressed arousals that follow sleep deprivation have been attributed to central mechanisms, rather than decreases in peripheral sensory organ function. Such mechanisms could include disturbances within the reticular formation of the brainstem, which integrates specific facilitory inputs, such as ascending pathways from auditory receptors, and inhibitory inputs from the cortex. It remains to be determined whether the combination of upper airway obstruction and depressed arousability from sleep contributes to the increased risk of sudden death reported for sleep-deprived infants.

Acoustic Stimulation↗
PubMed1987

Rapid eye movement sleep deprivation affects sleep similarly in castrated and noncastrated rats.

Twenty-four-hour recordings of electrophysiological correlates of the sleep-waking cycle in castrated and noncastrated Wistar rats were performed to validate the cuff pedestal technique in the deprivation of rapid eye movement sleep. An undisturbed pattern of sleep was found in both castrated and noncastrated rats when the cuffs were in the raised position. The lowering of the cuff for 4 days virtually abolished REMs in both groups of rats. During neither the dark nor the light period was there any difference between the castrated and noncastrated rats in the total amount of REMs rebound. The results accord with the data obtained by the conventional flowerpot procedure and show that castration does not influence the amount of REMs before, during, and after REMs deprivation in the rat. It is suggested that testicular testosterone, contrary to growth hormone, is not essential for the triggering of REMs sleep, although both have anabolic actions.

Analysis of Variance↗