Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SLEEP DEPRIVATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 973 records · Page 54Linked to original sources
PubMed1994

Waking electroencephalogram activity as a consequence of sleep and total sleep deprivation in the rat.

Effects of 6 hours of total sleep deprivation (TSD) by gentle handling and 6 hours of sleep on the waking electroencephalogram (EEG) activity of 14 Wistar rats were studied during the lights-on portion of the light-dark cycle under two TSD schedules: a) TSD 0800-1400 hours and sleep 1400-2000 hours, and b) sleep 0800-1400 hours and TSD 1400-2000 hours. EEG was recorded monopolarly from left and right parietals referred to ipsilateral reference electrodes. Spectral analysis was performed on samples of waking EEG during TSD (each 30 minutes) and during sleep (each 60 minutes after enforced awakening). The following significant changes were observed: TSD induced a linear increase in the absolute power of delta (1.46-3.42 Hz) and the full band (1.6-24.9 Hz) and produced a decrease in the interparietal correlation of theta. Sleep induced the opposite results. Theta relative power (power in a band expressed as a percentage of total power between 1.46 and 24.9 Hz) showed a circadian effect. It was higher at 1400 hours than at 0800 and 2000 hours after both sleep and TSD conditions. Six hours of TSD were enough to induce significant changes in the waking EEG regardless of position of TSD in the lights-on period of the light-dark cycle.

Animals↗
PubMed2006

Effects of partial sleep deprivation on within-format and cross-format priming.

STUDY OBJECTIVES: The purpose of this study was to examine the effects of sleep on long-term priming. We report the results of a preliminary experiment that enabled us to verify that priming can last for 4 hours, and we also report the results of a study of partial sleep-deprivation. DESIGN: Subjects performed 2 tasks: within-format and cross-format priming. SETTINGS: Sleep laboratory. PARTICIPANTS: Ninety-eight healthy young subjects participated in the 2 studies reported here: 48 in the preliminary experiment and 50 in the sleep-deprivation study. INTERVENTION: Testing after a 4-hour diurnal retention interval (Experiment 1) or after an equivalent interval filled with early or late sleep, or corresponding periods of wakefulness (Experiment 2). MEASUREMENTS AND RESULTS: A tachistoscopic identification paradigm, consisting of naming aloud briefly flashed drawings, was used to assess 2 priming conditions: a same-format or within-format condition (in which items were drawings in the study and test phases) and a different- or cross-format condition (in which the symbolic format of the items differed between the 2 phases: words/drawings). In Experiment 1, we revealed significant priming effects in both conditions after a 4-hour interval. In Experiment 2, only same-format priming effects were observed, but their magnitude was smaller than in Experiment 1. There was no significant difference in priming scores between the sleep and wake groups. CONCLUSIONS: Sleep does not appear to have a strong effect on priming. Instead, priming appears to be affected by circadian influences.

Adolescent↗
PubMed1986

The effects of REM sleep deprivation on striatal dopamine receptor sites.

3H-Spiroperidol binding to dopamine receptor sites of rat striatal tissue was studied following 24, 48, 72 and 96 hr of rapid eye movement sleep deprivation (REM dep.). The density of dopamine receptor binding sites (Bmax) was decreased after 48, 72, and 96 hr of REM dep. The apparent dissociation constant (KD) decreased after 96 hr, indicating an increase in apparent affinities. The control experimental animals also presented a time-dependent decrease of Bmax and KD as compared to unhandled controls. These results suggest that dopaminergic mechanisms may indeed be involved in the effects of REM sleep deprivation and/or stress.

Animals↗
PubMed1988

Deficient nocturnal surge of TSH secretion during sleep and sleep deprivation in rapid-cycling bipolar illness.

Rapid-cycling bipolar patients have a high prevalence of hypothyroidism, and this disturbance in their hypothalamic-pituitary-thyroid (HPT) function may provide a model for understanding the less severe thyroid dysfunction present in other forms of affective disorder. For these reasons, we investigated HPT function in eight rapid-cycling bipolar patients and eight normal controls by measuring plasma levels of thyroid-stimulating hormone (TSH) and cortisol every 30 min during a baseline 24-h period and during an additional night of sleep deprivation. Thyrotropin-releasing hormone (TRH) (500 micrograms) challenge tests were also performed in the patients. Controls exhibited a significant circadian variation in TSH with a nocturnal rise that was augmented by sleep deprivation. In the rapid cyclers, the nocturnal rise in TSH was absent, and sleep deprivation failed to raise their TSH levels significantly compared with baseline. Low nocturnal TSH levels were associated with blunted TSH responses to TRH infusions; due to the relatively brief sampling interval used in the TRH challenge tests, however, these results do not reliably discriminate between hypothalamic and pituitary dysfunction as an etiology for low nocturnal TSH levels. Additional studies are needed to determine the precise nature of the HPT disturbance in rapid-cycling patients.

Adult↗
PubMed2004

Augmentation of electroconvulsive therapy seizures with sleep deprivation.

Electroconvulsive therapy (ECT) is the fastest and most effective treatment for severe or treatment-resistant affective and psychotic disorders. Its therapeutic effect is obtained through a generalized tonic-clonic seizure of adequate duration. Several factors (older age, male gender, and the sessions of ECT themselves) increase seizure threshold and reduce seizure time. In our work, sleep deprivation was used as a strategy to enhance the ECT seizure. A matched sample design was conducted on the basis of the following variables: gender, age range, and seizure threshold. After the first ECT, when the initial seizure threshold was measured, subjects were assigned to ECT (electroconvulsive therapy) or SD+ECT (sleep deprivation + electroconvulsive therapy). Changes in the variable of seizure threshold were studied in both groups during the treatment course. A nonparametric analysis was implemented for 2 independent groups. During the treatment course, the SD+ECT group showed a decreased seizure threshold, from 190.4 mC in the first ECT session to 176.4 mC in the last ECT session, whereas the ECT group showed an increased seizure threshold, increasing from 190.4 mC to 321.91 mC. Sleep deprivation is an effective and safe technique used to lower the seizure threshold of ECT and to obtain an adequate seizure time without increasing the energy applied.

Aged↗
PubMed1999

Effects of menstrual cycle phase and oral contraceptives on alertness, cognitive performance, and circadian rhythms during sleep deprivation.

The influence of menstrual cycle phase and oral contraceptive use on neurobehavioral function and circadian rhythms were studied in healthy young women (n = 25) using a modified constant routine procedure during 24 h of sleep deprivation. Alertness and performance worsened across sleep deprivation and also varied with circadian phase. Entrained circadian rhythms of melatonin and body temperature were evident in women regardless of menstrual phase or oral contraceptive use. No significant difference in melatonin levels, duration, or phase was observed between women in the luteal and follicular phases, whereas oral contraceptives appeared to increase melatonin levels. Temperature levels were higher in the luteal phase and in oral contraceptive users compared to women in the follicular phase. Alertness on the maintenance of wakefulness test and some tests of cognitive performance were poorest for women in the follicular phase especially near the circadian trough of body temperature. These observations suggest that hormonal changes associated with the menstrual cycle and the use of oral contraceptives contribute to changes in nighttime waking neurobehavioral function and temperature level whereas these factors do not appear to affect circadian phase.

Adolescent↗
PubMed2004

Diurnal variation in the genital reflexes and hormone levels induced by paradoxical sleep deprivation and cocaine in male rats.

The purpose was to ascertain whether the genital reflexes induced by paradoxical sleep deprivation (PSD) in male rats show diurnal variation, and whether the hormonal rhythm of testosterone and progesterone is involved in these behaviors. Genital reflexes (penile erection -- PE, and ejaculation -- EJ) and hormone levels were assessed during a 24 h period at four testing times (0900, 1600, 2100 and 0400 h) in PSD rats injected with saline or cocaine. Results indicated that PE in PSD rats given saline or cocaine did not show diurnal variation while EJ responses were significantly reduced at 0400 h in the PSD-cocaine group. The home-cage control group testosterone concentrations were lower at 1600, 2100 and 0400 h than at 0900 h. At 0900 h, testosterone levels were significantly lower in the PSD groups than in the control group. In contrast, progesterone levels were significantly higher in PSD groups in relation to the control group at the four testing times. Thus, we observed strong diurnal variation in testosterone and progesterone in control rats whereas only EJ responses in PSD-cocaine seemed to be influenced by the time of day. These results suggest that progesterone may influence the modulation of male genital reflexes displayed by sleep-deprived rats.

Animals↗
PubMed2002

Sleep deprivation decreases glycogen in the cerebellum but not in the cortex of young rats.

We tested whether brain glycogen reserves were depleted by sleep deprivation (SD) in Long-Evans rats 20-59 days old. Animals were sleep deprived beginning at lights on and then immediately killed by microwave irradiation. Glycogen and glucose levels were measured by a fluorescence enzymatic assay. In all age groups, SD reduced cerebellar glycogen levels by an average of 26% after 6 h of SD. No changes were observed in the cortex after 6 h of SD, but in the oldest animals, 12 h of SD increased cortical glycogen levels. There was a developmental increase in basal glycogen levels in both the cortex and cerebellum that peaked at 34 days and declined thereafter. Robust differences in cortical and cerebellar glycogen levels in response to enforced waking may reflect regional differences in energy utilization and regulation during wakefulness. These results show that brain glycogen reserves are sensitive to SD.

Aging↗
PubMedDate not supplied

Spatial learning on the Morris Water Maze Test after a short-term paradoxical sleep deprivation in the rat.

Twelve rats were deprived of paradoxical sleep (PS) for eight hours using the small platform method. PS-deprived and control rats then learned either the standard allocentric version (using external cues) of the Morris Water Maze (MWM) or a delayed alternation version (changing the platform location between trials: MWM(DA)). Overall, rats learning the MWM(DA) made more quadrant entries than rats learning the allocentric version. Compared to other rats, PS-deprived rats crossed more quadrants only in the MWM(DA). These results show that MWM(DA) is a more complex task to learn and is more vulnerable to PS deprivation than allocentric spatial orientation. Since delayed alternation is dependent upon frontal structures, we propose that tasks involving the frontal cortex are more sensitive to short-term PS deprivation than tasks related to hippocampal structures.

Animals↗
PubMed2001

Fighting by sleep-deprived rats as a possible manifestation of panic: effects of sodium lactate.

Increased fighting is an effect of desynchronized sleep deprivation (DSD) in rats, and recently this behavior has been suggested to be spontaneous panic and equivalent to panic disorder. In the present study we tested this hypothesis by evaluating the effect of sodium lactate on this aggressiveness, because this substance is recognized to induce spontaneous panic attacks in patients. A total of 186 male albino Wistar rats, 250-350 g, 90-120 days of age, were submitted to DSD (multiple platform method) for 0, 4, or 5 days. At the end of the deprivation period the rats were divided into subgroups respectively injected intraperitoneally with 1.86, 2.98 and 3.72 g/kg of 1 M sodium lactate, or 1.86 and 3.72 g/kg of 2 M sodium lactate. The control animals were submitted to the same procedures but received equivalent injections of sodium chloride. Regardless of DSD time, sleep-deprived animals that received sodium lactate presented a significantly higher mean number of fights (0.13 +/- 0.02 fights/min) and a longer mean time spent in confrontation (2.43 +/- 0.66 s/min) than the controls (0.01 +/- 0.006 fights/min and 0.12 +/- 0.07 s/min, respectively; P<0.01, Student t-test). For the sodium lactate group, concentration of the solution and time of deprivation increased the number of fights, with the mean number of fights and mean duration of fighting episodes being greater with the 2.98 g/kg dose using 1 M lactate concentration. These results support the hypothesis that fighting induced by DSD is probably a spontaneous panic manifestation. However, additional investigations are necessary in order to accept this as a promising animal model for studies on panic disorder.

Aggression↗
PubMed1993

Effects of chronic total sleep deprivation on central noradrenergic receptors in rat brain.

The effect of chronic total sleep deprivation (TSD) on the regulation of central noradrenergic receptors was evaluated. Rats were subjected to 10 days of TSD by the disk-over-water method. As in previous TSD studies, these rats showed greater increases in food intake and energy expenditure and greater eventual declines in waking body temperature than their yoked-control (TSC) rats. After sacrifice, alpha 1-, alpha 2-, and beta-adrenoceptors were determined in 11 brain regions using radioligand binding assays with [3H]prazosin, [3H]rauwolscine, and 125I-iodocyanopindolol, respectively. Adrenoceptor density and affinity values were significantly different among TSD, TSC, and normally caged control rat groups only for the cerebellum, which showed higher alpha 2-binding density concomitant with lower affinity and lower beta-binding density than cage control rats. Such changes are attributable to apparatus or stimulus effects common to TSD and TSC rats. Given the absence of firm evidence for a TSD-induced downregulation of central noradrenergic receptors, the present results offer no support for the hypothesis of Siegel and Rogawski that a major function of paradoxical sleep is to upregulate these receptors.

Animals↗
PubMed2006

Preliminary findings of proton magnetic resonance spectroscopy in occipital cortex during sleep deprivation.

Proton magnetic resonance spectroscopy ((1)H MRS) has revealed biochemical alterations in various psychiatric disorders. Changes in brain metabolites may be caused not only by the disease's progression or response to treatment, but also by physiological variability. The aim of this study was to use (1)H MRS to assess the effects of specific short-term physiological states on major metabolites. Eight healthy women underwent (1)H MRS at the beginning and end of a 40-h period of sleep deprivation. The ratios of N-acetyl-aspartate (NAA), total creatine (tCr), and choline-containing compounds (Cho) to water (H(2)O) were determined from the occipital cortex during both baseline and photic stimulation conditions. During sleep deprivation, NAA/H(2)O decreased by 7% and Cho/H(2)O by 12%. Photic stimulation had no effect on the measured metabolites in the alert state, but in the sleep-deprived state the level of Cho/H(2)O increased during neuronal activation. The results suggest that NAA/H(2)O and Cho/H(2)O may depend on the state of alertness.

Adult↗
PubMed1985

DST in healthy volunteers and after sleep deprivation.

The dexamethasone suppression test (DST) was performed in 46 healthy volunteers and repeated in nine of them following total sleep deprivation (TSD). While only 2 postdexamethasone cortisol values were insufficiently suppressed (greater than 5 micrograms %) in control DSTs, 5 postdexamethasone cortisol values were above 5 micrograms % following TSD. The mean postdexamethasone value was increased from 1.55 +/- 1.06 to 4.47 +/- 5.86 micrograms % following TSD at 8.00 h. The authors conclude that sleep deprivation as a therapeutic approach and prolonged sleeplessness may bias DST results.

Adult↗
PubMed1994

Dissociated paradoxical sleep deprivation effects on inhibitory avoidance and conditioned fear.

Rats were submitted to paradoxical sleep deprivation (PSD) for 24, 72, or 96 h and were trained on a double aversively motivated task, encompassing a step-through inhibitory avoidance and a classical conditioning of fear to a brief tone serving as conditional stimulus. Retention test of the inhibitory avoidance was performed at the same apparatus of training (without tone presentation). Retention of conditioned fear was assessed in an open field apparatus, where the freezing reaction to the tone was measured. PSD for 24 and 72 h preceding the training session had no effect on either task. However, PSD during the 96 h preceding the training session impaired acquisition of inhibitory avoidance, but had no effect on classically conditioned fear. It is concluded that PSD had differential effects on the two tasks, both aversively motivated and trained at the same time and conditions.

Acoustic Stimulation↗
PubMed1995

Effects of pretraining paradoxical sleep deprivation upon two-way active avoidance.

In order to study whether paradoxical sleep (PS) is necessary to prepare subjects for the subsequent learning of a distributed two-way active avoidance conditioning, 10 rats were subjected to 5 h of paradoxical sleep deprivation (PSD group) by means of the platform method immediately before each of 5 acquisition sessions (one daily), as well as before a long-term retention (LTR) session (14 days). Another group of rats (PSD control group; n = 10) were placed on large platforms as a control for the side effects induced by PSD platforms. Rats in the dry control group (n = 10) did not receive any treatment. The number of avoidances of the PSD group was significantly lower on the 1st, 2nd and 3rd acquisition sessions compared to the PSD control group, and on the 2nd and 3rd sessions compared to the dry control group. PSD rats made significantly less intertrial crossings than dry controls on the 2nd and 3rd acquisition sessions, but no significant correlations were found between this variable and the number of avoidances. Therefore, our results are not fully in contradiction with the hypothesis that PS previous to the training sessions might prepare the animal for subsequent learning, although the influence of locomotor changes upon the performance of PSD subjects cannot be fully rejected.

Animals↗
PubMed1978

Effects of sleep deprivation on awakening thresholds and sensory evoked potentials in the rat.

The EEG desynchronization response to stimuli presented during slow-wave sleep was studied in 25 chronically implanted rats after 12 hr of sleep deprivation and during control periods of normal sleep. Compared to normal sleep, sleep after deprivation was accompanied by a significant decrease in the number of EEG desynchronization responses to auditory stimuli and by an additional disproportionate decrease in the number of sustained desynchronization responses. Thalamic auditory evoked potentials were not reduced in amplitude during postdeprivation sleep, thus the decrease in number of EEG desynchronization responses to the auditory stimuli was apparently not mediated by decreased responsiveness in the peripheral auditory system. On the other hand, postdeprivation sleep was not accompanied by any significant change in total number of EEG desynchronization responses to direct trigeminal nerve stimulation nor by any change in the duration of responses to trigeminal stimulation. The results suggest that recovery from sleep loss in accompanied not by a nonspecific increase in the threshold for arousal per se but instead by a selective increase in the threshold for arousal to certain classes of peripheral stimuli.

Acoustic Stimulation↗
PubMed1994

Cold thermoregulatory changes induced by sleep deprivation in men.

The aim of this study was to evaluate the thermoregulatory changes induced by 27-h of sleep deprivation (SD) in men at rest both in a comfortable ambient temperature and in cold air. A group of 12 male subjects were placed in a comfortable ambient temperature (dry bulb temperature, Tdb = 25 degrees C, relative humidity, rh = 40%-50%, clothing insulation = 1 clo) for 1 h and then they were submitted to a standard cold air test in a climatic chamber for 2 h (Tdb = 1 degree C, rh = 40%-50%, wind speed = 0.8 m.s-1, nude), before and after 27 h of sleep deprivation. Thermoregulatory changes (rectal temperature, Tre; mean skin temperature. Tsk; metabolic heat production M) were monitored continuously. At comfortable ambient temperature, no significant change was observed after SD for Tre, Tsk and M. During the cold test, Tre did not change but Tsk and M were higher after SD (P < 0.05). Increased M (+ 6%, P < 0.05) was related to earlier and higher shivering, with a possible increase in the sensitivity of the thermoregulatory system as shown by the shorter time to onset of continuous shivering (d): 8.66 (SEM 1.33) min versus 28.20 (SEM 1.33) min (P < 0.001) and by a higher Tsk observed at d: 27.60 (SEM 1.40) degrees C versus 21.40 (SEM 0.60) degrees C (P < 0.001). These results were associated with higher cold sensations and shivering following SD. They also suggested that SD modified thermoregulatory responses at a central level especially in a cold environment.

Adult↗