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At least 793 records · Page 44Linked to original sources
PubMed1983

Neither REM sleep deprivation nor rebound influences 3H-diazepam binding n rat brain.

Rats were placed on either small (subjected to REM sleep deprivation) or large circular platforms (stress controls) surrounded by water for 96 hours. Six animals from each group were either decapitated immediately following 96 hours or placed in cages and decapitated 6 hours later. Benzodiazepine receptor binding in rat brain cortices and brain stems was assessed using 3H-diazepam as the ligand. Scatchard analysis of these data showed that neither REM sleep deprivation nor REM sleep rebound affected the kinetics of 3H-diazepam binding (Bmax or apparent KD) in vitro.

Animals↗
PubMed1978

Electrophysiological changes induced by paradoxical sleep deprivation and lithium chloride poisoning in rats.

In an attempt to analyze the disruption of conditioned taste aversion (CTA) caused by pre-acquisition paradoxical sleep deprivation (PSD), the effect of poisoning (0.15 M LiCl, 4% body weight) on the sleep--wakefulness pattern was studied in 12 rats with chronically implanted electrodes. The polygraphic recording showed that poisoning reduced the total sleep time in the subsequent 3 h from 57 to 42% and REM sleep from 6 to 2%. The lithium chloride effect was still more pronounced after 24-h REM sleep deprivation: the total sleep time decreased from 67 to 46% and REM sleep from 13 to 2%. The change of sleep--wakefulness pattern, most pronounced during the first hour of poisoning, gradually returned to normal but REM sleep was significantly reduced even 3 h after poisoning. It is concluded that 24-h PSD does not alleviate the subsequent poisoning. On the other hand, the lithium chloride induced reduction of post-acquisition REM sleep many enhance the learning impairment caused by pre-acquisition PSD.

Activity Cycles↗
PubMed2007

Effects of caffeine on electrophysiological and neuropsychological indices after sleep deprivation.

Caffeine is regarded as a central nervous system (CNS) stimulant. The goal of this study was to analyze electrophysiological, motor, cognitive and behavioral changes produced by caffeine ingestion after sleep deprivation. Ten subjects were evaluated after sleep deprivation, comparing the ingestion of either 400 mg of caffeine or placebo, in a double-blind randomized study. The variables analyzed were: quantitative EEG, the event-related potential (ERP-P300) and cognitive responses. The most significant quantitative EEG results, which were characterized by moment x treatment interactions, were seen in alpha and theta relative power variables. A significant decrease in relative alpha and theta was observed in the caffeine group after sleep deprivation. In relation to caffeine stimulant effects, there were no significant differences in the other parameters.

Adult↗
PubMed1983

Physiological correlates of prolonged sleep deprivation in rats.

The issue of whether sleep is physiologically necessary has been unresolved because experiments that reported deleterious effects of sleep deprivation did not control for the stimuli used to prevent sleep. In this experiment, however, experimental and control rats received the same relatively mild physical stimuli, but stimulus presentations were timed to reduce sleep severely in experimental rats but not in controls. Experimental rats suffered severe pathology and death; control rats did not.

Adrenal Glands↗
PubMed1981

The effects of sleep deprivation on average evoked responses in depressed patients and in normals.

The effects of a single night of sleep deprivation on the amplitude and amplitude/stimulus intensity function of the visual evoked potential (EP) were studied in 16 patients with primary affective disorder and 20 normal controls. Visual EP amplitude and amplitude/intensity slopes tended to increase after sleep deprivation in the patient group, a direction found in other studies to be associated with a spontaneous mood improvement and changes with antidepressant medication. In contrast, normal volunteers who showed little or no mood elevation showed generally opposite EP effects. Taken together, the results suggest a similarity in the neurophysiological effect of sleep deprivation between patient and antidepressant medication in depressed patients.

Adolescent↗
PubMed2005

Partial sleep deprivation compromises gastric mucosal integrity in rats.

The gastric mucosa is most susceptible to stress that has been shown to induce mucosal damage in humans and animals. This study aims to explore the underlying mechanisms of partial sleep deprivation, as a source of psychophysiological stress, on gastric functions and its effect on mucosal integrity. Sprague-Dawley rats were partially sleep deprived (PSD) for 7 or 14 days by housing inside slowly rotating drums. Gastric tissues and plasma were sampled at the end of the sleep deprivation periods and mucosal lesion scores were evaluated. Morphological examination was performed after Hematoxylin and Eosin staining. Plasma levels of noradrenaline, adrenaline, gastrin, histamine and somatostatin were determined with enzyme immunoassays. Gastric acidity was measured with acid-base titration in pylorus ligated rats. Gastric mucosal blood flow was evaluated with Laser Doppler Flowmetry. It was found that gastric lesions were induced in about 30%-50% of the PSD rats. Gastric acidity as well as plasma levels of noradrenaline, gastrin and histamine were elevated. Gastric mucosal blood flow and plasma somatostatin level were on the contrary reduced, especially in rats with PSD for 14 days. It is concluded that partial sleep deprivation compromises gastric mucosal integrity by increasing gastric acidity, plasma levels of noradrenaline, gastrin, histamine, and decreasing gastric mucosal blood flow. These results provided experimental evidence on the gastric damaging effects of PSD and it could be one of the risk factors contributing to gastric ulcer formation.

Animals↗
PubMed1998

Repeated sleep deprivation once versus twice a week in combination with amitriptyline.

OBJECTIVE: Although a combination of antidepressive pharmacotherapy with repeated sleep deprivation therapy has proved to be an effective and easily applied treatment strategy, no systematic study investigating the most favourable interval between the sleep deprivation trials is available. METHOD: In a cross-over design, 44 patients with a major depressive episode (ICD-10) were randomly allocated to 4 weeks treatment with amitriptyline (150 mg/d) in combination with either late sleep deprivation (of the second half of the night, LSD) twice weekly during week 1 and 2 followed by LSDs once weekly during week 3 and 4 or vice versa. Two hypotheses were tested: Does LSD twice weekly during week 1 and 2 accelerate the clinical response compared with LSD once weekly? Does LSD twice weekly during week 3 and 4 improve the response rate compared with LSD once weekly? RESULTS: According to both observer rating (Hamilton Rating for Depression, 21-item version) and self-rating (Visual Analogue Mood Scale), no significant differences could be ascertained between the groups compared at any time of the investigation. With respect to drop-outs and immediate LSD effects there is a trend for patients undergoing twice weekly LSDs followed by once weekly LSD trials to have a more favourable treatment course than the control group. CONCLUSION: The hypotheses tested were answered in the negative. "High dose" LSD administration does not prove to be clearly superior to "low dose" LSD. This finding is in line with most of the corresponding data on antidepressive pharmacotherapy.

Adult↗
PubMed1977

[The value of EEG after sleep deprivation (author's transl)].

Seventy seven adult epileptics and 30 patients with clinically non epileptic seizures were subject to a 24 hours sleep deprivation. The waking records of these patients were normal or unspecific abnormal. After sleep deprivation 29 (37%) of epileptics had abnormal EEG with epileptiform or focal activity, more often in cases with frequent (26 (60%) patients out of 43) epileptic seizures. Patients with sporadic attacks only exceptionally showed specific EEG changes (3 patients (8,8%) out of 34). Drug induced sleep emerged to be diagnostically less helpful. Twenty nine out of 30 patients with clinical nonepileptic seizures had no additional abnormalities in the EEG after sleep deprivation.

Adolescent↗
PubMedDate not supplied

Circadian rhythms of water and alcohol intake: effect of REM-sleep deprivation and lesion of the suprachiasmatic nucleus.

The recently discovered increase in alcohol drinking produced by a 7 day period of rapid eye movement (REM)-sleep deprivation with a modified flowerpot technique and the subsequent decrease during REM-rebound were now examined through continual monitoring of drinking with a computer attached to drinkometers. REM-sleep deprivation abolished the circadian rhythms of both alcohol and water intake. The circadian rhythm of water drinking returned during the first post-deprivation day but alcohol drinking was almost eliminated during the first 18 hr and there was no circadian rhythm to the alcohol drinking on the following 3 days. In an additional study, the circadian rhythms of both water and alcohol intake were abolished by electrolytic lesioning of the suprachiasmatic nuclei. The lesion did not, however, alter the mean level of alcohol drinking. Thus the abolition of circadian rhythms is not sufficient for increasing alcohol consumption and the increase produced during REM-sleep deprivation appears to be mediated by other mechanisms.

Alcohol Drinking↗
PubMed1998

Clinical utility of sleep-deprived versus computer-assisted ambulatory 16-channel EEG in epilepsy patients: a multi-center study.

PURPOSE: The objective of this prospective study was to compare the usefulness of a sleep-deprived electroencephalogram (EEG) versus a computer-assisted 16-channel ambulatory EEG in patients with historical information consistent with epilepsy but with a normal or non-diagnostic initial routine EEG. METHODS: A total of 46 patients had both a 30-60 min sleep-deprived EEG and a computer-assisted ambulatory 24 h EEG. Each EEG was assigned a number and reviewed independently by two board-certified electroencephalographers for the presence of interictal epileptiform discharges and seizures. RESULTS: Both the sleep-deprived EEG and ambulatory EEG improved detection of epileptiform discharges by a similar amount (24% versus 33%); however, the ambulatory EEG detected seizures in 7/46 (15%) patients, and in three patients the seizures were solely detected by the computer. CONCLUSIONS: we conclude that the computer-assisted ambulatory EEG offers greater benefit than a sleep-deprived recording because in addition to detecting interictal epileptiform discharges, it may also capture seizures. The discovery of unsuspected seizures can significantly impact clinical management.

Ambulatory Care↗
PubMed1978

The influence of sleep deprivation on the duration of endogenous depressive episodes.

Out of 102 patients suffering from endogenous depression, it was possible to ascertain the duration of episodes in the case of 60 patients. Intraindividual comparisons among patients with unipolar depression show that sleep deprivation therapy causes a tendency to shorter depressive episodes. This tendency is related to the time of application of sleep deprivation: the sooner sleep deprivation is applied within an episode, the better the effect. Younger patients react better than older ones.

Depression↗
PubMed1994

Aerobic and anaerobic contributions to exhaustive high-intensity exercise after sleep deprivation.

The purpose of this study was to determine the effect of one night's sleep loss on the performance of high-intensity exercise and on the contribution of anaerobic and aerobic energy systems to the exercise. Seven males and seven females performed an all-out cycling exercise test during baseline testing and then on three consecutive days after a sleepless night. The work rates were 5.0 W kg-1 for the females and 6.0 W kg-1 for the males. The aerobic contribution was determined based on measured VO2 and the anaerobic contribution was determined by subtraction of the aerobic contribution from the total amount of work performed. The results of baseline tests and of tests performed following sleep loss were compared for evidence of an effect of sleep deprivation. The 25-30 h of sleep deprivation did not affect total work, the anaerobic contribution or the aerobic contribution (all P > 0.1), although there was a tendency (P = 0.13) for mean VO2 to decrease after the sleepless night. There were no interaction effects involving sex on total work, the anaerobic contribution or the aerobic contribution (all P > 0.1). The mean (+/- S.E.M.) values for total work (kJ) performed were: baseline, 21.9 +/- 2.7; after sleep loss, 21.1 +/- 2.5 (day 1), 21.7 +/- 2.5 (day 2), and 21.9 +/- 2.7 (day 3). It is concluded that, in both males and females, there are no changes in the contributions of the aerobic and anaerobic energy systems to high-intensity exercise performed following the loss of one night's sleep.

Adult↗
PubMed1982

Phencyclidine produces aggressive behavior in rapid eye movement sleep-deprived rats.

This study examined effects of acute doses of phencyclidine (PCP; 0.025, 0.05, 0.10, and 0.20 mg/kg intraperitoneally) on intra-specific aggressive behavior and muricide in normal rats and rats deprived of rapid eye movement (REM) sleep. Dose-related changes in intra-specific aggression and muricide occurred in REM sleep-deprived rats only. Dose-response curves are inverted-U shaped with the .05 mg/kg dose producing increases in aggression. Intra-specific aggression and muricide may serve as models of PCP-induced aggression in humans.

Aggression↗
PubMed2001

Patterns of response to repeated total sleep deprivations in depression.

BACKGROUND: Patterns of response and nonresponse in repeated sleep deprivation (SD) are of both clinical and scientific interest; as yet, studies have yielded inconsistent results. METHODS: Eighteen inpatients suffering from a major depression were subjected to a series of six scheduled total sleep deprivations within 3 weeks; 12 of them completed the whole protocol. All were under a constant antidepressant medication with amitriptyline. SD effects were measured using observer and self rating scales. RESULTS: Each single SD led to a significant improvement. Of the 12 patients who completed the protocol, seven were classified as responders at endpoint (i.e., 1 week after the sixth TSD). The majority of patients exhibited a pattern of responses and nonresponses randomly distributed over time. There was no temporal trend. The initial effect did not predict the average response to the following SDs. LIMITATIONS: One third of patients dropped out before completing the protocol which limits the scope of the study. CONCLUSIONS: Response to a single SD is not generalizable on a series of following SDs in an individual. The mechanism of action of SD does probably not involve mechanisms subjected to habituation or sensitization.

Amitriptyline↗
PubMed1996

Effects of a selective sleep deprivation on subsequent anaerobic performance.

The aim of the study was to investigate the effects of a partial sleep deprivation on a subsequent supramaximal exercise evaluated from the 30 second Wingate test, and on the following recovery. To take into account the active muscle mass, the Wingate test was performed against a constant braking force related to the data of a force-velocity test conducted on a Monark cycle ergometer (Model 814 E with weights) one week before the experimental test. Eight highly trained athletes were enrolled for this study. The changes in ventilatory and metabolic responses were analyzed during and upon completion of physical 30 second exercise, taking place after two nights, in other words, after a reference night and after a night with reduced sleep. Partial sleep deprivation was obtained by delaying bedtime until 3 a.m. The 30 second Wingate test was performed between 9 a.m. and noon the following days, using a Monark ergometer (Model 814 F). The analyses of change scores disclosed that there were no main significant effects for measures of ventilation, lactates and pH(v) levels under the two experimental conditions. The peak power, the mean power output and the peak velocity recorded after partial sleep deprivation were not modified in comparison with the values obtained after the reference night. These findings suggest that acute sleep loss did not contribute to alterations in supramaximal exercise.

Adolescent↗
PubMed2005

REM sleep deprivation affects extinction of cued but not contextual fear conditioning.

Previous research has demonstrated that rapid eye movement (REM), or paradoxical, sleep deprivation can interfere with the retention of certain types of learning tasks, particularly spatial learning. The present study investigated the effects of 6 h of REM sleep deprivation on the retention and extinction of both cued and contextual conditioning tasks in rats. Sleep-deprived animals showed normal retention of both types of conditioning tasks but retarded extinction of the cued task and a trend toward attenuated spontaneous recovery of the contextual task. The results provide further evidence for the involvement of REM sleep in learning and memory processes.

Acoustic Stimulation↗
PubMed1995

Sleep, sleep deprivation and infectious disease: studies in animals.

Common perceptions that the desire for sleep is increased during mild infectious diseases like colds and 'the flu' have fostered beliefs that sleep promotes recovery from infectious disease and that lack of sleep increases susceptibility to infections. However, until recently, the relationship between infectious disease and vigilance received relatively little systematic study. At present, several model systems provide evidence that infectious disease is accompanied by alterations in sleep. Indeed, increased sleepiness, like fever and anorexia, may be viewed as a facet of the acute phase response to infectious challenge. Recent studies also suggest that sleep, sleep deprivation and infectious disease may be related via mechanisms of the immune system (Fig. 1). Data are now accumulating to address questions such as whether immune processes alter sleep, whether sleep or sleep deprivation influences immune competence, and whether sleep facilitates recovery from infectious disease.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed2003

Effect of rapid eye movement sleep deprivation on allergen-induced airway responses in a rat model of asthma.

BACKGROUND: Nocturnal airway narrowing is a common characteristic of asthma that remains poorly understood. Sleep itself or rapid eye movement (REM) sleep has been suspected to play a role in the etiology of nocturnal asthma; however, only inconsistent findings have so far been produced. The purpose of this study was to examine the effect of sleep deprivation, particularly REM sleep, using the classical platform (flowerpot) method on asthmatic responses in a rat model of asthma, in a situation of immobilization stress. METHODS: After the rats had been randomly divided into three groups of 9 including (1) a caged control group, (2) a large (sham) platform group, and (3) a small platform group, we investigated the effect of REM sleep deprivation over a 72-hour period on both the antigen-induced immediate asthmatic response (IAR) and late asthmatic response (LAR) including the changes of stress hormones. RESULTS: The small platform group showed significantly lower plasma histamine levels and higher plasma adrenaline levels during the IAR compared to the control group (p < 0.05). The number of eosinophils in either the bronchoalveolar lavage fluid or the bronchial lamina propria during the LAR in the small platform group was reliably suppressed compared to the other groups (p < 0.05). No significant differences were found in the plasma corticosterone and noradrenaline levels among the three groups, irrespective of the phase of the asthmatic response. CONCLUSIONS: Our results indicate that REM sleep contributes to nocturnal asthma, possibly due to an alteration of the sympathetic nervous function.

Allergens↗