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PubMed1997

Cardiopulmonary interactions following REM sleep deprivation in Sprague-Dawley rats.

We characterized the effects of 48 h of rapid-eye-movement (REM) sleep deprivation on cardiovascular and respiratory variables and on sleep-related cardiopulmonary interactions in adult male Sprague-Dawley rats. Rats were instrumented for monitoring EEG, EMG, and aortic blood pressure. Respiratory rate and minute ventilation were measured by unrestrained single-chamber plethysmography. By using radiotelemetry to monitor blood pressure we clearly demonstrated progressive decreases in mean blood pressure with transitions from wakefulness to non-rapid-eye-movement and REM sleep which were unaffected by REM sleep deprivation. Mirror-image state-dependent increases in heart period suggest that baroreflexes were augmented during sleep with respect to wakefulness. REM sleep deprivation was also associated with lower blood pressure and longer heart period over all sleep/wake states, although this achieved statistical significance only during REM sleep and only during the first hour of recovery sleep. These cardiovascular changes coupled with the observed decreases in respiratory rate and minute ventilation suggest a further augmentation of baroreflexes following REM sleep deprivation.

Animals↗

PubMed1993

Effect of rapid eye movement sleep deprivation on rat brain monoamine oxidases.

Monoamine oxidase, monoamine oxidase-A, and monoamine oxidase-B activities were compared in free moving, rapid eye movement sleep-deprived, recovered, and control rat brains. The activities were estimated in the whole brain, cerebrum, cerebellum, whole brainstem, medulla, pons, and midbrain. The flowerpot method was used for continuing deprivation for one, two, or four days. Monoamine oxidase activity decreased significantly in the cerebrum and the cerebellum of the sleep-deprived rats, whereas monoamine oxidase-A and monoamine oxidase-B were differentially affected. Medullary MAO-A was the first to be affected, showing an increase after just one day of rapid eye movement sleep deprivation, while longer deprivation decreased its activity. The activity of monoamine oxidase-B was not significantly affected in any brain areas of the deprived rats until after two days of rapid eye movement sleep deprivation. All the altered enzyme activities returned to control levels after recovery. Control experiments suggest that the decrease was primarily caused by the rapid eye movement sleep deprivation and was not due to nonspecific effects. These findings are consistent with past studies and may help to explain earlier observations. The results support the involvement of aminergic mechanisms in rapid eye movement sleep. The plausible reasons for the changes in the activities of monoamine oxidases, after rapid eye movement sleep deprivation, are discussed.

Animals↗

PubMed1994

Increased limbic blood flow and total sleep deprivation in major depression with melancholia.

Single photon emission computed tomography (SPECT) with technetium-99m-d,l-hexamethyl-propylene amine oxime (99Tcm-HMPAO) was carried out in 20 melancholic patients before and after total sleep deprivation. Findings in 11 responders to total sleep deprivation (defined by > or = 40% improvement on the Hamilton Rating Scale for Depression) were compared with findings in nine nonresponders. On the basis of a semiquantitative evaluation of SPECT findings, responders showed relative hyperperfusion before sleep deprivation in the right anterior cingulate cortex and in the right and left fronto-orbital cortex and basal cingulate gyrus. Responders who showed > or = 50% improvement also showed hippocampal overactivation before sleep deprivation. It is possible that limbic overactivation may characterize depressed responders to total sleep deprivation as a distinct subtype. Another possibility is that the pattern of limbic hyperactivation reflects the increased number of bipolar patients in the responder group, with response to total sleep deprivation being only a covariate of this bipolar-unipolar distinction.

Adult↗

PubMed1996

Partial night sleep deprivation reduces natural killer and cellular immune responses in humans.

Prolonged and severe sleep deprivation is associated with alterations of natural and cellular immune function. To determine whether alterations of immune function also occur after even a modest loss of sleep, the effects of early-night partial sleep deprivation on circulating numbers of white blood cells, natural killer (NK) cell number and cytotoxicity, lymphokine-activated killer (LAK) cell number and activity, and stimulated interleukin-2 (IL-2) production were studied in 42 medically and psychiatrically healthy male volunteers. After a night of sleep deprivation between 10 P.M. and 3 A.M., a reduction of natural immune responses as measured by NK cell activity, NK activity per number of NK cells, LAK activity, and LAK activity per number of LAK precursors (CD16,56, CD25) was found. In addition, concanavalin A-stimulated IL-2 production was suppressed after sleep deprivation due to changes in both adherent and nonadherent cell populations. After a night of recovery sleep, NK activity returned to baseline levels and IL-2 production remained suppressed. These data implicate sleep in the modulation of immunity and demonstrate that even a modest disturbance of sleep produces a reduction of natural immune responses and T cell cytokine production.

Cell Adhesion↗

PubMed1992

Study of EEGs following 24-hour sleep deprivation in patients with posttraumatic epilepsy.

Routine and awake EEGs following 24-hour sleep deprivation were studied in 119 patients with closed head injury, 64 epileptics without any history of head injury and 53 healthy controls. The results were compared to CT brain scan findings. There were no epileptic discharges in routine EEGs, while EEGs after 24-hour sleep deprivation showed considerable activation, ranging from 28 to 37.5% in those with a history of head injury or epilepsy. No correlation was found between the period elapsed between the time of injury and the activation of the EEG. Most of the patients with EEG activation after sleep deprivation had abnormal CT scans. EEGs following 24-hour sleep deprivation therefore appear to be a useful adjunct to other methods used in detecting brain damage in patients with head injury or epilepsy.

Cerebral Cortex↗

PubMed1989

Sleep deprivation in the rat: X. Integration and discussion of the findings.

The results of a series of studies on total and selective sleep deprivation in the rat are integrated and discussed. These studies showed that total sleep deprivation, paradoxical sleep deprivation, and disruption and/or deprivation of non-rapid eye movement (NREM) sleep produced a reliable syndrome that included death, debilitated appearance, skin lesions, increased food intake, weight loss, increased energy expenditure, decreased body temperature during the late stages of deprivation, increased plasma norepinephrine, and decreased plasma thyroxine. The significance of this syndrome for the function of sleep is not entirely clear, but several changes suggested that sleep may be necessary for effective thermoregulation.

Animals↗

PubMedDate not supplied

Enzyme activity in sleep and sleep deprivation.

Liver tyrosine transaminase activity is low during the day when the rats are mostly asleep and high during the night when they are awake. When wakefulness was imposed for 8 hr during daylight on the day of the experiment and the rats were allowed to sleep for the following 3 hr during darkness, the tyrosine transaminase activity became high during the day and low at night. That this reversal in enzyme activity is not mediated by the pituitary-adrenal axis is demonstrated by the fact that in adrenalectomized rats tyrosine transaminase activity increased during the day in the sleep deprived rats. However, in these rats the enzyme activity did not become low in the sleep-deprived-sleeping condition. Changes in tryptophan pyrrolase activity during sleep deprivation were demonstrated to be mediated by the pituitary-adrenal axis.

Adrenal Glands↗

PubMed2000

The impact of sleep deprivation on decision making: a review.

Few sleep deprivation (SD) studies involve realism or high-level decision making, factors relevant to managers, military commanders, and so forth, who are undergoing prolonged work during crises. Instead, research has favored simple tasks sensitive to SD mostly because of their dull monotony. In contrast, complex rule-based, convergent, and logical tasks are unaffected by short-term SD, seemingly because of heightened participant interest and compensatory effort. However, recent findings show that despite this effort, SD still impairs decision making involving the unexpected, innovation, revising plans, competing distraction, and effective communication. Decision-making models developed outside SD provide useful perspectives on these latter effects, as does a neuropsychological explanation of sleep function. SD presents particular difficulties for sleep-deprived decision makers who require these latter skills during emergency situations.

Decision Making↗

PubMed1984

Delta sleep-inducing peptide-like material in rat brain as determined by enzyme immunoassay: effect of sleep deprivation.

The regional distribution of immunoreactive delta sleep-inducing peptide (IR-DSIP) and the effect of 24-h sleep deprivation on the IR-DSIP content was investigated in the rat brain by means of enzyme immunoassay (EIA) of the assayable IR-DSIP in the rat brain coeluted with authentic DSIP in the gel filtration. It is thus suggested that the present EIA method preferentially detects fee DSIP and not bound DSIP. IR-DSIP proved to be more concentrated in the limbic structures, although the contents were generally at a low level. Sleep deprivation and subsequent rebound sleep had no significant effect on the brain contents of 'free-form' DSIP.

Animals↗

PubMed2004

Simple instructions for partial sleep deprivation prior to pediatric EEG reduces the need for sedation.

OBJECTIVE: To study the effects of providing simple instructions for partial sleep deprivation on the necessity for sedation in children and adolescents undergoing electroencephalography (EEG). METHODS: Children and adolescents below 18 years undergoing non-urgent routine EEG were studied for the need for sedation during the EEG test. Two consecutive 3-year periods were reviewed. During the first 3 years no instructions for sleep deprivation were given, and during the second 3-year period, simple instructions were given to the patient or parents of young children to have less sleep prior to the EEG test. This was achieved by using the same sleep deprivation schedule irrespective of the age of the patient. RESULTS: In the first 3-year period between January 1996 and December 1998, 785 non-urgent routine EEG recordings were performed in which only 146 (19%) pediatric patients managed to fall asleep without the need for any sedation within 30 min of being ready for the sleep recording. When partial sleep deprivation was implemented in the 3-year period between January 2000 and December 2002, 449 (55%) out of 821 patients undergoing the test fell asleep in the laboratory without sedation, an overall increase of 36%. Analyzing the different age-specific groups, the maximal increase in the success for natural sleep following partial sleep deprivation was 44% for pediatric patients aged above 10 years. CONCLUSIONS: Simple instructions for partial sleep deprivation prior to the EEG reduced the need for sedation in children and adolescents undergoing the test.

Adolescent↗

PubMed2004

REM sleep deprivation induces changes in coping responses that are not reversed by amphetamine.

STUDY OBJECTIVE: Although sleep deprivation often occurs during stressful or threatening situations, the effects of sleep loss on defensive and coping behaviors are not well known. The purpose of the present study was to measure the effects of selective rapid eye movement (REM) sleep deprivation (RSD) on responses elicited by threatening situations and to assess the extent to which RSD-induced changes are reversed by amphetamine. DESIGN: Animals were divided into 3 groups; home-cage control, apparatus control, and REM sleep-deprived groups. The flowerpot method was used to produce RSD for up to 5 days. One set of rats was tested in the elevated plus maze, open field, shock-induced freezing, and analgesia tests. A second set of rats was evaluated for locomotor activity. A third set of animals was assessed in the defensive burying test. For the amphetamine studies, groups of home-cage control and REM sleep-deprived rats received an intraperitoneal injection of amphetamine prior to administration of the shock-induced freezing test or the defensive burying test. SETTING: Sleep Research Laboratory at UW-Madison. PARTICIPANTS AND INTERVENTIONS: 186 male Long-Evans rats approximately 3 months old. MEASUREMENTS AND RESULTS: RSD increased the proportion of time spent in open arms of the elevated plus maze and center of the open field, decreased freezing time, and reduced defensive burying. Amphetamine did not reverse RSD-induced changes in freezing or burying responses. CONCLUSIONS: RSD causes widespread abnormalities in coping and defensive responses in threatening situations; these deficits are not reversed and, in some cases, may be exacerbated by amphetamine.

Adaptation, Psychological↗

PubMed2002

Circadian clock resetting by sleep deprivation without exercise in Syrian hamsters: dark pulses revisited.

Circadian rhythms in Syrian hamsters can be phase shifted by procedures that stimulate wheel running ("exercise") in the mid-subjective day (the hamster's usual sleep period). The authors recently demonstrated that keeping hamsters awake by gentle handling, without continuous running, is sufficient to mimic this effect. Here, the authors assessed whether wakefulness, independent of wheel running, also mediates phase shifts to dark pulses during the midsubjective day in hamsters free-running in constant light (LL). With running wheels locked during a 3 h dark pulse on day 3 of LL, hamsters (N = 16) averaged only 43+/-15 min of spontaneous wake time and phase shifted only 24+/-43 min. When wheels were open during a dark pulse, two hamsters remained awake, ran continuously, and showed phase advance shifts of 7.3 h and 8.7 h, respectively, whereas the other hamsters were awake <60 min and shifted only 45+/-38 min. No animals stayed awake for 3 h without running. Additional time in LL (10 and 20 days) did not potentiate the waking or phase shift response to dark pulses. When all hamsters were sleep deprived with wheels locked during a dark pulse, phase advance shifts averaged 261+/-110 min and ranged up to 7.3 h. These shifts are large compared to those previously observed in response to the 3 h sleep deprivation procedure. Additional tests revealed that this potentiated shift response is dependent on LL prior to sleep deprivation but not LL after sleep deprivation. A final sleep deprivation test showed that a small part of the potentiation may be due to suppression of spontaneous wheel running by LL. These results indicate that some correlate of waking, other than continuous running, mediates the phase-shifting effect of dark pulses in the mid-subjective day. The mechanism by which LL potentiates shifting remains to be determined. The lack of effect of subsequent LL on the magnitude of shifts to sleep deprivation in the dark suggests that LL reduces responsivity to light by processes that take >3 h of dark to reverse.

Animals↗

PubMed1990

Sleep deprivation in bright and dim light: antidepressant effects on major depressive disorder.

Twenty-three patients with a major depressive disorder were deprived of a night's sleep twice weekly, one week staying up in the dimly lit living room of the ward (less than 60 lux), and one week in a brightly lit room (greater than 2000 lux). Immediate, but transient beneficial effects of sleep deprivation were observed primarily in eight patients (the 'responders'). The immediate effects did not differ greatly for the two conditions, indicating that exposure to light at night is an implausible explanation for the antidepressant effects of total sleep deprivation. There was some evidence that the bright light condition led to a more prolonged improvement of the responders.

Combined Modality Therapy↗

PubMed1995

Possible mechanism of rapid eye movement sleep deprivation induced increase in Na-K ATPase activity.

Rapid eye movement sleep deprivation increases Na-K ATPase activity and decreases aminergic neuronal firing rate as well as norepinephrine degrading enzyme, monoamine oxidase, activity. On the other hand, norepinephrine is known to increase Na-K ATPase activity. Hence, this study was conducted to find if the deprivation induced increase in Na-K ATPase activity is mediated by norepinephrine. Rapid eye movement sleep deprived rats were injected with either alpha-1 or beta adrenoceptor antagonist or alpha-2 adrenoceptor agonist and after 8 h the Na-K ATPase activity of the brain was estimated. In an attempt to simulate in vivo conditions, norepinephrine was added to an in vitro brain homogenate preparation in the presence or absence of alpha or beta adrenoceptor blockers and the enzyme activity was estimated. The results showed that the enzyme activity was decreased by alpha-1 antagonist as well as by alpha-2 agonist treatment in in vivo preparations. Norepinephrine increased enzyme activity in the in vitro preparation and the increase was prevented by the alpha-1 antagonist. The results of this study suggest that rapid eye movement sleep deprivation induced increase in Na-K ATPase activity may be mediated by norepinephrine acting on either alpha-1 and/or alpha-2 receptors.

Adrenergic Agonists↗

PubMed1998

Effects of tryptophan depletion in drug-free depressed patients who responded to total sleep deprivation.

BACKGROUND: There is some evidence that sleep deprivation (SD) might exert its antidepressant properties by involving serotonergic mechanisms. We investigated the effects of short-term tryptophan depletion (TD) on depressed patients who responded to a single night of total SD. METHODS: Drug-free depressed inpatients (n = 30) were randomly assigned to either TD or sham depletion. Tryptophan depletion was induced by a 24-hour low-tryptophan diet (day 1) followed the next morning by ingestion of a tryptophan-free amino acid mixture (day 2). During sham depletion, the diet and the amino acid beverage were supplemented with tryptophan. Sleep deprivation was performed from day 1 until day 2. Only SD responders received the amino acid beverage the morning after SD. Behavioral ratings and total and free plasma tryptophan levels were obtained before and after the test sessions. RESULTS: Twenty-two of 30 patients showed a favorable outcome after SD. As predicted, TD significantly lowered total and free plasma tryptophan levels, whereas both levels increased during sham depletion. No acute effects on mood were observed during the day after SD in either treatment group. Unexpectedly, TD, but not control testing, prevented the depressive relapse after the recovery night in most of the patients. CONCLUSIONS: Tryptophan depletion did not reverse the antidepressant effects of SD, but it prevented the relapse beyond a night of recovery sleep. These findings suggest that SD does not act via a single monoamine-related mechanism, but they allow the assumption that TD may induce neurochemical alterations that transiently improve depression.

Adult↗

PubMed2002

Sleep deprivation in the rat: X. Integration and discussion of the findings. 1989.

Animals↗

PubMedDate not supplied

Sleep apnea in normal and REM sleep-deprived normotensive Wistar-Kyoto and spontaneously hypertensive (SHR) rats.

The effects of hypertension and REM sleep deprivation on spontaneous and postsigh apneas have been studied in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats by simultaneously monitoring their respiration and sleep by the EEG. The amount of REM and non-REM sleep in SHR rats was identical to WKY rats under control as well as REM sleep-deprived recording conditions. Hypertension was associated with an increase in postsigh apneas, as was evident by the increased postsigh apnea index in non-REM and total sleep in SHR rats when compared to normotensive WKY rats. In contrast, REM sleep deprivation suppressed the postsigh apnea expression both in non-REM and total sleep in SHR rats. The incidence of spontaneous apneas was increased by a combination of hypertension and REM sleep deprivation, as was shown in REM-deprived SHR rats, while each of these conditions alone had no effect on spontaneous apneas. These results suggest a role for hypertension in the postsigh apnea genesis and the existence of partially distinct mechanisms for the two types of apneas.

Animals↗

PubMed2005

Increased prefrontal event-related current density after sleep deprivation.

To investigate how partial sleep loss affects temporal and spatial pattern of information flow, we analyzed sources of brain electrical activity during continuous attention test. Sixteen physicians recruited from the university hospitals participated in the study. Each participant served as his own control. All participants underwent two test sessions including the Stanford Sleepiness Scale (SSS), the Beck Depression Inventory (BDI), the Selective Reminding Test (SRT), and the Continuous Attention Test (CAT). The CAT items were used as stimuli in event-related potential (ERP) recordings. EEG was recorded from 21 electrodes, according to the international 10-20 system. The sources of bioelectrical activity were computed with low resolution electromagnetic tomography (LORETA). Estimated sleep time was significantly shorter on nights spent on duty than on nights of normal sleep at home. Sleep loss resulted in significant increase in SSS and BDI scoring, and impairment of immediate recall. Performance on the CAT remained relatively intact. Under the sleep loss condition compared to baseline, significant differences in brain activity occurred only for targets. Within the P1 time frame, sleep loss led to greater activation in the right Brodmann's area 9/10. For the N1 component, significant differences were localized on the lateral surface of the right frontal lobe, in Brodmann's areas 8 and 9. No significant effects of sleep deprivation on the P3 component were found. Our results are consistent with earlier data indicating that increased activation of the prefrontal cortex allows the maintainance of performance during periods of sleep loss.

Adult↗