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At least 865 records · Page 48Linked to original sources
PubMed2003

Sleep deprivation inhibits expression of NADPH-d and NOS while activating microglia and astroglia in the rat hippocampus.

This study investigated the expression of nitric oxide (NO)-synthesizing enzymes and the glial reaction in the rat hippocampal formation following sleep deprivation for 5 days. Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) reactivity was markedly reduced in the hippocampal CA1, CA2 and CA3 sectors as well as in the dentate gyrus, suggesting a suppression of NO production in these areas. Microglial cells were hypertrophic and showed an up-regulation of complement type 3 receptors as determined by antibody OX-42. However, expression of major histocompatibility complex class I and II antigens, and antigen of monocyte/macrophage lineage marked by OX-18, OX-6 and ED1, respectively, was undetected. Astrocytes also displayed hypertrophied processes with enhanced glial fibrillary acidic protein (GFAP) immunoreactivity. Western blots of hippocampal tissues corroborated the above-mentioned morphological findings in that expression of NO-synthase (NOS) was decreased while that of OX-42 and GFAP was increased in the sleep-deprived rats. Since NO is thought to be involved in memory consolidation processes in the hippocampus during sleep, the inhibition of NADPH-d and NOS reactivities may account for the memory decline after long-term sleep deprivation. The concomitant reactions in microglia and astrocytes suggest the involvement of these cells in the deleterious effect of prolonged sleep deprivation.

Animals↗
PubMed2004

Activation of c-fos in GABAergic neurones in the preoptic area during sleep and in response to sleep deprivation.

Neurones in the median preoptic nucleus (MnPN) and the ventrolateral preoptic area (vlPOA) express immunoreactivity for c-Fos protein following sustained sleep, and display elevated discharge rates during both non-REM and REM sleep compared to waking. We evaluated the hypothesis that MnPN and vlPOA sleep-active neurones are GABAergic by combining staining for c-Fos protein with staining for glutamic acid decarboxylase (GAD). In a group of six rats exhibiting spontaneous total sleep times averaging 82.2 +/- 5.1% of the 2 h immediately prior to death, >75% of MnPN neurones that were Fos-immunoreactive (IR) were also GAD-IR. Similar results were obtained in the vlPOA. In a group of 11 rats exhibiting spontaneous sleep times ranging from 20 to 92%, the number of Fos + GAD-IR neurones in MnPN and vlPOA was positively correlated with total sleep time. Compared to control animals, Fos + GAD-IR cell counts in the MnPN were significantly elevated in rats that were sleep deprived for 24 h and permitted 2 h of recovery sleep. These findings demonstrate that a majority of MnPN and vlPOA neurones that express Fos-IR during sustained spontaneous sleep are GABAergic. They also demonstrate that sleep deprivation is associated with increased activation of GABAergic neurones in the MnPN and vlPOA.

Animals↗
PubMed2001

Nap polygraphic recordings after partial sleep deprivation in patients with suspected epileptic seizures.

A review of the literature shows that nap recordings make a significant contribution to epilepsy studies, providing evidence of specific EEG findings in patients suspected of having epilepsy. In addition, sleep deprivation can cause paroxysmal EEG activity and clinical seizures. We studied retrospectively 686 patients, 51.8% males and 48.2% females, who had experienced at least one episode classified from the clinical point of view as epileptic in origin. They were divided into six age groups. Patients underwent a two-hour (1 P.M.-3 P.M.) nap-video-polygraphic recording (EEG 13 channels using the standard 10-20 system, EOG, ECG, EMG and respiration), following a partial sleep deprivation (1 to 3 h) the night before. A second recording was made in 40 patients. In 35.3% of patients, a complete sleep cycle was obtained; in 64.6% sufficient light and deep NREM sleep was obtained, but not REM stage; in 9.3%, we only observed drowsiness and stage 1 of sleep, and this group was excluded from the analysis. Interictal and/or ictal epileptic discharges were observed during the first nap recording in 245 patients (40.4% of the sample). In addition, in 40 patients (11%) with normal or inconclusive first nap EEG, a second recording was able to demonstrate epileptic abnormalities in 35% of cases. Because of its good cost/benefit ratio and availability in most western laboratories, we consider the 'nap plus partial sleep deprivation' method as advantageous over other activation procedures.

Adolescent↗
PubMed1978

REM sleep deprivation and pain thresholds in rats.

The relationship between REM sleep deprivation and pain threshold was measured using 36 Sprague-Dawley female rats. Relative to that of the controls, a significant lowering of threshold to painful electrical stimulation was observed during each of the post-treatment tests, i.e., immediate, and after 3- and 24-hr. recovery periods, for the animals which had been REM deprived.

Animals↗
PubMed2005

Melatonin treatment of winter depression following total sleep deprivation: waking EEG and mood correlates.

Patients with winter depression (seasonal affective disorder (SAD)) commonly complain of sleepiness. Sleepiness can be objectively measured by spectral analysis of the waking electroencephalogram (EEG) in the 1-10 Hz band. The waking EEG was measured every 3 h in 16 female SAD patients and 13 age-matched control women throughout a total sleep deprivation of 30 h. Melatonin (or placebo) under double-blind conditions was administered subsequently (0.5 mg at 1700 h for 6 days), appropriately timed to phase advance circadian rhythms, followed by reassessment in the laboratory for 12 h. The increase in EEG power density in a narrow theta band (5-5.99 Hz, derivation Fz-Cz) during the 30 h protocol was significantly attenuated in patients compared with controls (difference between linear trends p=0.037). Sleepiness (p=0.092) and energy (p=0.045) self-ratings followed a similar pattern. Six patients improved after sleep deprivation (> or =50% reduction on SIGH-SAD(22) score). EEG power density dynamics was correlated with clinical response to sleep deprivation: the steeper the build-up (as in controls), the better the improvement (p<0.05). There was no differential effect of melatonin or placebo on any measure; both treatments stabilized the improvement. Overall, patients with winter depression manifest similar wake EEG characteristics as long sleepers or late chronotype with respect to an insufficient build-up of homeostatic sleep pressure. Sleep deprivation was an effective antidepressant treatment for some patients, but evening melatonin was not more efficacious than placebo in sustaining this antidepressant effect.

Adolescent↗
PubMedDate not supplied

Antidepressant effects of sleep deprivation and phototherapy.

In contrast to drugs, sleep deprivation and phototherapy rapidly induce depressive remissions, which are rapidly reversible. These characteristics make them useful tools for prospective, longitudinal studies of the psychobiology of depression. It seems likely that discovery of the mechanism of action of these two antidepressant procedures would increase our understanding of the pathogenesis of depression and lead to novel, rapidly acting pharmacological treatments. Further progress in this direction depends on careful delineation of which conditions of the procedures are necessary for their antidepressant efficacy and identification and pharmacological manipulation of biological correlates of the procedures that may be relevant to their mechanism of action. Analogies between the two procedures suggest that similar mechanisms may be involved in both.

Atenolol↗
PubMed1979

Prediction of lofepramine-response in depression based on response to partial sleep deprivation.

The improvement of depression after partial sleep deprivation in the second half of the night (sd) is tested for its predictory power for the therapeutical efficacy of pharmacotherapy with lofepramine. In a group of 15 patients with depression, we found that in contradiction to the findings of Wirz-Justice and collaborators (1976), the velocity of the antidepressive effect of sd has no predictive value. On the other hand, the amount of depression improvement after sd is of predictive value. This is independent of the time of occurrence of the improvement peak after sd. An improvement of more than 35% measured in the Bf-S or in the H.DRS on the first or the second day after sd is highly predictive for a good response to three weeks of 210 mg lofepramine per day (p = .05).

Clinical Trials as Topic↗
PubMed2003

Influence of a functional polymorphism within the angiotensin I-converting enzyme gene on partial sleep deprivation in patients with major depression.

Partial sleep deprivation (PSD) exerts transient antidepressant efficacy. As a potential mechanism of action an enhancement of dopaminergic neurotransmission within the CNS is discussed. Because genetic variations influencing neurotransmission could have an impact on therapeutic outcome and stability of improvement, we investigated the functional insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene to examine a possible influence on the dopaminergic pathway. We included 56 patients with major depression (DSM-IV). Psychiatric ratings including the HAM-D6 scale were assessed prior to and after PSD and related to the different genotypes. The ACE I/D polymorphism was determined following PCR amplification using genomic DNA. A total of 58.1% of the patients were PSD responders. As expected, the therapeutical effect of PSD was transient and most patients experienced an exacerbation of depressive symptoms on day 2. Subdivision according ACE gene variants showed a significantly less pronounced relapse of symptoms in ACE gene D-allele carriers (P=0.02). Our results give first hints that the ACE I/I genotype, probably influencing dopaminergic neurotransmission, could be an indicator for relapse after PSD. This should result in earlier and more intense additional therapeutic interventions in this group of patients.

Adult↗
PubMedDate not supplied

[Prenatal experience and postnatal development of the rat hippocampus: sleep deprivation of pregnant rats].

The effects of sleep deprivation in pregnancy on the development of hippocampal function of the offspring have been investigated. For this purpose we compared electrophysiological characteristics in the hippocampal slices of 15-20-old-day rats of the control and two experimental groups. In the first experimental group the pups were taken from mother for weighting three times during the first postnatal week and then weekly. Another experimental group was brought up without handling. We found that CA1 population spikes developed to significantly less amplitude in experimental groups of rat pups. This phenomenon was observed at higher intensity of monosynaptic activation, although near-threshold stimuli didn't reveal any differences among groups. However, under paired-pulse stimulation (70 ms inter-pulse interval) small amplitudes in the hippocampal slices of experimental animals could facilitate up to control value, and second in pair responses didn't differ from corresponding control. Our data doesn't confirm the hypothesis about decreased connectivity in the hippocampus of experimental rats, but the efficacy of CA3-CA1 inputs seems to be lower. Besides excitatory transmission, the effectiveness of inhibition of paired-pulse facilitation at 15 ms inter-pulse interval was also significantly decreased. The observed effects of prenatal influences seem to develop under postnatal experience. We observed significant trend to more pronounced modifications upon age especially in the case of early handling and testing.

Animals↗
PubMed1990

Moderate exercise and hemodilution during sleep deprivation.

The effect of 52 h of sleep deprivation (SD) upon blood constituents was studied in 12 young women aged 21.5 +/- 0.4 years. Subjects were individually isolated without time cues, performing a sequence of cognitive tasks. Significant decreases in hematocrit (p less than 0.002) and red cell count (p less than 0.04) developed, mainly over the first 28 h of SD, reaching a subsequent plateau or partial recovery. The calculated plasma volume also increased by 10.7 +/- 3.1% at 52 h, with recovery to a 6.9 +/- 3.2% increase the following day. About 1 L of water was retained over the first 30 h of SD, with a subsequent partial elimination of this excess. Plasma albumin and total protein concentrations were largely sustained in the face of the plasma expansion. The plasma pH showed a progressive fall from a baseline value of 7.381 +/- 0.014 to 7.332 +/- 0.006 at 52 h, while plasma bicarbonate decreased from a baseline figure of 31.2 +/- 0.7 to 26-27 mM/L (p less than 0.05). After 8 weeks, all subjects repeated the experiment, with the introduction of 30 min of exercise in the 40th h of wakefulness. Hematocrit and plasma volume changes were similar to those of the first experiment up to the time of exercise, but hematocrit decreased and plasma volume increased after the exercise bout, rather than reaching a plateau. Plasma pH increased with exercise, but returned to the previous low level at 52 h. Any arousing effect of the exercise bout was transient. The plasma expansion reflects metabolic and/or respiratory acidosis, plus possible effects of a prolonged period without recumbency.

Adult↗
PubMed2000

[Circadian fluctuations in the muscular efficiency of athletes: with sleep versus sleep deprivation].

The influence of time of day on muscular performance was studied. From part of the results of two different studies (EAS et EPS), the effects of sleep deprivation were appreciated. Seven times over the 24-h period, developed torque and myoelectric activity were estimated during maximal isometric voluntary contractions using an isokinetic dynamometer: elbow flexion for EAS in standardised sleep, and knee extension for EPS in complete sleep deprivation. The results showed nycthemeral changes in torque in both conditions (p < 0.005), with maximal values recorded at the beginning of night. Although during sleep deprivation (EPS) the rhythm followed neurophysiological factors, during EAS, this rhythm was accounted for by the variations in the contractile state of muscle.

Adult↗
PubMed1986

An analgesic effect of enkephalinase inhibition is modulated by monoamine oxidase-B and REM sleep deprivations.

Both the MAO-B inhibitor deprenyl (2.5-10 mg/kg, ip, 60 min prior) and the MAO-B substrate beta-phenylethylamine (PEA, 40 micrograms, icv) potentiated the analgesic action of the enkephalinase inhibitor phosphoramidon (250 micrograms, icv) in animals allowed normal sleep. The enhancing effect of PEA on phosphoramidon analgesia was further potentiated by deprenyl (5 mg/kg, ip) pretreatment. Deprenyl (5 mg/kg, ip) or PEA (40 micrograms, iv) given alone did not induce analgesia in animals allowed undisturbed sleep. REM sleep deprivation (REMSD) decreased the basal pain threshold and abolished the analgesic effect of phosphoramidon. The administration of deprenyl and/or PEA failed to restore the analgesic effect of phosphoramidon in REM sleep deprived animals. The results indicate that excess PEA has a stimulatory effect on the analgesic activity of endogenously released enkephalins in rats allowed undisturbed sleep but not in REM sleep deprived animals. It is suggested that the failure of phosphoramidon to induce analgesia after REMSD, is probably due to a functional insufficiency of an enkephalinergic system.

Animals↗
PubMed1976

6-Hydroxydopamine and the aggressive behavior induced by marihuana in REM sleep-deprived rats.

6-Hydroxydopamine (6OH-DA) pretreatment increased the aggressive behavior induced by marihuana in REM sleep-deprived rats. Brain catecholamine assays revealed that 6OH-DA depleted popamine (DA) and norepinephrine (NE) to a different extent, increasing the DA/NE ratio. Intraventricular injection of NE significantly decreased the aggressive behavior of these animals, whereas control solution or DA injections had no effect. The possible role played by DA and NE in the aggressive behavior induced by marihuana in REM sleep-deprived rats is discussed.

Aggression↗
PubMed2001

Nineteen-hour variation of postural sway, alertness and rectal temperature during sleep deprivation.

Nineteen-hour variation of postural sway, alertness and rectal temperature during sleep deprivation were studied. Alertness decreased gradually at night and remained low until morning. Postural sway in the eyes-closed condition increased during early morning. In six of the eight subjects the greatest sway was observed during the 3-h period when rectal temperature was at its minimum. It is suggested that unbearable sleepiness during sleep deprivation will give rise to measurable impairment of postural balance especially during the time zone of temperature nadir.

Adult↗
PubMed1975

The treatment of psychotic depression by sleep deprivation: a replication study.

A replication study of the effects of single-night sleep deprivation therapy was carried out as a preliminary to a controlled comparison with orthodox antidepressent measures. The results show that sleep deprivation therapy was acceptable to a majority of the patients studied, and was followed by an improvement in over half those who completed treatment. Adverse effects were minimal. The authors feel that further clinical and physiological study is warranted.

Adult↗
PubMed1979

Five variations of sleep deprivation in a depressed woman.

Systematic variation in aspects of the sleep-wakefulness cycle of a depressed woman showed that recovery occurred reliably after 19 to 20 hours sustained wakefulness, unrelated to diurnal rhythm. Depression returned during as little as 15 minutes sleep. The effect of sleep deprivation was a specific response, probably unrelated to REM sleep.

Aged↗
PubMed2004

Age-related effects on genital reflexes induced by paradoxical sleep deprivation and cocaine in rats.

Although sexual function often decreases with age, a recent study demonstrated that paradoxical sleep deprivation (PSD) was effective in inducing penile erection (PE) in 60% of 22-month-old PSD rats after acute cocaine injection, whereas this behavior was absent in non-PSD control rats. The present study sought to compare alterations in genital reflexes (PE and ejaculation-EJ) induced by PSD followed by acute cocaine or saline at different points in the life span of male rats. Rats of different ages (3, 6, 10, 12, 18, 22 and 28 months), were given a single injection of either saline or cocaine (7 mg/kg, i.p.) after a 4-day period of PSD, and then evaluated for genital reflexes. Results indicated that genital reflexes in PSD rats given saline become less frequent with age and disappear after the age of 18 months. However, cocaine potentiated and prolonged these behaviors until the age of 22 months. Although a number of factors are involved in such a complex phenomenon as PE, we suggest that the previously documented dopamine receptor supersensitivity induced by PSD may be an important contributor to the potentiation by cocaine of genital reflexes after sleep deprivation.

Aging↗
PubMed2005

The effects of total sleep deprivation on the generation of random sequences of key-presses, numbers and nouns.

According to a recent hypothesis, executive functions should be particularly vulnerable to the effects of total sleep deprivation. Random generation is a task that taps executive functions. In three experiments we examined the effects of total sleep deprivation on random generation of key-presses, numbers, and nouns, in particular on the suppression of prepotent responses and the selection of next responses by way of applying a local-representativeness heuristic. With random key-presses suppression of prepotent responses did not suffer from lack of sleep, but it became poorer at a sufficiently high pacing rate. In contrast, suppression of prepotent responses suffered when numbers and nouns were generated. According to these findings different types of random generation tasks involve different types of inhibitory process. With only four response alternatives, but not with larger response sets, application of the local-representativeness heuristic was impaired after a night without sleep. In terms of a simple formal model, serial-order representations of the preceding responses are used in selecting the next response only for the small response set, and not for larger response sets. Thus, serial-order representations are likely to suffer from loss of sleep. These findings strongly suggest that random generation involves multiple processes and that total sleep deprivation does not impair all sorts of executive functions, but only some.

Adult↗