Changes In REM Sleep Research Articles

Sleep phenotype characterization of peripheral and central mouse models of myotonic dystrophy

Excessive daytime sleepiness and associated alterations in REM sleep patterns are among the most characteristic non-muscular features of myotonic dystrophy (DM). The symptoms of DM are caused by an expanded C (C) UG repeat that sequesters muscleblind-like protein 1 (MBNL1) and MBNL2, proteins that regulates alternative splicing required for fetal to adult developments. A recent study strongly suggests that major pathological changes in the DM brain are attributable to MBNL2 sequestration by toxic RNAs and dysregulation of specific alternative splicing events required for normal adult CNS function. We thus performed sleep EEG/EMG evaluations on Mbnl1 and Mbnl2 knockout (KO) mice. Adult wild and KO mice of Mbnl1 or Mbnl2 at 6 month of age (Mbnl1; n = 7, Mbnl2; n = 8) were implanted with EEG and EMG electrodes along with E-mitters. Sleep deprivation was performed for 6 h after one full day of baseline by gentle handling. Mbnl1 and Mbnl2 KOs had normal amounts, and natural diurnal distributions, of wakefulness and NREM sleep in the 12:12 LD condition. Shorter sleep latency and modest wake fragmentation during dark periods (frequent/shorter wake episodes) were observed in the Mbnl2 KO mice. However, the most profound sleep phenotypes observed in the Mbnl2 KO mice were an increase in REM sleep amounts, associated with increased numbers of REM sleep episodes, and increased EEG theta power. This change was most notable during the dark/active period. No direct transition from Wake to REM sleep, an EEG/EMG phenotype equivalent to behavioral cataplexy, was seen in either WT or Mbnl2 KO mice. A change in REM sleep in Mbnl2 KOs was also observed during rebound sleep after a 6-h sleep deprivation period initiated at ZT 0, where a more profound REM sleep rebound was observed in Mbnl2 KO mice, compared to WT mice. These REM specific changes were not observed in the Mbnl1 KO mice. Our results indicate that Mbnl2, but not Mbnl1, KO mice exhibit increased REM sleep propensity, suggesting REM-associated sleep abnormality in Mbnl2 KO are caused by dysregulation of specific alternative splicing events in the brain, and this may be one of the most important sleep abnormalities in DM. REM sleep characteristics in DM might be a residual of infant-type REM sleep, as infants of altricial species, including human and mice, spend large majority of time in REM sleep.

Phase of nasal cycle during sleep tends to be associated with sleep stage

The phenomena of periodic cycles of vascular engorgement on the nasal cavity mucosa that alternate between right and left sides are termed the "nasal cycle." The physiologic mechanisms underlying this cycle have not been entirely clarified, even more so during sleep. In this study, we measured the periodic patterns of the normal nasal cycle, not only during wakefulness but also during sleep. Our team utilized a method for functional rhinologic assessment, the portable rhinoflowmeter (Rhinocycle, Rhinometrics, Lynge, Denmark), measuring airflow independently through each nostril during 24 hours on 20 healthy subjects aged 20 to 56 years, and without any nasal pathology or diagnosed medical, psychiatric, or sleep disorders. In addition, a nocturnal polysomnogram was simultaneously performed during sleep. Nineteen of 20 subjects showed a detectable nasal cycle, and 16 of 19 subjects presented a change of the cyclic phase during sleep. The mean nasal cycle duration was 234.2 ± 282.4 minutes (median, 164.1 minutes), although variation was considerable. The mean cycle duration time during sleep was significantly longer than that in wakefulness (P <0.005). The reversal of cyclic phase during sleep tended to be associated with REM sleep (68.8%) and postural changes (18.8%). It never occurred in slow-wave sleep. Nasal cycle duration during sleep is longer than in wakefulness. Changes in laterality of nasal cycle frequently coincide with switches in posture, tend to occur in REM sleep, never occur in slow-wave sleep, and may be absent in subjects with severe nasal septal deviations.

Blood Chemistry, Acid-Base, Electrolyte, Blood Lactate Metabolism and Sleep at 3480 m in Mountain Marathon Runners

Altered blood chemistry, acid-base and electrolyte are suggested determinants of sleep disturbance, with frequent arousal at high altitude even in well and long-trained altitude marathon runners. In this sample of experienced altitude marathon runners with maximal aerobic power at sea level of 61.4 ± 2.7 ml/kg-1·min-1 we found that pO2 and percent of oxygen saturation (%SO2) were lower at2050 mand3480 mthan at sea level; pO2 was higher after 38 - 41 hours than after 30 - 31 hours of acclimatization at3480 m(P < 0.05). After ascentto3480 m%SO2 decreased (P < 0.003). Com- pared to sea level values, pH increased at high altitude (P < 0.05) consistent with changes in pCO2 and (P < 0.05). Nocturnal %SpaO2 at a sleeping altitude of3480 mwas lower (P < 0.05) than at sea level. At high altitude, the percent of wake (W) time and delay falling asleep (DFA) increased, whereas non-rapid eye movement sleep (N-REM), REM sleep and total sleep time (TST) decreased (P < 0.05). Simple regression analysis disclosed a significant correlation between the changes in TST and the percent of REM sleep and the changes in %SpaO2 recorded during sleep (P < 0.05). Simple regression analysis showed a positive correlation between the changes in pO2 at higher altitude and the percent of W and of TST (P < 0.05). The changes in pO2, tCO2 and [HCO3-] correlated negatively and significantly with the percent of REM sleep changes at high altitude (P < 0.05). The TST changes at high altitude correlated positively with the changes in pO2 and pH and correlated negatively with the changes in %SO2, pCO2, tCO2, and [HCO3-] (P < 0.05). The changes in the percent of W at high altitude correlated significantly and positively with the changes in bases excess [BE] at high altitude (P < 0.05). The changes in the percent of REM sleep correlated significantly and positively with the changes in [iCa++] and [BE] and negatively with the changes in buffered bases [BB] and [BEeffective] (P < 0.05). The change in the percent of NREM + REM sleep at high altitude correlated significantly and positively with the changes in [BE] and [BB] concentration (P < 0.05). The increase in DFA at high altitude correlated significantly and negatively with the changes in pCO2 and significantly and negatively with the changes in [K+] (P < 0.05). Simple regression analysis demonstrated that the changes in pH at high altitude correlated positively and significantly with the percent of W and the DFA and negatively with the percent of changes in NREM sleep, REM sleep, NREM + REM sleep (P < 0.05). The decrease in the TST at high altitude correlated significantly and negatively with the changes in pCO2, tCO2, [HCO3-] and [K+] (P < 0.05). Our data demonstrate that the arterialized ear lobe techniques we used for evaluating most of the changes in blood chemistry, acid-base, electrolyte and blood lactate metabolism aresuitable for clinical and laboratory assessment and are important predictors of the quality and quantity of acclimatization and sleep at high altitude.

Significance of REM Sleep in Depression: Effects on Neurogenesis

Significance of REM Sleep in Depression: Effects on Neurogenesis

TASK-3 as a potential antidepressant target

Modulation of TASK-3 ( Kcnk9) potassium channels affect neurotransmitter release in thalamocortical centers and other sleep-related nuclei having the capacity to regulate arousal cycles and REM sleep changes associated with mood disorders and antidepressant action. Circumstantial evidence from this and previous studies suggest the potential for TASK-3 to be a novel antidepressant therapeutic target; TASK-3 knock-out mice display augmented circadian amplitude and exhibit sleep architecture characterized by suppressed REM activity. Detailed analysis of locomotor activity indicates that the amplitudes of activity bout duration and bout number are augmented in TASK-3 mutants well beyond that seen in wildtypes, findings substantiated by amplitude increases in body temperature and EEG recordings of sleep stage bouts. Polysomnographic analysis of TASK-3 mutants reveals increases in nocturnal active wake and suppressed REM sleep time while increased slow wave sleep typifies the inactive phase, findings that have implications for the cognitive impact of reduced TASK-3 activity. In direct measures of their resistance to despair behavior, TASK-3 knock-outs displayed significant decreases in immobility relative to wildtype controls in both tail suspension and forced swim tests. Treatment of wildtype animals with the antidepressant Fluoxetine markedly reduced REM sleep, while leaving active wake and slow wave sleep relatively intact. Remarkably, these effects were absent in TASK-3 mutants indicating that TASK-3 is either directly involved in the mechanism of this drug's action, or participates in parallel pathways that achieve the same effect. Together, these results support the TASK-3 channel to act as a therapeutic target for antidepressant action.

Circadian variation of sleep during the follicular and luteal phases of the menstrual cycle.

Women experience insomnia more frequently than men. Menstrual cycle changes in reproductive hormones and circadian rhythms may contribute to sleep disruptions. Our aim, therefore, was to clarify the interaction between menstrual and circadian processes as it affects sleep. Participants entered the laboratory during the mid-follicular (MF) and mid-luteal (ML) phases of their menstrual cycle for an ultra-rapid sleep-wake cycle (URSW) procedure, consisting of 36 cycles of 60-min wake episodes alternating with 60-min nap opportunities. This procedure concluded with an ad libitum nap episode. Time-isolation suite. Eight unmedicated, physically and mentally healthy females with regular ovulatory menstrual cycles. N/A. Polysomnographic sleep from nocturnal sleep episodes and 60-min naps; subjective alertness; core body temperature (CBT); salivary melatonin; urinary estradiol; and urinary progesterone. Increased CBT values at night and decreased CBT amplitude were observed during ML compared to MF. Circadian phase of CBT and the circadian melatonin profile were unaffected by menstrual phase. All analyzed sleep parameters showed a circadian variation throughout the URSW procedure, with no menstrual phase differences observed for most, including slow wave sleep (SWS). The circadian variation of REM sleep duration, however, was sensitive to menstrual phase, with reduced REM sleep during ML at circadian phase 0 degrees and 30 degrees. Moderate but significant changes in REM sleep across the menstrual and circadian cycles were observed. These results support an interaction between circadian and menstrual processes in the regulation of REM sleep.

Discontinuation of hypnotics during cognitive behavioural therapy for insomnia.

BackgroundIn practical sleep medicine, therapists face the question of whether or not to discontinue the ongoing use of hypnotics in patients, as well as the possible effects of discontinuation. The aim of this study was to evaluate the effects of discontinuing third-generation hypnotics on the results of cognitive-behavioural therapy (CBT) for primary insomnia in patients after long-term abuse.MethodsTwenty-eight outpatients were treated by CBT for 8 weeks. The treatment outcome was estimated by means of differences among subjective clinical scales and polysomnography variables assessed before and after the treatment period. The therapeutic effect in a subgroup of 15 patients who had previously received hypnotics and were successively withdrawn during weeks 2–6 was compared to the effect achieved in patients who had not used hypnotics before CBT.ResultsThere were no significant differences in baseline subjective and objective sleep characteristics between the hypnotic abusers and non-abusers. According to clinical scales and most polysomnographic measures, CBT was highly effective in both groups of subjects; it produced the greatest changes in total sleep time, REM sleep and sleep efficiency. Unexpectedly, discontinuation of hypnotics, as a factor in the analysis, was followed by an additional improvement of sleep efficiency and wake after sleep onset parameters.ConclusionOur study confirmed the efficacy of CBT in both hypnotic-abusing and non-abusing patients with chronic insomnia. The results of this study suggest that tapered withdrawal of third-generation hypnotics during CBT therapy for chronic insomnia could be associated with improvement rather than worsening of sleep continuity.

Effects of Eszopiclone and Zolpidem on Sleep and Waking States in the Adult Guinea Pig

The present study was designed to compare and contrast the effects of eszopiclone and zolpidem on the states of sleep and wakefulness in chronically instrumented, unanesthetized adult guinea pigs. Adult guinea pigs were implanted with electrodes to record sleep and waking states and to perform a frequency analysis of the EEG. Eszopiclone (1 and 3 mg/kg) and zolpidem (1 and 3 mg/kg) were administered intraperitoneally. The administration of eszopiclone (1 and 3 mg/kg) resulted in a significant dose-dependent increase in NREM sleep. Zolpidem produced a significant increase in NREM sleep, but only at a dose of 3 mg/kg. The following changes in NREM and REM sleep, as well as in the power spectra, were all significant when the effects of 1 and 3 mg/kg of eszopiclone were compared with responses induced with 1 and 3 mg/kg of zolpidem, respectively: The increase in NREM sleep produced by eszopiclone was greater than that following the administration of zolpidem. The mean latency to NREM sleep following the administration of eszopiclone was significantly shorter than zolpidem. Eszopiclone significantly increased the latency to REM sleep. The mean duration of episodes of NREM sleep was increased by eszopiclone, but not by zolpidem. The EEG power increased in the delta band and decreased in the theta band during NREM sleep following the administration of eszopiclone. No significant changes occurred in any of the frequency bands analyzed following zolpidem administration. The differences in the effects of eszopiclone and zolpidem on sleep and waking states and the power spectra of the EEG likely reflect the fact that eszopiclone and zolpidem bind to different subunits of the GABAA receptor complex.

Up‐regulated neuronal COX‐2 expression after cortical spreading depression is involved in non‐REM sleep induction in rats

Cortical spreading depression is an excitatory wave of depolarization spreading throughout cerebral cortex at a rate of 2-5 mm/min and has been implicated in various neurological disorders, such as epilepsy, migraine aura, and trauma. Although sleepiness or sleep is often induced by these neurological disorders, the cellular and molecular mechanism has remained unclear. To investigate whether and how the sleep-wake behavior is altered by such aberrant brain activity, we induced cortical spreading depression in freely moving rats, monitoring REM and non-REM (NREM) sleep and sleep-associated changes in cyclooxygenase (COX)-2 and prostaglandins (PGs). In such a model for aberrant neuronal excitation in the cerebral cortex, the amount of NREM sleep, but not of REM sleep, increased subsequently for several hours, with an up-regulated expression of COX-2 in cortical neurons and considerable production of PGs. A specific inhibitor of COX-2 completely arrested the increase in NREM sleep. These results indicate that up-regulated neuronal COX-2 would be involved in aberrant brain excitation-induced NREM sleep via production of PGs.

Dissociable learning-dependent changes in REM and non-REM sleep in declarative and procedural memory systems

Sleep spindles and rapid eye movements have been found to increase following an intense period of learning on a combination of procedural memory tasks. It is not clear whether these changes are task specific, or the result of learning in general. The current study investigated changes in spindles, rapid eye movements, K-complexes and EEG spectral power following learning in good sleepers randomly assigned to one of four learning conditions: Pursuit Rotor ( n = 9), Mirror Tracing ( n = 9), Paired Associates ( n = 9), and non-learning controls ( n = 9). Following Pursuit Rotor learning, there was an increase in the duration of Stage 2 sleep, spindle density (number of spindles/min), average spindle duration, and an increase in low frequency sigma power (12–14 Hz) at occipital regions during SWS and at frontal regions during Stage 2 sleep in the second half of the night. These findings are consistent with previous findings that Pursuit Rotor learning is consolidated during Stage 2 sleep, and provide additional data to suggest that spindles across all non-REM stages may be a mechanism for brain plasticity. Following Paired Associates learning, theta power increased significantly at central regions during REM sleep. This study provides the first evidence that REM sleep theta activity is involved in declarative memory consolidation. Together, these findings support the hypothesis that brain plasticity during sleep does not involve a unitary process; that is, different types of learning have unique sleep-related memory consolidation mechanisms that act in dissociable brain regions at different times throughout the night.

Transient fear-induced alterations in evoked release of norepinephrine and GABA in amygdala slices

Presentation of a tonal cue that previously had been associated with a fearful experience (footshock) produces alterations in arousal and sleep that occur after the fearful cue is no longer presented. To begin investigating neurochemical mechanisms that may underlie the effects of fearful cue presentation, we measured release of [ 3H]-norepinephrine ([ 3H]-NE]) and [ 14C]-γ-amino-butyric acid ([ 14C]-GABA) from brain regions known to regulate arousal states and REM sleep. Depolarization-evoked release of [ 3H]-NE from amygdalar slices of mice, which were trained to recognize a tone as a fearful cue, was suppressed at 2–3 h after exposure of animals to the fearful cue, but recovered after 4–5 h. Interestingly, depolarization-evoked release of [ 14C]-GABA was significantly increased in the amygdala, and also showed a tendency for enhancement in the hippocampus, NPO, and DRN at 2–3 h after cue presentation. The changes in [ 14C]-GABA release were also transient; 4–5 h after cue presentation no significant differences were detected between samples derived from experimental groups which experienced fearful or neutral cues. The similar time course of fearful cue-induced changes in neurotransmitter release and changes in arousal and REM sleep suggests that alterations in amygdalar neurotransmission may be involved in the changes in arousal and sleep that occur after fear.

Age-related changes in cholinergic neurons in the laterodorsal and the pedunculo-pontine tegmental nuclei of cats: A combined light and electron microscopic study

In aged cats, light microscopic studies revealed significant decrease in the soma size of choline acetyltransferase (ChAT)-positive neurons in the laterodorsal and pedunculo-pontine tegmental nuclei (LDT and PPT), compared with adult control animals. In addition, a significant reduction of the total dendritic length and total dendritic segment number of ChAT-positive neurons was detected in both the LDT and PPT of aged cats. However, in contrast to the changes of soma and dendrites, no significant changes in the number of ChAT-positive neurons in aged were found comparing to that in the control cats in both the LDT and PPT; nor were there differences in the staining intensity of the somata of neurons in the adult and aged cats. Electron microscopic analysis highlighted degenerative changes in cholinergic neurons in the LDT and PPT of aged cats which included somata with intracytoplasmic vacuoles, darkened mitochondria, depletion of dendritic microtubules and severe demyelination of axons. These data indicate that profound atrophic changes occur in cholinergic systems of the LDT and PPT as a consequence of the aging process. These alterations likely reflect the cellular bases for the age-related changes in REM sleep that occur in old animals.

Article reviewed: Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men

Article reviewed: Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men

Post-traumatic stress disorder and sleep—what a nightmare!

According to DSM IV criteria, sleep disturbances are incorporated in the definition of post-traumatic stress disorder (PTSD). These include the re-experiencing symptoms (nightmares, criteria B) and a hyperarousal state (difficulty initiating and maintaining sleep, criteria D). PTSD patients commonly complain of sleep disturbances. Moreover, insomnia, restless sleep and trauma-related dreams might be the primary complaint of some patients. However, although subjective sleep disturbances are considered characteristic of PTSD, sleep laboratory studies have provided inconsistent evidence of objective sleep disorders. A variety of sleep architectures and sleep patterns has been reported in PTSD. However, only a few studies have controlled for comorbidities. Thus, uncertainty exists to what extent the sustained complaints of sleep disturbances in chronic PTSD are specifically related to the impact of exposure to traumatic stress, or rather are a consequence of comorbid disorders. Specific changes in REM sleep suggest a pathophysiologic role of REM sleep abnormality in PTSD (e.g. anxiety dreams, increased REM density, exaggerated startle response, decreased dream recall and elevated awakening thresholds from REM sleep). However, again, studies have failed to show consistent changes in percentage of REM sleep or in REM latency. There might be a coexistence of pressure to REM along with inhibitory forces of REM that result in high variability of REM parameters across patients. Alternatively, changes in REM sleep might reflect the effect of comorbid psychiatric disorders that results in inconsistent findings between patients. The current review tries to address these issues based on recent studies carried out in this field.

Age-related changes in sleep in the rat.

Human sleep in old age is characterized by a number of changes, including reductions in sleep efficiency, amounts of visually scored slow-wave and REM sleep, and amplitude of the diurnal sleep/wake rhythm. In older rats, some, but not all, of these traits have been reported, including a decrease in the mean duration of sleep bouts, an increase in the number of sleep bouts, and a modest reduction of REM sleep. Studies of the diurnal rhythm of total sleep have had varied results. There are, however, virtually no data indicating at what point across the rat's lifetime the changes seen in old age begin to occur. In order to more fully characterize sleep in older rats, and to develop data on when they first appear, we have examined sleep in young adult (3 months), middle-aged (12 months), and older (24 months) rats during 24 hours under constant dim light. Analyses of variance revealed no age-related changes in total sleep, NREM or REM sleep, wake time after sleep onset, or three different measures of the amplitude of the sleep/wake circadian rhythm. There were, however, significant age-related reductions in high-voltage NREM sleep ("HS2"), the mean length of sleep bouts, and REM-onset duration. These were seen in the 1-year-old rats, indicating that the changes seen in the older animals were evident by midlife.

A polysomnographic study of sleep patterns in normal humans with low- or high-anxiety personality traits.

To clarify the effects of anxiety-related personality traits on sleep patterns, polysomnographic examinations (PSG) were performed over 4 consecutive nights on normal humans who tested within the low- or high-anxiety ranges. The subjects consisted of two groups of six male university students who scored either less than 45 points (low-anxiety group) or more than 55 points (high-anxiety group) on the Spielberger's State Trait Anxiety Inventory. Compared to the levels of sleep change in the high-anxiety group, the low-anxiety group exhibited a greater change in REM sleep and stage 2 sleep. The REM sleep in the low-anxiety group was shorter on the first and second nights compared to the third and fourth nights, and the stage 2 sleep was longer on the first night than on the remaining three nights. Thus, the low-anxiety group showed a first-night effect followed by partial recovery on the second night, while the high-anxiety group exhibited no obvious first-night effect. These results suggest that there is a difference in sleep patterns, assessed by consecutive PSG, between those with low- and high-anxiety traits, and that anxiety-related personality traits attenuate the occurrence of the first-night effect, reflecting a lower adaptability to a novel environment.

Heart rate variability: sleep stage, time of night, and arousal influences

Spectral analysis was used to assess heart rate variability in consecutive 5-min epochs during the night in 12 normal adults. Simultaneous time coding of EEG and digitized EKG allowed examination of heart rate variability as a function of sleep stage, time of night and presence of EEG arousal. The results replicated previous studies in showing increases in high frequency components and decreases in low frequency components of heart rate variability across NREM sleep stages and opposite changes in REM sleep and wake. These results are consistent with sympathetic nervous system activation during REM sleep and wake periods. The shift in heart rate variability seen during REM sleep began in NREM sleep several minutes prior to standardly scored REM and often continued beyond the end of REM sleep. EEG arousals during Stage 2 and to some extent REM sleep were also associated with changes in heart rate variability which were consistent with sympathetic activation. An examination of beat to beat intervals in proximity to EEG arousals showed heart rate acceleration at least 10 beats prior to the EEG arousal. The arousal data along with Stage 2 sleep transition data support the contention that increases in central nervous system sympathetic activity precede and possibly play a role in the initiation of REM sleep and arousals during sleep.

Prolonged enhancement of REM sleep produced by carbachol microinjection into the amygdala.

The effect on sleep organization of carbachol microinjected into different amygdaloid nuclei was analysed in 12 cats. Single carbachol doses of 8 micrograms in 0.50 microliter saline were delivered unilaterally or bilaterally into the central, basal, lateral or basolateral amygdaloid nucleus. Carbachol administration into the central nucleus induced a prolonged (5 days) enhancement of both REM sleep and its preceeding slow wave sleep episodes with PGO waves (sommeil phasique a ondes lentes, SPHOL), which was more pronounced following bilateral than unilateral carbachol administration. However, neither SPHOL nor REM sleep changes were produced by administration of carbachol into the other amygdaloid nuclei. We conclude that cholinergic activation of the central amygdaloid nucleus produces a long-term facilitation of REM sleep occurrence.

Sleep effects following intrathecal administration of the 5-HT 1A agonist 8-OH-DPAT and the NMDA antagonist AP-5 in rats

The modulating effect of an intrathecally (i.t.) administered 5-HT 1A agonist and an NMDA antagonist on sleep, waking and EEG power spectra was investigated in rats. The 5-HT 1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) (38 nmol) increased total slow wave sleep (TSWS) and decreased waking over the 8 h recording period. The TSWS increase was mostly due to an increase in SWS1. Sleep latency to SWS1 was also reduced. The NMDA antagonist dl-2-amino 5-phosphonovaleric acid (AP-5) (31.5 nmol) reduced waking. SWS1 was increased, but TSWS was not changed. An increase in REM sleep was seen during the last part of the recording. Combined treatment with 8-OH-DPAT and AP-5 reduced waking and increasd TSWSS. No change in REM sleep was seen. There were no systematic changes in either waking, TSWS or REM fronto-frontal or fronto-parietal EEG power spectrum after any of the treatments. The results suggest that in the spinal cord stimulation of 5-HT 1A receptors have a dampening effect on transmission of sensory information, leading to deactivation and thereby increased possibilities for sleep induction. Blockade of the NMDA receptors may also lead to a small dampening of sensory transmission with similar consequences.

Changes of sleep EEG slow-wave activity in response to sleep manipulations: to what extent are they related to changes in REM sleep latency?

Sleep interventions may have direct effects on slow-wave activity (SWA, i.e. power of the sleep EEG signal in the 0.75-4.5 Hz range) as well as indirect ones caused by changes in REM sleep (REMS) latency. The effects of changes in REMS latency on SWA were investigated by analysing simulations with a mathematical model. Mean SWA in the first non-REMS episode shows an initial increase and a later decline as a function of REMS latency. In the second non-REMS episode, mean SWA decreases with increasing REMS latency. These results of the simulations were validated with experimental data. In the evaluation of the effects of sleep interventions on SWA the effects of the timing of REMS have to be accounted for. The analysis of SWA over a sufficiently long constant amount of time spent in non-REMS proves to be relatively independent of REMS latency, which allows conclusions about the effects of sleep interventions on SWA per se.