Rapid Eye Movement Sleep Episodes Research Articles

Simultaneous real-time measurement of EEG/EMG and l-glutamate in mice: A biosensor study of neuronal activity during sleep

We report on electroencephalograph (EEG) and electromyograph (EMG) measurements concurrently with real-time changes in l-glutamate concentration. These data reveal a link between sleep state and extracellular neurotransmitter changes in a freely-moving (tethered) mouse. This study reveals, for the first time in mice, that the extracellular l-glutamate concentration in the pre-frontal cortex (PFC) increases during periods of extended wakefulness, decreases during extended sleep episodes and spikes during periods of REM sleep. Individual sleep epochs (10 s in duration) were scored as wake, slow-wave (SW) sleep or rapid eye movement (REM) sleep, and then correlated as a function of time with measured changes in l-glutamate concentrations. The observed l-glutamate levels show a statistically significant increase of 0.86 ± 0.26 μM ( p < 0.05) over 37 wake episodes recorded from all mice ( n = 6). Over the course of 49 measured sleep periods longer than 15 min, l-glutamate concentrations decline by a similar amount (0.88 ± 0.37 μM, p < 0.08). The analysis of 163 individual REM sleep episodes greater than one min in length across all mice ( n = 6) demonstrates a significant rise in l-glutamate levels as compared to the 1 min preceding REM sleep onset (RM-ANOVA, DF = 20, F = 6.458, p < 0.001). The observed rapid changes in l-glutamate concentration during REM sleep last only between 1 and 3 min. The approach described can also be extended to other regions of the brain which are hypothesized to play a role in sleep. This study highlights the importance of obtaining simultaneous measurements of neurotransmitter levels in conjunction with sleep markers to help elucidate the underlying physiological and ultimately the genetic components of sleep.

Loss of Goosecoid-like and DiGeorge syndrome critical region 14 in interpeduncular nucleus results in altered regulation of rapid eye movement sleep

Sleep and wakefulness are regulated primarily by inhibitory interactions between the hypothalamus and brainstem. The expression of the states of rapid eye movement (REM) sleep and non-REM (NREM) sleep also are correlated with the activity of groups of REM-off and REM-on neurons in the dorsal brainstem. However, the contribution of ventral brainstem nuclei to sleep regulation has been little characterized to date. Here we examined sleep and wakefulness in mice deficient in a homeobox transcription factor, Goosecoid-like (Gscl), which is one of the genes deleted in DiGeorge syndrome or 22q11 deletion syndrome. The expression of Gscl is restricted to the interpeduncular nucleus (IP) in the ventral region of the midbrain-hindbrain transition. The IP has reciprocal connections with several cell groups implicated in sleep/wakefulness regulation. Although Gscl(-/-) mice have apparently normal anatomy and connections of the IP, they exhibited a reduced total time spent in REM sleep and fewer REM sleep episodes. In addition, Gscl(-/-) mice showed reduced theta power during REM sleep and increased arousability during REM sleep. Gscl(-/-) mice also lacked the expression of DiGeorge syndrome critical region 14 (Dgcr14) in the IP. These results indicate that the absence of Gscl and Dgcr14 in the IP results in altered regulation of REM sleep.

Fear conditioning fragments REM sleep in stress-sensitive Wistar–Kyoto, but not Wistar, rats

Pavlovian conditioning is commonly used to investigate the mechanisms of fear learning. Because the Wistar–Kyoto (WKY) rat strain is particularly stress-sensitive, we investigated the effects of a psychological stressor on sleep in WKY compared to Wistar (WIS) rats. Male WKY and WIS rats were either fear-conditioned to tone cues or received electric foot shocks alone. In the fear-conditioning procedure, animals were exposed to 10 tones (800Hz, 90dB, 5s), each co-terminating with a foot shock (1.0mA, 0.5s), at 30-s intervals. In the shock stress procedure, animals received 10 foot shocks at 30-s intervals, without tones. All subjects underwent a tone-only test both 24h (Day 1) and again two weeks (Day 14) later. Rapid eye movement sleep (REMS) continuity was investigated by partitioning REMS episodes into single (inter-REMS episode interval >3min) and sequential (interval ≤3min) episodes. In the fear-conditioned group, freezing increased from baseline in both strains, but the increase was maintained on Day 14 in WKY rats only. In fear-conditioned WKY rats, total REMS amount increased on Day 1, sequential REMS amount increased on Day 1 and Day 14, and single REMS amount decreased on Day 14. Alterations were due to changes in the number of sequential and single REMS episodes. Shock stress had no significant effect on REMS microarchitecture in either strain. The shift toward sequential REMS in fear-conditioned WKY rats may represent REMS fragmentation, and may provide a model for investigating the neurobiological mechanisms of sleep disturbances reported in posttraumatic stress disorder.

Interictal epileptiform discharges and phasic phenomena of REM sleep

The objective of this study was to assess the effect of phasic rapid eye movement (REM) sleep events on interictal epileptiform discharges (IEDs). Twelve patients with focal epilepsy and IEDs during REM sleep were examined by video-EEG monitoring. The number of IEDs was calculated in different REM sleep episodes according to the rate of rapid eye movements. A negative correlation was identified between the occurrence of rapid eye movements and IEDs, indicating that the suppression of propagation of IEDs during REM sleep is enhanced by phasic REM sleep events, probably as a result of phasic activation of cholinergic neurons of the ponto-mesencephalic tegmentum. This study demonstrates that the degree of EEG desynchronization and IEDs is influenced by REM density.

Endogenous Melatonin is Not Obligatory for the Regulation of the Rat Sleep-Wake Cycle

Though melatonin and melatonin receptor agonists are in clinical use and under development for treating insomnia, the role of endogenous melatonin in the regulation of the sleep-wake cycle remains uncertain. Some clinical case reports suggest that reduced nocturnal melatonin secretion is linked to sleep disruption, but pineal-gland removal in experimental animals has given variable results. The present study examined the effects of pinealectomy on the diurnal sleep-wake cycle of rats implanted with a radiotransmitter to allow continuous measurement of cortical electroencephalogram, electromyogram, and core temperature (Tc) without restraint in their home cages. Tc was slightly (0.2 degrees C) but significantly lower after pineal removal. The total amount and diurnal distribution of locomotor activity, wake, non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep were unaltered in pinealectomized rats compared to sham-operated controls. Sleep consolidation measured by determining wake, NREM sleep, and REM sleep bout length and frequency was also unchanged. The EEG power spectrum during NREM sleep was unchanged, but a significant decrease in theta power (5-8 Hz) during REM sleep episodes was found. Our data provide no evidence that endogenous circulating melatonin plays a role in regulating the sleep-wake cycle in rats. However, because cortical theta oscillations are generated in the CA1-3 layer of the hippocampus, neurons known to express melatonin receptors, this suggests that a lack of melatonin following pineal removal influences the function of these neurons and is consistent with previous work suggesting that endogenous melatonin is an important regulator of hippocampal physiology.

Sleep induced by stimulation in the human pedunculopontine nucleus area

The pedunculopontine nucleus is part of the reticular ascending arousal system and is involved in locomotion and sleep. Two patients with Parkinson disease received electrodes that stimulated the pedunculopontine nucleus area to alleviate their severe gait impairment. Instead, we found that low-frequency stimulation of the pedunculopontine nucleus area increased alertness, whereas high-frequency stimulation induced non-rapid eye movement sleep. In addition, the sudden withdrawal of the low-frequency stimulation was consistently followed by rapid eye movement sleep episodes in 1 patient. These data have the potential to benefit patients who suffer from sleep disorders.

Endogenous ouabain-like compounds in locus coeruleus modulate rapid eye movement sleep in rats

Although the detailed mechanism of spontaneous generation and regulation of rapid eye movement sleep (REMS) is yet unknown, it has been reported that noradrenergic REM-OFF neurons in the locus coeruleus (LC) cease firing during REMS and, if they are kept active, REMS is significantly reduced. On the other hand, the activity as well as expression of Na-K ATPase has been shown to increase in the LC following REMS deprivation. Ouabain is a specific inhibitor of Na-K ATPase, and endogenous ouabain-like compounds are present in the brain. These findings led us to propose that a decrease in the level of ouabain-like compounds spontaneously available in and around the LC would stimulate and increase the REM-OFF neuronal activities in this region and thus would reduce REMS. To test this hypothesis, we generated anti-ouabain antibodies and then microinjected it bilaterally into the LC in freely moving chronically prepared rats and recorded electrophysiological signals for evaluation of sleep-wakefulness states; suitable control experiments were also conducted. Injection of anti-ouabain antibodies into the LC, but not into adjacent brain areas, significantly reduced percent REMS (mean +/- SEM) from 7.12 (+/-0.74) to 3.63 (+/-0.65). The decrease in REMS was due to reduction in the mean frequency of REMS episode, which is likely due to increased excitation of the LC REM-OFF neurons. Control microinjections of normal IgG did not elicit this effect. These results support our hypothesis that interactions of naturally available endogenous ouabain-like compounds with the Na-K ATPase in the LC modulate spontaneous REMS.

Orexin neurons are necessary for the circadian control of REM sleep.

The orexin-producing neurons are hypothesized to be essential for the circadian control of sleep/wake behavior, but it remains unknown whether these rhythms are mediated by the orexin peptides or by other signaling molecules released by these neurons such as glutamate or dynorphin. To determine the roles of these neurotransmitters, we examined the circadian rhythms of sleep/wake behavior in mice lacking the orexin neurons (ataxin-3 [Atx] mice) and mice lacking just the orexin neuropeptides (orexin knockout [KO] mice). We instrumented mice for recordings of sleep-wake behavior, locomotor activity (LMA), and body temperature (Tb) and recorded behavior after 6 days in constant darkness. The amplitude of the rapid eye movement (REM) sleep rhythm was substantially reduced in Atx mice but preserved in orexin KO mice. This blunted rhythm in Atx mice was caused by an increase in the amount of REM sleep during the subjective night (active period) due to more transitions into REM sleep and longer REM sleep episodes. In contrast, the circadian variations of Tb, LMA, Wake, non-REM sleep, and cataplexy were normal, suggesting that the circadian timekeeping system and other output pathways are intact in both Atx and KO mice. These results indicate that the orexin neurons are necessary for the circadian suppression of REM sleep. Blunting of the REM sleep rhythm in Atx mice but not in orexin KO mice suggests that other signaling molecules such as dynorphin or glutamate may act in concert with orexins to suppress REM sleep during the active period.

Small platform sleep deprivation selectively increases the average duration of rapid eye movement sleep episodes during sleep rebound

The single platform-on-water (flower pot) method is extensively used for depriving rapid eye movement sleep (REMS). Detailed comparison of sleep–wake architecture, recorded during the rebound period after spending three days on either a small or large platform, could separate the effects of REMS deficit from other stress factors caused by the procedure. A further aim of the study was to find the most characteristic REMS parameter of the rebound originating from REMS deficit. Rats were kept on a small or large platform for 72 h. Their fronto-parietal electroencephalogram, electromyogram and motility were recorded during the 24 h rebound at the beginning of the passive phase. A similar period of a home cage group was also recorded. The most typical differences between the two rebound groups were the increased cumulative time and longer average duration of REMS episodes without significant change in the number of these episodes of the small platform animals during the passive phase. Results obtained by cosinor analysis were in accordance with the findings above. Since we did not find any difference in the average duration of REMS episodes comparing the large platform rebound group and the home cage group, we concluded that the increased mean duration of REMS episodes is a selective marker for the rebound caused by small platform sleep deprivation, while other changes in sleep architecture may be the consequence of stress and also some sleep deficit.

The Time Course of the Probability of Transition Into and Out of REM Sleep

A model of rapid eye movement (REM) sleep expression is proposed that assumes underlying regulatory mechanisms operating as inhomogenous Poisson processes, the overt results of which are the transitions into and out of REM sleep. Based on spontaneously occurring REM sleep episodes ("Episode") and intervals without REM sleep ("Interval"), 3 variables are defined and evaluated over discrete 15-second epochs using a nonlinear logistic regression method: "Propensity" is the instantaneous rate of into-REM transition occurrence throughout an Interval, "Volatility" is the instantaneous rate of out-of-REM transition occurrence throughout an Episode, and "Opportunity" is the probability of being in non-REM (NREM) sleep at a given time throughout an Interval, a requisite for transition. 12:12 light:dark cycle, isolated boxes. Sixteen male Sprague-Dawley rats. None. Spontaneous sleep cycles. The highest levels of volatility and propensity occur, respectively, at the very beginning of Episodes and Intervals. The new condition stabilizes rapidly, and variables reach nadirs at minute 1.25 and 2.50, respectively. Afterward, volatility increases markedly, reaching values close to the initial level. Propensity increases moderately, the increment being stronger through NREM sleep bouts occurring at the end of long Intervals. Short-term homeostasis is evidenced by longer REM sleep episodes lowering propensity in the following Interval. The stabilization after transitions into Episodes or Intervals and the destabilization after remaining for some time in either condition may be described as resulting from continuous processes building up during Episodes and intervals. These processes underlie the overt occurrence of transitions.

Behavioral sleep in the walrus

In this study we examined behavioral sleep in the walrus, the only living species of the family Odobenidae. The behavior of four 1.5–2-year-old captive walruses was videotaped continuously for 7–17 days and scored in 1-min epochs. When walruses had access to water and land, behavioral sleep, the combined amount of quiet and rapid eye movement (REM) sleep, occupied on average 17 ± 4% of 24 h ( n = 4) with the majority of sleep occurring on land. All walruses alternated periods of almost continuous swimming lasting for 40–84 h with periods of rest on land lasting for 2–19 h. When in water they were predominantly awake (88–99% of the time). On land walruses were asleep on average 40–74% of the time. The total sleep time varied between 0 and 60% of 24 h with the daily amount of REM sleep ranging from 0 to 5% of 24 h. In water, walruses slept while floating at the surface, lying on the bottom or standing and leaning against the pool wall. REM sleep in water occurred in all positions. On land the breathing pattern was regular during quiet sleep (most pauses were <30 s) and arrhythmic in REM sleep (apneas lasted up to 160 s). While in water the irregularity of breathing further increased (apneas were >4 min) and all REM sleep episodes occurred during a single apnea. Data indicate that the pattern of sleep and breathing in walruses is similar to the Otariidae seals while on land and the Phocidae seals while in water.

The effects of testosterone on sleep and sleep-disordered breathing in men: Its bidirectional interaction with erectile function

As a major androgen with a key role in developing and maintaining male sexual characteristics, testosterone exerts a broad range of actions regulating several systems throughout human life. This article reviews data on the role of sleep in modulating endocrine release, as well as data on the effects of testosterone and androgen-replacement therapy on sleep architecture and breathing. This review also discusses the interaction of testosterone and sleep, with a particular emphasis on bilateral effects. Changes in nocturnal testosterone are sleep-related, with levels rising during sleep and falling on waking, whereas circadian effects are apparently marginal. Peak testosterone levels coincide with rapid-eye movement (REM) sleep onset. The decreasing sleep efficiency and numbers of REM sleep episodes with altered REM sleep latency observed in older men are associated with lower concentrations of circulating testosterone. The well-established male preponderance of sleep apnea suggests that sex hormones are involved in the pathogenesis of this breathing disorder. In addition, androgens are most certainly key players in the central and peripheral modulation of erectile function. Among other effects, sleep curtailment has been shown to lead to reduced levels of circulating androgens in healthy men and male rodents, and this highlights the biological significance of sleep homeostasis for endocrine regulation.

Rapid eye movement (REM) sleep homeostatic regulatory processes in the rat: Changes in the sleep–wake stages and electroencephalographic power spectra

The aim of this study was to elucidate physiological processes that are involved in the homeostatic regulation of REM sleep. Adult rats were chronically instrumented with sleep–wake recording electrodes. Following post-surgical recovery, rats were habituated extensively for freely moving polygraphic recording conditions. On the first experimental recording day (baseline day, BLD), polygraphic signs of undisturbed sleep–wake activities were recorded for 4 h (between 11:00 AM and 3:00 PM). During the second experimental recording day (REM sleep deprivation day, RDD), rats were selectively deprived of REM sleep for the first 2 h and then allowed to have normal sleep–wake for the following 2 h. The results demonstrated that during the first 2 h, compared to BLD, RDD recordings exhibited 87.80% less time in REM sleep and 16% more time in non-REM (NREM) sleep. The total percentages of wakefulness remained comparable between the BLD and RDD. During the RDD, the mean number of REM sleep episodes was much higher than in the BLD, indicating increased REM sleep drive. Electroencephalographic (EEG) power spectral analysis revealed that selective REM sleep deprivation increased delta power but decreased theta power during the residual REM sleep. During the last 2 h, after REM sleep deprivation, rats spent 51% more time in REM sleep compared to the BLD. Also during this period, the number of REM sleep episodes with the shortest (5–30 s) and longest (> 120 s) duration increased during the RDD. These findings suggest that the REM sleep homeostatic process involves increased delta- and decreased theta-frequency wave activities in the cortical EEG.

Increased EEG spectral power density during sleep following short‐term sleep deprivation in pigeons (Columba livia): evidence for avian sleep homeostasis

Birds provide a unique opportunity to evaluate current theories for the function of sleep. Like mammalian sleep, avian sleep is composed of two states, slow-wave sleep (SWS) and rapid eye-movement (REM) sleep that apparently evolved independently in mammals and birds. Despite this resemblance, however, it has been unclear whether avian SWS shows a compensatory response to sleep loss (i.e., homeostatic regulation), a fundamental aspect of mammalian sleep potentially linked to the function of SWS. Here, we prevented pigeons (Columba livia) from taking their normal naps during the last 8 h of the day. Although time spent in SWS did not change significantly following short-term sleep deprivation, electroencephalogram (EEG) slow-wave activity (SWA; i.e., 0.78-2.34 Hz power density) during SWS increased significantly during the first 3 h of the recovery night when compared with the undisturbed night, and progressively declined thereafter in a manner comparable to that observed in similarly sleep-deprived mammals. SWA was also elevated during REM sleep on the recovery night, a response that might reflect increased SWS pressure and the concomitant 'spill-over' of SWS-related EEG activity into short episodes of REM sleep. As in rodents, power density during SWS also increased in higher frequencies (9-25 Hz) in response to short-term sleep deprivation. Finally, time spent in REM sleep increased following sleep deprivation. The mammalian-like increase in EEG spectral power density across both low and high frequencies, and the increase in time spent in REM sleep following sleep deprivation suggest that some aspects of avian and mammalian sleep are regulated in a similar manner.

Predator-induced plasticity in sleep architecture in wild-caught Norway rats (Rattus norvegicus)

Sleep is a prominent behaviour in the lives of animals, but the unresponsiveness that characterizes sleep makes it dangerous. Mammalian sleep is composed of two neurophysiological states: slow wave sleep (SWS) and rapid-eye-movement (REM) sleep. Given that the intensity of stimuli required to induce an arousal to wakefulness is highest during deep SWS or REM sleep, mammals may be most vulnerable during these states. If true, then animals should selectively reduce deep SWS and REM sleep following an increase in the risk of predation. To test this prediction, we simulated a predatory encounter with 10 wild-caught Norway rats (Rattus norvegicus), which are perhaps more likely to exhibit natural anti-predator responses than laboratory strains. Immediately following the encounter, rats spent more time awake and less time in SWS and REM sleep. The reduction of SWS was due to the shorter duration of SWS episodes, whereas the reduction of REM sleep was due to a lower number of REM sleep episodes. The onset of SWS and REM sleep was delayed post-encounter by about 20 and 100min, respectively. The reduction of REM sleep was disproportionately large during the first quarter of the sleep phase, and slow wave activity (SWA) (0.5–4.5Hz power density) was lower during the first 10min of SWS post-encounter. An increase in SWA and REM sleep was observed later in the sleep phase, which may reflect sleep homeostasis. These results suggest that aspects of sleep architecture can be adjusted to the prevailing risk of predation.

Iron deficiency anemia in infancy is associated with altered temporal organization of sleep states in childhood.

The highest prevalence of iron deficiency anemia (IDA) in infancy coincides with a time of rapid changes in sleep organization. Since IDA in infancy is associated with long-lasting neurofunctional effects despite iron treatment, the normal development of sleep patterns might be affected. Night polysomnographic recordings were performed in 55 healthy 4-y-old children (former IDA = 27, nonanemic controls = 28). Both groups were followed from infancy and were similar in background characteristics. The duration of each waking episode was measured, as was the duration of each episode of nonrapid eye movement (NREM) sleep stages 1 (NREM1), 2 (NREM2), and 3-4 (SWS), and rapid eye movement (REM) sleep. The data were analyzed according to the successive thirds of the total sleep time (TST). Relative to controls, former IDA children showed: a) longer duration of REM sleep episodes in the first third and shorter in the last third; b) more REM sleep episodes in the first third and fewer in the second third; and c) shorter latency to the first REM sleep episode and shorter NREM stage 2 and SWS episodes within the first sleep cycle. The results show that early IDA is associated with long-lasting alterations in the temporal organization of sleep patterns.

Differential effects of psychological and physical stress on the sleep pattern in rats.

In the present study, we investigated the acute effects of 2 different kinds of stress, namely physical stress (foot shock) and psychological stress (non-foot shock) induced by the communication box method, on the sleep patterns of rats. The sleep patterns were recorded for 6 h immediately after 1 h of stress. Physical and psychological stress had almost opposite effects on the sleep patterns: In the physical stress group, hourly total rapid eye movement (REM) sleep and total non-REM sleep were significantly inhibited, whereas psychological stress enhanced hourly total REM sleep but not total non-REM sleep. Further results showed that total REM sleep, total non-REM sleep, total sleep and the total number of REM sleep episodes in 5 h were reduced, and that sleep latency was prolonged compared to the control group. On the other hand, in the psychological stress group, the total REM sleep in 5 h was increased significantly due to the prolongation of the average duration of REM sleep episodes and reduced REM sleep latency. In addition, the plasma of corticosterone increased significantly after physical stress but not after psychological stress. These results suggested that the sleep patterns, particularly the patterns of REM sleep following physical and psychological stress, are probably regulated by 2 different pathways.

Short light–dark cycles affect sleep in mice

Environmental light has a strong impact on human physiology and behaviour, including cognitive functioning and alertness. Previous studies have shown that short light-dark (LD) cycles influence sleep in the albino rat. Rapid eye movement (REM) sleep increases after the onset of darkness and increases after light onset. In the present study, we investigated whether light affects sleep in mice. To this purpose the electroencephalogram and electromyogram of nine adult male C57BL/6 mice was recorded under 12 : 12 h baseline LD conditions, followed by 24 h continuous darkness (DD) and 6 days with LD cycles of different durations (2 h, 30 min, 14 min, 10 min, 4 min and 2 min), presented in a randomized order. NREM sleep was evenly distributed over the light and dark intervals of all short LD cycles. REM sleep, however, was increased during the dark intervals of short (10-30 min) LD cycles. Analysis showed that in these LD cycles, the increment in REM sleep was maximal in the second minute after dark onset, where the percentage of epochs with REM sleep increased significantly to 175% of baseline values. This increase was attributable to an increase in REM sleep episode duration. The recorded responses show that sleep in mice is affected by photic stimulation. The results demonstrate that pigmented animals can show REM sleep induction after dark onset and indicate that light has significant effects on the regulation of sleep.

The effects of atropine on changes in the sleep patterns induced by psychological stress in rats

The present study was designed to investigate the acute effects of psychological stress on the sleep patterns of rats and the potential mechanisms underlying these effects. Psychological stress was induced using a communication box. In a preliminary study, sleep recording was performed for 6 h immediately after 1-h stress in rats. The results showed that psychological stress significantly enhanced the total amount of rapid eye movement (REM) sleep by prolonging the average duration of REM sleep episodes during first 3 h of sleep, whereas the total amount of non-rapid eye movement sleep was not influenced. In a second study, three doses of atropine (3, 10, or 30 nmol) were intracerebroventricularly microinjected into the rats. Total REM sleep was inhibited by the highest dose of atropine during the first 3 h of sleep in the stressed group but not in the control group; the inhibition of total REM sleep was due to a reduction in the average duration of REM sleep episodes. These results suggest that the increase in total REM sleep induced by stress was related to the activation of cholinergic neurons. In addition, plasma corticosterone—an index of hypothalamic–pituitary–adrenal (HPA) axis activity in response to stress—was examined after psychological stress. The concentration of corticosterone did not change significantly. Therefore, the abnormal sleep patterns could not be simply attributed to the HPA axis. These results indicate that the changes in sleep patterns induced by stress were related to cholinergic neurons, but not the HPA axis.

Ultradian cycles in mice: definitions and links with REMS and NREMS

Sleep can be organized in two quite different ways across homeothermic species: either in one block (monophasic), or in several bouts across the 24 h (polyphasic). Yet, the main relationships between variables, as well as regulating mechanisms, are likely to be similar. Correlations and theories on sleep regulation should thus be examined on both types of sleepers. In previous studies on monophasic humans, we have shown preferential links between the number of ultradian cycles and the rapid eye movement sleep (REMS) time, rather than with its counterpart non-rapid eye movement sleep (NREMS). Here, the sleep of 26 polyphasic mice was examined, both to better describe the NREMS distribution, which is far more complex than in humans, and to replicate the analyses performed on humans. As in humans, the strongest links with the number of cycles were with REMS. Links were not significant with NREMS taken as a whole, although positive correlations were found with the NREMS immediately preceding REMS episodes and inversely significant with the residue. This convergence between monophasic and polyphasic patterns supports the central role played by REMS in sleep alternation.