Showing papers on "Slow-wave sleep published in 1999"

Reactivation of Hippocampal Cell Assemblies: Effects of Behavioral State, Experience, and EEG Dynamics

Abstract: During slow wave sleep (SWS), traces of neuronal activity patterns from preceding behavior can be observed in rat hippocampus and neocortex. The spontaneous reactivation of these patterns is manifested as the reinstatement of the distribution of pairwise firing-rate correlations within a population of simultaneously recorded neurons. The effects of behavioral state [quiet wakefulness, SWS, and rapid eye movement (REM)], interactions between two successive spatial experiences, and global modulation during 200 Hz electroencephalographic (EEG) "ripples" on pattern reinstatement were studied in CA1 pyramidal cell population recordings. Pairwise firing-rate correlations during often repeated experiences accounted for a significant proportion of the variance in these interactions in subsequent SWS or quiet wakefulness and, to a lesser degree, during SWS before the experience on a given day. The latter effect was absent for novel experiences, suggesting that a persistent memory trace develops with experience. Pattern reinstatement was strongest during sharp wave-ripple oscillations, suggesting that these events may reflect system convergence onto attractor states corresponding to previous experiences. When two different experiences occurred in succession, the statistically independent effects of both were evident in subsequent SWS. Thus, the patterns of neural activity reemerge spontaneously, and in an interleaved manner, and do not necessarily reflect persistence of an active memory (i.e., reverberation). Firing-rate correlations during REM sleep were not related to the preceding familiar experience, possibly as a consequence of trace decay during the intervening SWS. REM episodes also did not detectably influence the correlation structure in subsequent SWS, suggesting a lack of strengthening of memory traces during REM sleep, at least in the case of familiar experiences.

Ageing and the circadian and homeostatic regulation of human sleep during forced desynchrony of rest, melatonin and temperature rhythms

Abstract: 1. The circadian timing system has been implicated in age-related changes in sleep structure, timing and consolidation in humans. 2. We investigated the circadian regulation of sleep in 13 older men and women and 11 young men by forced desynchrony of polysomnographically recorded sleep episodes (total, 482; 9 h 20 min each) and the circadian rhythms of plasma melatonin and core body temperature. 3. Stage 4 sleep was reduced in older people. Overall levels of rapid eye movement (REM) sleep were not significantly affected by age. The latencies to REM sleep were shorter in older people when sleep coincided with the melatonin rhythm. REM sleep was increased in the first quarter of the sleep episode and the increase of REM sleep in the course of sleep was diminished in older people. 4. Sleep propensity co-varied with the circadian rhythms of body temperature and plasma melatonin in both age groups. Sleep latencies were longest just before the onset of melatonin secretion and short sleep latencies were observed close to the temperature nadir. In older people sleep latencies were longer close to the crest of the melatonin rhythm. 5. In older people sleep duration was reduced at all circadian phases and sleep consolidation deteriorated more rapidly during the course of sleep, especially when the second half of the sleep episode occurred after the crest of the melatonin rhythm. 6. The data demonstrate age-related decrements in sleep consolidation and increased susceptibility to circadian phase misalignment in older people. These changes, and the associated internal phase advance of the propensity to awaken from sleep, appear to be related to the interaction between a reduction in the homeostatic drive for sleep and a reduced strength of the circadian signal promoting sleep in the early morning.

Effects of early and late nocturnal sleep on priming and spatial memory

Abstract: A wordstem priming task (nondeclarative memory), and a mental spatial rotation task (declarative memory) were presented to subjects of an experimental "sleep" group (n = 11) and of a "wake" control group (n = 10). Repetition priming effects and recall of spatial memory were tested after 3-hr retention intervals, which followed learning and were placed either in the early or in the late half of the night. Sleep group subjects slept during the retention intervals while subjects of the wake group stayed awake. As expected, early retention sleep was dominated by slow wave sleep (SWS), whereas rapid eye movement (REM) sleep prevailed during late retention sleep. After early retention sleep, recall of spatial memory was superior to that after late retention sleep (p < 0.01), and also to that after retention intervals of wakefulness (p < 0.05). In contrast, priming was more effective after late than early retention sleep (p < 0.05). It appears that early sleep dominated by SWS facilitates consolidation of declarative memory whereas late sleep dominated by REM sleep facilitates consolidation of nondeclarative memory.

Night terrors, sleepwalking, and confusional arousals in the general population: their frequency and relationship to other sleep and mental disorders.

Abstract: BACKGROUND: Arousal parasomnias (night terrors, sleepwalking, and confusional arousals) have seldom been investigated in the adult general population. Clinical studies of parasomnias, however, show that these disorders may be indicators of underlying mental disorders and may have serious consequences. METHOD: A representative sample of the United Kingdom population (N = 4972) was interviewed by telephone with the Sleep-EVAL system. RESULTS: Night terrors were reported by 2.2% (95% CI = 1.8% to 2.6%) of the sample, sleepwalking by 2.0% (1.6% to 2.4%), and confusional arousals by 4.2% (3.6% to 4.8%). The rate of these 3 parasomnias decreased significantly with age, but no gender difference was observed. Multivariate models identified the following independent factors as associated with confusional arousals (odds ratio [OR]): age of 15-24 years (OR = 4.1), shift work (OR = 2.1), hypnagogic hallucinations (OR = 3.3), deep sleep (OR = 1.6), daytime sleepiness (OR = 1.9), sleep talking (OR = 1.7), daily smoking (OR = 1.7), adjustment disorder (OR = 3.1), and bipolar disorder (OR = 13.0). Factors associated with night terrors were subjective sense of choking or blocked breathing at night (OR = 5.1), obstructive sleep apnea syndrome (OR = 4.1), alcohol consumption at bedtime (OR = 3.9), violent or injury-causing behaviors during sleep (OR = 3.2), hypnagogic hallucinations (OR = 2.2), and nightmares at least 1 night per month (OR = 4.0). Factors associated with sleepwalking were age of 15-24 years (OR = 5.2), subjective sense of choking or blocked breathing at night (OR = 5.1), sleep talking (OR = 5.0), and a road accident in the past year (OR = 3.9) after controlling for possible effects of sleep deprivation, life stress, and mental and sleep disorders. CONCLUSION: Arousal parasomnias, especially night terrors and confusional arousals, are often the expression of a mental disorder. Other life or medical conditions, such as shift work or excessive need of sleep for confusional arousals and stressful events for sleepwalking, may also trigger parasomnias. Prevalence rates are based on self-reported data and, consequently, are likely underestimated. Language: en

Effects of selective slow wave sleep disruption on musculoskeletal pain and fatigue in middle aged women.

Abstract: Objective. To determine whether disrupted slow wave sleep (SWS) would evoke musculoskeletal pain, fatigue, and an alpha electroencephalograph (EEG) sleep pattern. We selectively deprived 12 healthy, middle aged, sedentary women without muscle discomfort of SWS for 3 consecutive nights. Effects were assessed for the following measures: polysomnographic sleep, musculoskeletal tender point pain threshold, skinfold tenderness, reactive hyperemia (inflammatory flare response), somatic symptoms, and mood state. Methods. Sleep was recorded and scored using standard methods. On selective SWS deprivation (SWSD) nights, when delta waves (indicative of SWS) were detected on EEG, a computer generated tone (maximum 85 decibels) was delivered until delta waves disappeared. Musculoskeletal tender points were measured by dolorimetry; skinfold tenderness was assessed by skin roll procedure; and reactive hyperemia was assessed with a cotton swab test. Subjects completed questionnaires on bodily feelings, symptoms, and mood. Results. On each SWSD night, SWS was decreased significantly with minimal alterations in total sleep time, sleep efficiency, and other sleep stages. Subjects showed a 24% decrease in musculoskeletal pain threshold after the third SWSD night. They also reported increased discomfort, tiredness, fatigue, and reduced vigor. The flare response (area of vasodilatation) in skin was greater than baseline after the first, and again, after the third SWSD night. However, the automated program for SWSD did not evoke an alpha EEG sleep pattern. Conclusion. Disrupting SWS, without reducing total sleep or sleep efficiency, for several consecutive nights is associated with decreased pain threshold, increased discomfort, fatigue, and the inflammatory flare response in skin. These results suggest that disrupted sleep is probably an important factor in the pathophysiology of symptoms in fibromyalgia.

Effects of sleep and sleep deprivation on catecholamine and interleukin-2 levels in humans: clinical implications.

Abstract: The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on catecholamine and interleukin-2 (IL-2) levels in humans. Circulating levels of catecholamines and IL-2 were sampled every 30 min during 2 nights: undisturbed, baseline sleep and partial sleep deprivation-late night (PSD-L; awake from 0300-0600 h) in 17 healthy male volunteers. Sleep was monitored somnopolygraphically. Sleep onset was associated with a significant (P < 0.05) decline of circulating concentrations of norepinephrine and epinephrine, with a nocturnal nadir that occurred 1 h after nocturnal sleep. On the PSD-L night, levels of norepinephrine and epinephrine significantly (P < 0.05) increased in association with nocturnal awakening. During stage 3-4 sleep, levels of norepinephrine, but not epinephrine, were significantly lower (P < 0.05) compared to average levels during the awake period, stages 1-2 sleep, and rapid eye movement sleep. Nocturnal levels of circulating IL-2 did not change with sleep onset or in relation to PSD-L or the various sleep stages. We conclude that sleep onset is associated with changes in levels of circulating catecholamines. Loss of sleep and disordered sleep with decreases in slow wave sleep may serve to elevate nocturnal catecholamine levels and contribute to cardiovascular disease.

Genetic determinants of sleep regulation in inbred mice.

Abstract: Genetic variation in the expression and regulation of sleep was assessed in six inbred mice strains (AK, C, B6, BR, D2, 129). The amount, distribution, and fragmentation of the behavioral states wakefulness (W), slow-wave sleep (SWS), and paradoxical sleep (PS), as well as EEG delta power in SWS, were determined and compared among strains and between baseline and recovery from a 6-hour sleep deprivation (SD) starting at lights-on. In baseline, the most striking strain differences concerned sleep amount, the onset and duration of the main rest period, and SWS fragmentation. The time course of delta power in SWS during the main rest period was similar between strains. Immediately following the SD, high delta power values were reached (higher for AK than for 129). However, the relative increase in delta power, compared to the first 6 hours of the baseline rest period, was not strain-specific. Over the first 6 hours of recovery, W was decreased and PS increased in AK, B6, BR, and 129. In C and D2, time spent in any of the states was not affected by the SD. In contrast, in the recovery dark period, SWS and PS were invariably increased. In recovery, SWS fragmentation was strongly reduced for D2, resulting in the disappearance of the strain differences observed in baseline. Since these inbred strains are fully homozygous and thus can be considered genetic clones, the sleep-related strain differences reported here can be attributed to differences in genotype. Therefore, this study provides a basis for the identification of genetic factors underlying sleep and its regulation.

Sleep deprivation effects on the activity of the hypothalamic–pituitary–adrenal and growth axes: potential clinical implications

Abstract: OBJECTIVES Although several studies have shown that sleep deprivation is associated with increased slow wave sleep during the recovery night, the effects of sleep deprivation on cortisol and growth hormone (GH) secretion the next day and recovery night have not been assessed systematically. We hypothesized that increased slow wave sleep postsleep deprivation is associated with decreased cortisol levels and that the enhanced GH secretion is driven by the decreased activity of the HPA axis. DESIGN AND SUBJECTS After four consecutive nights in the Sleep Laboratory, 10 healthy young men were totally deprived of sleep during the fifth night, and then allowed to sleep again on nights six and seven. Twenty-four hour blood sampling was performed serially every 30 minutes on the fourth day, immediately following the previous night of sleep and on the sixth day, immediately after sleep deprivation. MEASUREMENT Eight-hour sleep laboratory recording, including electroencephologram, electro-oculogram and electromyogram. Plasma cortisol and GH levels using specific immunoassay techniques. RESULTS Mean plasma and time-integrated (AUC) cortisol levels were lower during the postdeprivation nighttime period than on the fourth night (P < 0.05). Pulsatile analysis showed significant reduction of both the 24 h and daytime peak area (P < 0.05) and of the pulse amplitude (P < 0.01), but not of the pulse frequency. Also, the amount of time-integrated GH was significantly higher for the first 4 h of the postdeprivation night compared to the predeprivation night (P < 0.05). Cross-correlation analyses between the absolute values of the time-series of each hormone value and percentage of each sleep stage per half hour revealed that slow wave sleep was negatively correlated with cortisol and positively correlated with GH with slow wave sleep preceding the secretion of these hormones. In contrast, indices of sleep disturbance, i.e. wake and stage 1 sleep, were positively correlated with cortisol and negatively correlated with GH. CONCLUSION We conclude that sleep deprivation results in a significant reduction of cortisol secretion the next day and this reduction appears to be, to a large extent, driven by the increase of slow wave sleep during the recovery night. We propose that reduction of CRH and cortisol secretion may be the mechanism through which sleep deprivation relieves depression temporarily. Furthermore, deep sleep has an inhibitory effect on the HPA axis while it enhances the activity of the GH axis. In contrast, sleep disturbance has a stimulatory effect on the HPA axis and a suppressive effect on the GH axis. These results are consistent with the observed hypocortisolism in idiopathic hypersomnia and HPA axis relative activation in chronic insomnia. Finally, our findings support previous hypotheses about the restitution and immunoenhancement role of slow wave (deep) sleep.

Brain Gene Expression During REM Sleep Depends on Prior Waking Experience

Abstract: In most mammalian species studied, two distinct and successive phases of sleep, slow wave (SW), and rapid eye movement (REM), can be recognized on the basis of their EEG profiles and associated behaviors. Both phases have been implicated in the offline sensorimotor processing of daytime events, but the molecular mechanisms remain elusive. We studied brain expression of the plasticity-associated immediate-early gene (IEG) zif-268 during SW and REM sleep in rats exposed to rich sensorimotor experience in the preceding waking period. Whereas nonexposed controls show generalized zif-268 down-regulation during SW and REM sleep, zif-268 is upregulated during REM sleep in the cerebral cortex and the hippocampus of exposed animals. We suggest that this phenomenon represents a window of increased neuronal plasticity during REM sleep that follows enriched waking experience.

Heart rate variability during waking and sleep in healthy males and females.

Abstract: Study Objectives: The study goal was to investigate autonomic activity with heart rate variability analysis during different sleep stages in males and females. Design: The study utilized a 2 Groups (males, females) X 4 States (waking, stage 2 sleep, stage 4 sleep, rapid-eye movement sleep) mixed design with one repeated, within-subjects factor (i.e., state). Setting: The study was carried out in the sleep laboratory of the Thomas N. Lynn Institute for Healthcare Research. Participants: Twenty-four healthy adults (fourteen females and ten males). Interventions: NA Measurements and Results: All participants underwent polysomnographic monitoring and electrocardiogram recordings during pre-sleep waking and one night of sleep. Fifteen-minute segments of beat-to-beat heart rate intervals during waking, stage 2 sleep, stage 4 sleep, and REM sleep were subjected to spectral analysis. Compared to NREM sleep, REM sleep was associated with decreased high frequency (HF) band power, and significantly increased low frequency (LF) to (HF) ratio. Compared to females, males showed significantly elevated LF/HF ratio during REM sleep. Males also demonstrated significantly decreased HF band power during waking when compared to females. No significant sleep- or gender-related changes in LF band power were found. Conclusions: The results confirmed changes in autonomic activity from waking to sleep, with marked differences between NREM and REM sleep. These changes were primarily due to stage-related alterations in vagal tone. REM sleep was characterized by increased sympathetic dominance, secondary to vagal withdrawal. The data also suggested gender differences in autonomic functioning during waking and sleep, with decreased vagal tone during waking and increased sympathetic dominance during REM sleep in the males.

Melatonin as a therapy in REM sleep behavior disorder patients: an open-labeled pilot study on the possible influence of melatonin on REM-sleep regulation.

Abstract: REM sleep behavior disorder (RBD) is clinically impressive by virtue of its vigorous sleep behaviors usually accompanying vivid, striking dreams. The main feature of the disorder, REM sleep without muscle atonia, has been shown in a variety of diseases; therefore, the disorder might possibly be underestimated. In an open-labeled trial, we treated six consecutive RBD patients over a 6-week period with 3 mg melatonin given within 30 minutes before bedtime. There was a dramatic clinical improvement in five of the six patients within a week which extended beyond the end of treatment for weeks or months. A second polysomnogram performed 6 weeks after the beginning of treatment showed a significant tendency toward normalization of the percentage of REM sleep, a significant reduction of 30-second epochs, scored as REM sleep without muscle atonia, a significant reduction of stage-shifts in REM, and a significant reduction in epochs considered as movement time in REM. All other sleep parameters were not changed consistently. We hypothesize that internal desynchrony might be a part of the underlying pathophysiology in RBD. Our data might give first evidence to the hypothesis that exogenous melatonin, administered to patients with internal desynchrony at the time of the maximal rise of melatonin secretion, might increase the overall amplitude of the circadian pacemaker by reentraining the suprachiasmatic nucleus and thereby restore circadian driven rhythms, one of them being the circadian modulation of REM sleep.

Effects of method, duration, and sleep stage on rebounds from sleep deprivation in the rat

Abstract: Total sleep deprivation (TSD) of rats for 24 hours or less by continually enforced locomotion has consistently produced subsequent rebounds of slow-wave or high-amplitude EEG activity in NREM sleep, which has contributed to the widely held view that this EEG activity reflects particularly "intense" or restorative sleep. These rebounds usually have been accompanied by substantial rebounds of REM sleep. In contrast, chronic TSD (2 weeks or longer) by the disk-over-water (DOW) method has produced only huge, long-lasting rebounds of REM sleep with no rebound of high-amplitude NREM sleep. To evaluate whether the different rebounds result from different methods or from different lengths of deprivation, rats were subjected to 24-hour TSD by the DOW method. Rebounds included increases in high-amplitude and slow-wave activity; i.e., the methods produced similar rebound patterns following short-term TSD. (Chronic TSD by continually enforced locomotion would be strategically difficult and severely confounded with motor fatigue.) Rats subjected to DOW-TSD for 4 days, well before the development of severe TSD symptoms, showed primarily REM sleep rebounds. Rats subjected to 1 day of selective REM sleep deprivation, but not their closely yoked control rats, showed large, significant REM sleep rebounds, which evidently were not induced by the stress of the deprivation method per se. The combined findings prompted reexamination of published evidence relevant to "sleep intensity," including "negative rebounds," rebounds in other species, the effects of stress and fatigue, depth of sleep indicators, and extended sleep. The review points out pitfalls in the designation of any specific pattern as intense sleep.

Effect of mouth leak on effectiveness of nasal bilevel ventilatory assistance and sleep architecture

Abstract: Mouth leak is common during nasal ventilatory assistance, but its effects on ventilatory support and on sleep architecture are unknown. The acute effect of sealing the mouth on sleep architecture and transcutaneous carbon dioxide tension (Ptc,CO2) was tested in 9 patients (7 hypercapnic) on longterm nasal bilevel ventilation with symptomatic mouth leak. Patients slept with nasal bilevel ventilation at their usual settings on two nights in random order. On one night, the mouth was taped closed. Leak was measured with a pneumotachograph. Median leak fell from 0.35+/-0.07 (mean +/- SEM) L x s(-1) untaped to 0.06+/-0.03 L x s(-1) taped. Ptc,CO2 fell in 8/9, including all hypercapnic patients. Across all patients, the mean Ptc,CO2 fell by 1.02+/-0.28 kPa (7.7+/-2.1 mm Hg) with taping (p = 0.007). Arousal index fell in every patient. Mean arousal index fell from 35.0+/-3.0 to 13.9+/-1.2 h(-1) (p<0.0001), and rapid eye movement (REM) sleep increased from 12.9+/-1.5% to 21.1+/-1.8% sleep time (p = 0.0016). Slow wave sleep changed inconsistently, from a mean of 13.1+/-1.6% to 19.5+/-2.2% of sleep (p = 0.09). Sleep latency and efficiency were unchanged. In four healthy volunteers ventilator-induced awake hypopharyngeal pressure swing during timed bilevel ventilation fell by 35+/-5% L(-1) x s(-1) of voluntary mouth leak (p<0.0001). Mouth leak reduces effective nasal bilevel ventilatory support, increases transcutaneous carbon dioxide tension, and disrupts sleep architecture.

Memory consolidation in human sleep depends on inhibition of glucocorticoid release.

Abstract: Early sleep dominated by slow-wave sleep has been found to be particularly relevant for declarative memory formation via hippocampo-neocortical networks. Concurrently, early nocturnal sleep is characterized by an inhibition of glucocorticoid release from the adrenals. Here, we show in healthy humans that this inhibition serves to support declarative memory consolidation during sleep. Elevating plasma glucocorticoid concentration during early sleep by administration of cortisol impaired consolidation of paired associate words, but not of non-declarative memory of visuomotor skills. Since glucocorticoid concentration was enhanced only during retention sleep, but not during acquisition or retrieval, a specific effect on the consolidation process is indicated. Blocking mineralocorticoid receptors by canrenoate did not affect memory, suggesting inactivation of glucocorticoid receptors to be the essential prerequisite for memory consolidation during early sleep.

Circadian regulation of human sleep and age-related changes in its timing, consolidation and EEG characteristics.

Abstract: The light-entrainable circadian pacemaker located in the suprachiasmatic nucleus of the hypothalamus regulates the timing and consolidation of sleep by generating a paradoxical rhythm of sleep propensity; the circadian drive for wakefulness peaks at the end of the day spent awake, ie close to the onset of melatonin secretion at 21.00-22.00 h and the circadian drive for sleep crests shortly before habitual waking-up time. With advancing age, ie after early adulthood, sleep consolidation declines, and time of awakening and the rhythms of body temperature, plasma melatonin and cortisol shift to an earlier clock hour. The variability of the phase relationship between the sleep-wake cycle and circadian rhythms increases, and in old age sleep is more susceptible to internal arousing stimuli associated with circadian misalignment. The propensity to awaken from sleep advances relative to the body temperature nadir in older people, a change that is opposite to the phase delay of awakening relative to internal circadian rhythms associated with morningness in young people. Age-related changes do not appear to be associated with a shortening of the circadian period or a reduction of the circadian drive for wake maintenance. These changes may be related to changes in the sleep process itself, such as reductions in slow-wave sleep and sleep spindles as well as a reduced strength of the circadian signal promoting sleep in the early morning hours. Putative mediators and modulators of circadian sleep regulation are discussed.

Modeling hypersomnolence in sleep-disordered breathing. A novel approach using survival analysis.

Abstract: The etiology of excessive daytime sleepiness in patients with sleep-disordered breathing (SDB) is not well defined. In this study, we examined the relationships between several clinical and polysomnographic parameters and the degree of hypersomnolence in 741 patients with SDB (apnea-hypopnea index [AHI] >/= 10 events/h). The study sample was obese (body mass index [BMI]: 35.3 +/- 8.5 kg/m2) and had evidence of moderate SDB (AHI: 47.6 +/- 29.3 events/h). Hypersomnolence was quantified with the multiple sleep latency test (MSLT) and survival analysis was used to assess the risk factors for hypersomnolence. In a multivariate proportional hazards model, AHI and nocturnal hypoxemia were independent predictors of hypersomnolence (MSLT /= 60 events/h, respectively. A positive association between hypersomnolence and oxyhemoglobin desaturation (DeltaSaO2) was observed with RR of 1.00, 1.18, 1.43, and 1.94 for a DeltaSaO2 of 15%, respectively. Sleep fragmentation, as assessed by the distribution of sleep stages, was also an independent predictor of hypersomnolence. Using stage 1 sleep as a reference, an increase in stage 2 and slow wave sleep (SWS) were protective from hypersomnolence. For a 10% increase in stage 2 or SWS the adjusted RR for hypersomnolence were 0.93 and 0.79, respectively. REM sleep showed no significant association with the degree of hypersomnolence. These results suggest that AHI, nocturnal hypoxemia, and sleep fragmentation are independent determinants of hypersomnolence in SDB.

Rapid Eye Movement Sleep

Abstract: Eyelid Condition at Birth: Relationship to Adult Mammalian Sleep-waking Patterns, E Aserinsky Phylogeny and Evolution of Rapid Eye Movement (REM) Sleep, M G Frank Ontogenesis of REM Sleep, M Segawa Initiation of Rapid Eye Movement Sleep: Beyond the Brainstem, A R Morrison, L D Sanford, and R J Ross Muscle Atonia in REM Sleep, Y -Y Lai and J M Siegel PGO Wave Generation: Mechanism and Functional Significance, S Datta Norepinephrine and REM Sleep, P-H Luppi, D Gervasoni, C Peyron, C Rampon, B Barbagli, R Boissard, and P Fort New Directions for the Study of Cholinergic REM Sleep Generation: Specifying Pre- and Postsynaptic Mechanisms, M L Capece, H A Baghdoyan, and R Lydic Functional Role of Serotonin 5-HT1 and 5-HT2 Receptor in the Regulation of REM Sleep, J M Monti and D Monti Possible Role of GABA in the Regulation of REM Sleep with Special Reference to REM-OFF Neurons, B N Mallick, S Kaur, S K Jha, and J M Siegel Nitric Oxide: A Diffusible Modulator of Physiological Traits and Behavioral States, T O Leonard and R Lydic Neurotransmitters Changes and REM Sleep, T Kodama Spatio-Temporal Distribution of Neuronal Activities and REM Sleep, S Inoue, U K Saha, and T Musha Different Physiological Properties of Two Populations of PS-on Neurons in the Mesopontine Tegmentum, Y Koyama, Y Kayama, and K Sakai Hormones and REM Sleep, F Obal Jr and J M Krueger Endogenous Sleep Substances and REM Sleep, S Inoue, K Honda, M Kimura, and S-Q Zhang Brain Energy, Production, and Sleep Occurrence, R Cespuglio, H Faradji-Prevautel, and L Netchiporouk Rapid Eye Movement Sleep: From Cerebral Metabolism to Functional Brain Mapping, P Maquet and C Phillips REM Sleep and Apnea, D W Carley and M Radulovacki Thermoregulatory Control of the nonREM-REM Sleep Cycle, R Szymusiak, Md Noor Alam, and D McGinty REM Sleep Across Age and Sex, K Mishima, T Shimizu, and Y Hishikawa The Function of Fetal/Neonatal REM Sleep, M Mirmiran and Y G H Maas REM Sleep Deprivation Alters Factors Affecting Neuronal Excitability: Role of Norepinephrine and Its Possible Mechanism of Action, B N Mallick, H V A Adya, and s Thankachan REM Sleep Deprivation and Behavioral Changes, G W Vogel Cellular and Molecular Changes Occurring During REM Sleep, O Prospero-Garcia, L Navarro, E Murillo-Rodriguez, M Sanchez-Alavez, R Guzman-Marin, M Mendez-Diaz, M Gomez-Chavarin, A Jimenez-Anguiano, and R Drucker-Colin Intensity of REM Sleep, K Takahashi Why We Believe What We Believe About REM-Sleep Regulation, H Benington Hypothesis on REM Sleep from the Viewpoint of Neuronal Dynamics, M Nakao and M Yamamoto

The effects of leptin on REM sleep and slow wave delta in rats are reversed by food deprivation

Abstract: Leptin (ob protein) is an adipose tissue derived circulating hormone that acts at specific receptors in the hypothalamus to reduce food intake. The protein is also critically involved in energy balance and metabolic status. Here the effect of leptin on sleep architecture in rats was evaluated because food consumption and metabolic status are known to influence sleep. Sprague-Dawley rats were chronically implanted with electrodes for EEG and EMG recording and diurnal sleep parameters were quantified over 9-h periods following leptin administration. Murine recombinant leptin (rMuLep) was administered systemically to rats that either had undergone 18 h of prior food deprivation or had received food ad libitum. In the normally fed rats, leptin significantly decreased the duration of rapid eye movement sleep (REMS) by about 30% and increased the duration of slow wave sleep (SWS) by about 13%, the latter effect reflecting enhanced power in the delta frequency band. These results are consistent with studies that have linked changes in metabolic rate with effects on sleep. Leptin administration has previously been shown to alter neuroendocrine parameters that could have mediated these changes in sleep architecture. Unexpectedly, prior food deprivation negated the effect of leptin on both REMS and SWS, a result that emphasizes the significance of the apparent coupling between sleep parameters and energy status.

High nocturnal body temperatures and disturbed sleep in women with primary dysmenorrhea.

Abstract: Primary dysmenorrhea is characterized by painful uterine cramps, near and during menstruation, that have an impact on personal life and productivity. The effect on sleep of this recurring pain has not been established. We compared sleep, nocturnal body temperatures, and hormone profiles during the menstrual cycle of 10 young women who suffered from primary dysmenorrhea, without any menstrual-associated mood disturbances, and 8 women who had normal menstrual cycles. Dysmenorrheic pain significantly decreased subjective sleep quality, sleep efficiency, and rapid eye movement (REM) sleep but not slow wave sleep (SWS), compared with pain-free phases of the menstrual cycle and compared with the controls. Even before menstruation, in the absence of pain, the women with dysmenorrhea had different sleep patterns, nocturnal body temperatures, and hormone levels compared with the controls. In the mid-follicular, mid-luteal, and menstrual phases, the dysmenorrheics had elevated morning estrogen concentrations, higher mean in-bed temperatures, and less REM sleep compared with the controls, as well as higher luteal phase prolactin levels. Both groups of women had less REM sleep when their body temperatures were high during the luteal and menstrual phases, implying that REM sleep is sensitive to elevated body temperatures. We have shown that dysmenorrhea is not only a disorder of menstruation but is manifest throughout the menstrual cycle. Furthermore, dysmenorrheic pain disturbs sleep, which may exacerbate the effect of the pain on daytime functioning.

Autonomic cardiovascular control in children with obstructive sleep apnea

Abstract: Autonomic cardiorespiratory control changes with sleep-wake states and is influenced by sleep-related breathing disorders. Power spectrum (PS) analysis of instantaneous fluctuations in heart rate (HR) is used to investigate the role of the autonomic nervous system (ANS) in cardiorespiratory control. The two spectral regions of interest are the low frequency component (LF) and high frequency component (HF). The aim of the present study was to investigate the autonomic cardiorespiratory control in children with obstructive sleep apnea (OSA) syndrome. We studied 10 children with OSA versus 10 normal children. All subjects underwent whole night polysomnography. Spectral analysis of the HR and breathing signals was performed for 256 second long, artifact-free epochs in each sleep-wake state. The LF power was higher in the OSA group compared with control subjects for all states, reflecting enhanced sympathetic activity in OSA subjects. The results indicated sympathetic predominance during REM sleep in all subjects and parasympathetic predominance in slow wave sleep only in controls. The autonomic balance (LF/HF) was significantly higher in OSA patients than in control subjects, at all stages during night sleep, and while awake before sleep onset. An index of overall autonomic balance (ABI) was computed for each subject and correlated well with the measured respiratory disturbance index (RDI).

The effects of sleep inertia on decision-making performance.

Abstract: Sleep inertia, the performance impairment that occurs immediately after awakening, has not been studied previously in relation to decision-making performance. Twelve subjects were monitored in the sleep laboratory for one night and twice awoken by a fire alarm (slow wave sleep, SWS and REM sleep). Decision making was measured over 10 3-min trials using the 'Fire Chief' computer task under conditions of baseline. SWS and REM arousal. The most important finding was that sleep inertia reduces decision-making performance for at least 30 min with the greatest impairments (in terms of both performance and subjective ratings) being found within 3 min after abrupt nocturnal awakening. Decision-making performance was as little as 51% of optimum (i.e. baseline) during these first few minutes. However, after 30 min. performance may still be as much as 20% below optimum. The initial effects of sleep inertia during the first 9 min are significantly greater after SWS arousal than after REM arousal, but this difference is not sustained. Decision-making performance after REM arousal showed more variability than after SWS arousal. Subjects reported being significantly sleepier and less clear-headed following both SWS and REM awakenings compared with baseline and this was sustained across the full 30 min. In order to generalize this finding to real-life situations, further research is required on the effects of continuous noise, emotional arousal and physical activity on the severity and duration of sleep inertia.

Sleep and activity rhythms are related to circadian phase in the blind.

Abstract: Study objectives: Sleep is controlled by both circadian and homeostatic mechanisms. As the light-dark cycle is the most important time cue in humans, blind individuals may have circadian rhythm disorders including sleep. The aim of the study was to assess sleep with simultaneous measurement of an endogenous marker of the circadian clock, namely 6-sulphatoxymelatonin (aMT6s). Setting and participants: 59 registered blind subjects were studied in their own homes. Design: Subjects completed daily sleep and nap diaries for at least four weeks, wore activity monitors continuously, and collected urine samples over 48 hours each week for 3-5 weeks for assessment of aMT6s rhythms. Results: The most sensitive indicator of a circadian rhythm disorder was day-time napping. Subjects with normally entrained (NE) aMT6s rhythms had fewer naps of a shorter duration than abnormally entrained (AE) or free- running (FR) subjects. The timing of these naps was not random; significantly more naps occurred within a five-hour range before and after the aMT6s acrophase (phi (I�)) than outside this range. Disorders in the timing and duration of night sleep in AE subjects manifested as either a permanent advance (advanced sleep phase syndrome, ASPS) or delay (delayed sleep phase syndrome, DSPS). In FR subjects there were transient advances and delays in sleep timing that paralleled aMT6s timing with increased night sleep duration and reduced number and duration of day-time naps associated with a normal aMT6s phase. Conclusions: Changes in sleep and activity rhythms reflect changes in circadian phase.

Changes in forebrain function from waking to REM sleep in depression: preliminary analyses of [18F]FDG PET studies.

Abstract: Based on recent functional brain imaging studies of healthy human REM sleep, we hypothesized that alterations in REM sleep in mood disorder patients reflect a functional dysregulation within limbic and paralimbic forebrain structures during that sleep state. Six unipolar depressed subjects and eight healthy subjects underwent separate [18F]2-fluoro-2-deoxy-d-glucose ([18F]FDG) PET scans during waking and during their first REM period of sleep. Statistical parametric mapping contrasts were performed to detect changes in relative regional cerebral glucose metabolism (rCMRglu) from waking to REM sleep in each group as well as interactions in patterns of change between groups. Clinical and EEG sleep comparisons from an undisturbed night of sleep were also performed. In contrast to healthy control subjects, depressed patients did not show increases in rCMRglu in anterior paralimbic structures in REM sleep compared to waking. Depressed subjects showed greater increases from waking to REM sleep in rCMRglu in the tectal area and a series of left hemispheric areas including sensorimotor cortex, inferior temporal cortex, uncal gyrus-amygdala, and subicular complex than did the control subjects. These observations indicate that changes in limbic and paralimbic function from waking to REM sleep differ significantly from normal in depressed patients.

Juvenile Parkinson’s disease with REM sleep behavior disorder, sleepiness, and daytime REM onset

Abstract: We describe an unmedicated patient with juvenile PD with difficulties maintaining wakefulness and the atonia of REM sleep. Laboratory testing showed enhanced muscle activity in REM sleep consistent with a history of dream enactment behavior (i.e., REM sleep behavior disorder) and daytime sleepiness, and REM-sleep onsets on multiple sleep latency testing. The results emphasize the potential role of dopamine and basal ganglia circuits in the modulation of activated behavioral states (e.g., wakefulness and REM sleep).