Showing papers on "Slow-wave sleep published in 2011"

Sleep and sleep disorders in older adults.

Abstract: A common but significant change associated with aging is a profound disruption to the daily sleep-wake cycle. It has been estimated that as many as 50% of older adults complain about difficulty initiating or maintaining sleep. Poor sleep results in increased risk of significant morbidity and mortality. Moreover, in younger adults, compromised sleep has been shown to have a consistent effect on cognitive function, which may suggest that sleep problems contribute to the cognitive changes that accompany older age. The multifactorial nature of variables affecting sleep in old age cannot be overstated. Changes in sleep have been thought to reflect normal developmental processes, which can be further compromised by sleep disturbances secondary to medical or psychiatric diseases (e.g., chronic pain, dementia, depression), a primary sleep disorder that can itself be age-related (e.g., Sleep Disordered Breathing and Periodic Limb Movements During Sleep), or some combination of any of these factors. Given that changes in sleep quality and quantity in later life have implications for quality of life and level of functioning, it is imperative to distinguish the normal age-related sleep changes from those originating from pathological processes.

Development of the Brain's Default Mode Network from Wakefulness to Slow Wave Sleep

Abstract: Falling asleep is paralleled by a loss of conscious awareness and reduced capacity to process external stimuli. Little is known on sleep-associated changes of spontaneously synchronized anatomical networks as detected by resting-state functional magnetic resonance imaging (rs-fMRI). We employed functional connectivity analysis of rs-fMRI series obtained from 25 healthy participants, covering all non-rapid eye movement (NREM) sleep stages. We focused on the default mode network (DMN) and its anticorrelated network (ACN) that are involved in internal and external awareness during wakefulness. Using independent component analysis, cross-correlation analysis (CCA), and intraindividual dynamic network tracking, we found significant changes in DMN/ACN integrity throughout the NREM sleep. With increasing sleep depth, contributions of the posterior cingulate cortex (PCC)/retrosplenial cortex (RspC), parahippocampal gyrus, and medial prefrontal cortex to the DMN decreased. CCA revealed a breakdown of corticocortical functional connectivity, particularly between the posterior and anterior midline node of the DMN and the DMN and the ACN. Dynamic tracking of the DMN from wakefulness into slow wave sleep in a single subject added insights into intraindividual network fluctuations. Results resonate with a role of the PCC/RspC for the regulation of consciousness. We further submit that preserved corticocortical synchronization could represent a prerequisite for maintaining internal and external awareness.

Labile or stable: opposing consequences for memory when reactivated during waking and sleep

Abstract: Memory reactivation underlying consolidation can occur during periods of sleep or in waking where wakeful memory reactivation is susceptible to disruption. Contrary to prior predictions, the authors find that memory reactivation during slow-wave sleep immediately stabilizes memories in the absence of REM sleep. Memory consolidation is a dynamic process. Reconsolidation theory assumes that reactivation during wakefulness transiently destabilizes memories, requiring them to reconsolidate in order to persist. Memory reactivation also occurs during slow-wave sleep (SWS) and is assumed to underlie the consolidating effect of sleep. Here, we tested whether the same principle of transient destabilization applies to memory reactivation during SWS. We reactivated memories in humans by presenting associated odor cues either during SWS or wakefulness. Reactivation was followed by an interference task to probe memory stability. As we expected, reactivation during waking destabilized memories. In contrast, reactivation during SWS immediately stabilized memories, thereby directly increasing their resistance to interference. Functional magnetic resonance imaging revealed that reactivation during SWS mainly activated hippocampal and posterior cortical regions, whereas reactivation during wakefulness primarily activated prefrontal cortical areas. Our results show that reactivation of memory serves distinct functions depending on the brain state of wakefulness or sleep.

Changes in Sleep as a Function of Adolescent Development

Abstract: Adolescence is marked by dramatic changes in sleep. Older adolescents go to bed later, have an increased preference for evening activities, and sleep less than younger adolescents. This behavior change is driven by external factors, notably increased pressures from academic, social, and extracurricular activities and by biological circadian factors. There are also substantial changes in sleep architecture across adolescence, with dramatic declines in slow wave sleep, and slow wave activity (delta, ~ 0.5–4.5 Hz). These changes are associated with underlying changes in brain structure and organization, with a decrease in synaptic density likely underlying the reduction in high amplitude slow waveforms. While changes in sleep across adolescence are a normal part of development, many adolescents are getting insufficient sleep and are consequently, less likely to perform well at school, more likely to develop mood-related disturbances, be obese, and are at greater risk for traffic accidents, alcohol and drug abuse.

Acute Optogenetic Silencing of Orexin/Hypocretin Neurons Induces Slow-Wave Sleep in Mice

Abstract: Orexin/hypocretin neurons have a crucial role in the regulation of sleep and wakefulness. To help determine how these neurons promote wakefulness, we generated transgenic mice in which orexin neurons expressed halorhodopsin (orexin/Halo mice), an orange light-activated neuronal silencer. Slice patch-clamp recordings of orexin neurons that expressed halorhodopsin demonstrated that orange light photic illumination immediately hyperpolarized membrane potential and inhibited orexin neuron discharge in proportion to illumination intensity. Acute silencing of orexin neurons in vivo during the day (the inactive period) induced synchronization of the electroencephalogram and a reduction in amplitude of the electromyogram that is characteristic of slow-wave sleep (SWS). In contrast, orexin neuron photoinhibition was ineffective during the night (active period). Acute photoinhibition of orexin neurons during the day in orexin/Halo mice also reduced discharge of neurons in an orexin terminal field, the dorsal raphe (DR) nucleus. However, serotonergic DR neurons exhibited normal discharge rates in mice lacking orexin neurons. Thus, although usually highly dependent on orexin neuronal activity, serotonergic DR neuronal activity can be regulated appropriately in the chronic absence of orexin input. Together, these results demonstrate that acute inhibition of orexin neurons results in time-of-day-dependent induction of SWS and in reduced firing rate of neurons in an efferent projection site thought to be involved in arousal state regulation. The results presented here advance our understanding of the role of orexin neurons in the regulation of sleep/wakefulness and may be relevant to the mechanisms that underlie symptom progression in narcolepsy.

Properties of Slow Oscillation during Slow-Wave Sleep and Anesthesia in Cats

Abstract: Deep anesthesia is commonly used as a model of slow-wave sleep (SWS). Ketamine-xylazine anesthesia reproduces the main features of sleep slow oscillation: slow, large-amplitude waves in field potential, which are generated by the alternation of hyperpolarized and depolarized states of cortical neurons. However, direct quantitative comparison of field potential and membrane potential fluctuations during natural sleep and anesthesia is lacking, so it remains unclear how well the properties of sleep slow oscillation are reproduced by the ketamine-xylazine anesthesia model. Here, we used field potential and intracellular recordings in different cortical areas in the cat to directly compare properties of slow oscillation during natural sleep and ketamine-xylazine anesthesia. During SWS cortical activity showed higher power in the slow/delta (0.1-4 Hz) and spindle (8-14 Hz) frequency range, whereas under anesthesia the power in the gamma band (30-100 Hz) was higher. During anesthesia, slow waves were more rhythmic and more synchronous across the cortex. Intracellular recordings revealed that silent states were longer and the amplitude of membrane potential around transition between active and silent states was bigger under anesthesia. Slow waves were mostly uniform across cortical areas under anesthesia, but in SWS, they were most pronounced in associative and visual areas but smaller and less regular in somatosensory and motor cortices. We conclude that, although the main features of the slow oscillation in sleep and anesthesia appear similar, multiple cellular and network features are differently expressed during natural SWS compared with ketamine-xylazine anesthesia.

Sleep spindles and hippocampal functional connectivity in human NREM sleep.

Abstract: We investigated human hippocampal functional connectivity in wakefulness and throughout non-rapid eye movement sleep. Young healthy subjects underwent simultaneous EEG and functional magnetic resonance imaging (fMRI) measurements at 1.5 T under resting conditions in the descent to deep sleep. Continuous 5 min epochs representing a unique sleep stage (i.e., wakefulness, sleep stages 1 and 2, or slow-wave sleep) were extracted. fMRI time series of subregions of the hippocampal formation (HF) (cornu ammonis, dentate gyrus, and subiculum) were extracted based on cytoarchitectonical probability maps. We observed sleep stage-dependent changes in HF functional coupling. The HF was integrated to variable strength in the default mode network (DMN) in wakefulness and light sleep stages but not in slow-wave sleep. The strongest functional connectivity between the HF and neocortex was observed in sleep stage 2 (compared with both slow-wave sleep and wakefulness). We observed a strong interaction of sleep spindle occurrence and HF functional connectivity in sleep stage 2, with increased HF/neocortical connectivity during spindles. Moreover, the cornu ammonis exhibited strongest functional connectivity with the DMN during wakefulness, while the subiculum dominated hippocampal functional connectivity to frontal brain regions during sleep stage 2. Increased connectivity between HF and neocortical regions in sleep stage 2 suggests an increased capacity for possible global information transfer, while connectivity in slow-wave sleep is reflecting a functional system optimal for segregated information reprocessing. Our data may be relevant to differentiating sleep stage-specific contributions to neural plasticity as proposed in sleep-dependent memory consolidation.

Decreased Slow Wave Sleep Increases Risk of Developing Hypertension in Elderly Men

Abstract: The importance of sleep to health and cardiovascular disease has become increasingly apparent. Sleep disordered breathing (SDB), sleep duration, and sleep architecture may all influence metabolism and neurohormonal systems, yet no prior study has evaluated these sleep characteristics concurrently in relation to incident hypertension. Our objective was to determine if incident hypertension is associated with polysomnography (PSG) measures of SDB, sleep duration, and sleep architecture in older men. Participants were784 community dwelling, ambulatory men ≥65 years (mean age 75.1±4.9 years) from the Outcomes of Sleep Disorders in Older Men Study (MrOs Sleep Study) who did not have hypertension at the time of their in-home PSG sleep studies (2003-2005); and who returned for follow-up (2007-2009). Of 784 older men included in this report, 243 met criteria for incident hypertension after a mean follow-up of 3.4 years. In unadjusted analyses, incident hypertension was associated with increased hypoxemia, increased sleep stages N1 and N2 and decreased stage N3 (slow wave sleep, SWS). After adjustment for age, non-white race, study site, and body mass index, the only sleep index to remain significantly associated with incident HTN was SWS percent (odds ratio for lowest to highest quartile of SWS: 1.83, 95% CI 1.18, 2.85). No attenuation of this association was seen after accounting for sleep duration, sleep fragmentation and indices of SDB. Percentage time in SWS was inversely associated with incident HTN, independent of sleep duration and fragmentation, and SDB. Selective deprivation of SWS may contribute to adverse blood pressure in older men.

Electrophysiological correlates of behavioural changes in vigilance in vegetative state and minimally conscious state

Abstract: The existence of normal sleep in patients in a vegetative state is still a matter of debate. Previous electrophysiological sleep studies in patients with disorders of consciousness did not differentiate patients in a vegetative state from patients in a minimally conscious state. Using high-density electroencephalographic sleep recordings, 11 patients with disorders of consciousness (six in a minimally conscious state, five in a vegetative state) were studied to correlate the electrophysiological changes associated with sleep to behavioural changes in vigilance (sustained eye closure and muscle inactivity). All minimally conscious patients showed clear electroencephalographic changes associated with decreases in behavioural vigilance. In the five minimally conscious patients showing sustained behavioural sleep periods, we identified several electrophysiological characteristics typical of normal sleep. In particular, all minimally conscious patients showed an alternating non-rapid eye movement/rapid eye movement sleep pattern and a homoeostatic decline of electroencephalographic slow wave activity through the night. In contrast, for most patients in a vegetative state, while preserved behavioural sleep was observed, the electroencephalographic patterns remained virtually unchanged during periods with the eyes closed compared to periods of behavioural wakefulness (eyes open and muscle activity). No slow wave sleep or rapid eye movement sleep stages could be identified and no homoeostatic regulation of sleep-related slow wave activity was observed over the night-time period. In conclusion, we observed behavioural, but no electrophysiological, sleep wake patterns in patients in a vegetative state, while there were near-to-normal patterns of sleep in patients in a minimally conscious state. These results shed light on the relationship between sleep electrophysiology and the level of consciousness in severely brain-damaged patients. We suggest that the study of sleep and homoeostatic regulation of slow wave activity may provide a complementary tool for the assessment of brain function in minimally conscious state and vegetative state patients.

Involvement of cytokines in slow wave sleep

Abstract: Cytokines such as tumor necrosis factor alpha (TNFα) and interleukin-1 beta (IL1β) play a role in sleep regulation in health and disease. TNFα or IL1β injection enhances non-rapid eye movement sleep. Inhibition of TNFα or IL1β reduces spontaneous sleep. Mice lacking TNFα or IL1β receptors sleep less. In normal humans and in multiple disease states, plasma levels of TNFα covary with EEG slow wave activity (SWA) and sleep propensity. Many of the symptoms induced by sleep loss, for example, sleepiness, fatigue, poor cognition, enhanced sensitivity to pain, are elicited by injection of exogenous TNFα or IL1β. IL1β or TNFα applied unilaterally to the surface of the cortex induces state-dependent enhancement of EEG SWA ipsilaterally, suggesting greater regional sleep intensity. Interventions such as unilateral somatosensory stimulation enhance localized sleep EEG SWA, blood flow, and somatosensory cortical expression of IL1β and TNFα. State oscillations occur within cortical columns. One such state shares properties with whole animal sleep in that it is dependent on prior cellular activity, shows homeostasis, and is induced by TNFα. Extracellular ATP released during neuro- and gliotransmission enhances cytokine release via purine type 2 receptors. An ATP agonist enhances sleep, while ATP antagonists inhibit sleep. Mice lacking the P2X7 receptor have attenuated sleep rebound responses after sleep loss. TNFα and IL1β alter neuron sensitivity by changing neuromodulator/neurotransmitter receptor expression, allowing the neuron to scale its activity to the presynaptic neurons. TNFα's role in synaptic scaling is well characterized. Because the sensitivity of the postsynaptic neuron is changed, the same input will result in a different network output signal and this is a state change. The top-down paradigm of sleep regulation requires intentional action from sleep/wake regulatory brain circuits to initiate whole-organism sleep. This raises unresolved questions as to how such purposeful action might itself be initiated. In the new paradigm, sleep is initiated within networks and local sleep is a direct consequence of prior local cell activity. Whole-organism sleep is a bottom-up, self-organizing, and emergent property of the collective states of networks throughout the brain.

Hippocampal memory consolidation during sleep: a comparison of mammals and birds.

Abstract: The transition from wakefulness to sleep is marked by pronounced changes in brain activity. The brain rhythms that characterize the two main types of mammalian sleep, slow-wave sleep (SWS) and rapid eye movement (REM) sleep, are thought to be involved in the functions of sleep. In particular, recent theories suggest that the synchronous slow-oscillation of neocortical neuronal membrane potentials, the defining feature of SWS, is involved in processing information acquired during wakefulness. According to the Standard Model of memory consolidation, during wakefulness the hippocampus receives input from neocortical regions involved in the initial encoding of an experience and binds this information into a coherent memory trace that is then transferred to the neocortex during SWS where it is stored and integrated within preexisting memory traces. Evidence suggests that this process selectively involves direct connections from the hippocampus to the prefrontal cortex (PFC), a multimodal, high-order association region implicated in coordinating the storage and recall of remote memories in the neocortex. The slow-oscillation is thought to orchestrate the transfer of information from the hippocampus by temporally coupling hippocampal sharp-wave/ripples (SWRs) and thalamocortical spindles. SWRs are synchronous bursts of hippocampal activity, during which waking neuronal firing patterns are reactivated in the hippocampus and neocortex in a coordinated manner. Thalamocortical spindles are brief 7–14 Hz oscillations that may facilitate the encoding of information reactivated during SWRs. By temporally coupling the readout of information from the hippocampus with conditions conducive to encoding in the neocortex, the slow-oscillation is thought to mediate the transfer of information from the hippocampus to the neocortex. Although several lines of evidence are consistent with this function for mammalian SWS, it is unclear whether SWS serves a similar function in birds, the only taxonomic group other than mammals to exhibit SWS and REM sleep. Based on our review of research on avian sleep, neuroanatomy, and memory, although involved in some forms of memory consolidation, avian sleep does not appear to be involved in transferring hippocampal memories to other brain regions. Despite exhibiting the slow-oscillation, SWRs and spindles have not been found in birds. Moreover, although birds independently evolved a brain region—the caudolateral nidopallium (NCL)—involved in performing high-order cognitive functions similar to those performed by the PFC, direct connections between the NCL and hippocampus have not been found in birds, and evidence for the transfer of information from the hippocampus to the NCL or other extra-hippocampal regions is lacking. Although based on the absence of evidence for various traits, collectively, these findings suggest that unlike mammalian SWS, avian SWS may not be involved in transferring memories from the hippocampus. Furthermore, it suggests that the slow-oscillation, the defining feature of mammalian and avian SWS, may serve a more general function independent of that related to coordinating the transfer of information from the hippocampus to the PFC in mammals. Given that SWS is homeostatically regulated (a process intimately related to the slow-oscillation) in mammals and birds, functional hypotheses linked to this process may apply to both taxonomic groups.

The role of presleep negative emotion in sleep physiology

Abstract: Although daytime emotional stressful events are often presumed to cause sleep disturbances, the few studies of stressful life events on sleep physiology have resulted in various and contradictory findings. As research has focused in particular on stress in itself, the present study is the first to investigate the effect using polysomnography (PSG). Results indicate a significant increase in sleep fragmentation, as expressed by decreased sleep efficiency, total sleep time, percentage of rapid eye movement (REM) sleep, and an increased wake after sleep onset latency, total time awake, latency to SWS, number of awakenings and number of awakenings from REM sleep. The results demonstrate that negative emotion correlates with enhanced sleep fragmentation helping us to understand why sleep patterns change and how sleep disturbances may develop.

Local sleep homeostasis in the avian brain: convergence of sleep function in mammals and birds?

Abstract: The function of the brain activity that defines slow wave sleep (SWS) and rapid eye movement (REM) sleep in mammals is unknown. During SWS, the level of electroencephalogram slow wave activity (SWA or 0.5–4.5 Hz power density) increases and decreases as a function of prior time spent awake and asleep, respectively. Such dynamics occur in response to waking brain use, as SWA increases locally in brain regions used more extensively during prior wakefulness. Thus, SWA is thought to reflect homeostatically regulated processes potentially tied to maintaining optimal brain functioning. Interestingly, birds also engage in SWS and REM sleep, a similarity that arose via convergent evolution, as sleeping reptiles and amphibians do not show similar brain activity. Although birds deprived of sleep show global increases in SWA during subsequent sleep, it is unclear whether avian sleep is likewise regulated locally. Here, we provide, to our knowledge, the first electrophysiological evidence for local sleep homeostasis in the avian brain. After staying awake watching David Attenborough's The Life of Birds with only one eye, SWA and the slope of slow waves (a purported marker of synaptic strength) increased only in the hyperpallium—a primary visual processing region—neurologically connected to the stimulated eye. Asymmetries were specific to the hyperpallium, as the non-visual mesopallium showed a symmetric increase in SWA and wave slope. Thus, hypotheses for the function of mammalian SWS that rely on local sleep homeostasis may apply also to birds.

Decreased sleep efficiency, increased wake after sleep onset and increased cortical arousals in late pregnancy.

Abstract: Background Anecdotal reports of sleep disturbance during pregnancy are abundant; however, objective measurement of sleep changes has so far produced conflicting results. Aims To objectively measure sleep architecture and investigate subjective sleep quality in the first and third trimester of pregnancy, when compared to the nonpregnant state. Methods Twenty-seven women in the third trimester of pregnancy, 21 women in the first trimester of pregnancy and 24 nonpregnant control women underwent overnight polysomnography and completed questionnaires regarding sleep quality and mood. Results Women in the third trimester of pregnancy had poorer sleep efficiency, more awakenings, less stage 4 sleep, more stage 1 sleep and fewer minutes in rapid eye movement sleep when compared to the control group. Cortical arousals were seen more often during pregnancy, particularly in response to respiratory events and limb movements. Sleep during the first trimester was affected to a lesser extent, with more wake time after sleep onset and less stage 4 sleep when compared to the controls. Conclusions Sleep during pregnancy is compromised by higher amounts of wake and cortical arousals leading to sleep fragmentation, with greater amounts of light sleep and less deep sleep. Mood state did not have an effect on sleep. Given the impact of sleep on well-being, this study increases our understanding of the characteristics of sleep during pregnancy, to help recognise when severe sleep disruption may warrant referral to a specialist for appropriate diagnosis and treatment.

Sleep following alcohol intoxication in healthy, young adults: effects of sex and family history of alcoholism.

Abstract: Background: This study evaluated sex and family history of alcoholism as moderators of subjective ratings of sleepiness/sleep quality and polysomnography (PSG) following alcohol intoxication in healthy, young adults. Methods: Ninety-three healthy adults [mean age 24.4 ± 2.7 years, 59 women, 29 subjects with a positive family history of alcoholism (FH+)] were recruited. After screening PSG, participants consumed alcohol (sex/weight adjusted dosing) to intoxication [peak breath alcohol concentration (BrAC) of 0.11 ± 0.01 g% for men and women] or matching placebo between 20:30 and 22:00 hours. Sleep was monitored using PSG between 23:00 and 07:00 hours. Participants completed the Stanford Sleepiness Scale and Karolinska Sleepiness Scale at bedtime and on awakening and a validated post-sleep questionnaire. Results: Following alcohol, total sleep time, sleep efficiency, nighttime awakenings, and wake after sleep onset were more disrupted in women than men, with no differences by family history status. Alcohol reduced sleep onset latency, sleep efficiency, and rapid eye movement sleep while increasing wakefulness and slow wave sleep across the entire night compared with placebo. Alcohol also generally increased sleep consolidation in the first half of the night, but decreased it during the second half. Sleepiness ratings were higher following alcohol, particularly in women at bedtime. Morning sleep quality ratings were lower following alcohol than placebo. Conclusions: Alcohol intoxication increases subjective sleepiness and disrupts sleep objectively more in healthy women than in men, with no differences evident by family history of alcoholism status. Evaluating moderators of alcohol effects on sleep may provide insight into the role of sleep in problem drinking.

Cognitive, psychomotor and polysomnographic effects of trazodone in primary insomniacs

Abstract: Trazodone is prescribed widely as a sleep aid, although it is indicated for depression, not insomnia. Its daytime cognitive and psychomotor effects have not been investigated systematically in insomniacs. The primary goal of this study was to quantify, in primary insomniacs, the hypnotic efficacy of trazodone and subsequent daytime impairments. Sixteen primary insomniacs (mean age 44 years) participated, with insomnia confirmed by overnight polysomnography (sleep efficiency ≤ 85%). Trazodone 50 mg was administered to participants 30 min before bedtime for 7 days in a 3-week, within-subjects, randomized, double-blind, placebo-controlled design. Subjective effects, equilibrium (anterior/posterior body sway), short-term memory, verbal learning, simulated driving and muscle endurance were assessed the morning after days 1 and 7 of drug administration. Sleep was evaluated with overnight polysomnography and modified Multiple Sleep Latency Tests (MSLT) on days 1 and 7. Trazodone produced small but significant impairments of short-term memory, verbal learning, equilibrium and arm muscle endurance across time-points. Relative to placebo across test days, trazodone was associated with fewer night-time awakenings, minutes of Stage 1 sleep and self-reports of difficulty sleeping. On day 7 only, slow wave sleep was greater and objective measures of daytime sleepiness lower with trazodone than with placebo. Although trazodone is efficacious for sleep maintenance difficulties, its associated cognitive and motor impairments may provide a modest caveat to health-care providers.

Delta wave power: an independent sleep phenotype or epiphenomenon?

Abstract: Electroencephalographic (EEG) δ waves during non-rapid eye movement sleep (NREMS) after sleep deprivation are enhanced That observation eventually led to the use of EEG δ power as a parameter to model process S in the two-process model of sleep It works remarkably well as a model parameter because it often co-varies with sleep duration and intensity Nevertheless there is a large volume of literature indicating that EEG δ power is regulated independently of sleep duration For example, high amplitude EEG δ waves occur in wakefulness after systemic atropine administration or after hyperventilation in children Human neonates have periods of sleep with an almost flat EEG Similarly, elderly people have reduced EEG δ power, yet retain substantial NREMS Rats provided with a cafeteria diet have excess duration of NREMS but simultaneously decreased EEG δ power for days Mice challenged with influenza virus have excessive EEG δ power and NREMS In contrast, if mice lacking TNF receptors are infected, they still sleep more but have reduced EEG δ power Sleep regulatory substances, eg, IL1, TNF, and GHRH, directly injected unilaterally onto the cortex induce state-dependent ipsilateral enhancement of EEG δ power without changing duration of organism sleep IL1 given systemically enhances duration of NREMS but reduces EEG δ power in mice Benzodiazepines enhance NREMS but inhibit EEG δ power If duration of NREMS is an indicator of prior sleepiness then simultaneous EEG δ power may or may not be a useful index of sleepiness Finally, most sleep regulatory substances are cerebral vasodilators and blood flow affects EEG δ power In conclusion, it seems unlikely that a single EEG measure will be reliable as a marker of sleepiness for all conditions Citation: Davis CJ; Clinton JM; Jewett KA; Zielinski MR; Krueger JM EEG delta wave power: An independent sleep phenotype or epiphenomenon? J Clin Sleep Med 2011;7(5):Supplement S16–S18

Ostriches sleep like platypuses

Abstract: Mammals and birds engage in two distinct states of sleep, slow wave sleep (SWS) and rapid eye movement (REM) sleep. SWS is characterized by slow, high amplitude brain waves, while REM sleep is characterized by fast, low amplitude waves, known as activation, occurring with rapid eye movements and reduced muscle tone. However, monotremes (platypuses and echidnas), the most basal (or ‘ancient’) group of living mammals, show only a single sleep state that combines elements of SWS and REM sleep, suggesting that these states became temporally segregated in the common ancestor to marsupial and eutherian mammals. Whether sleep in basal birds resembles that of monotremes or other mammals and birds is unknown. Here, we provide the first description of brain activity during sleep in ostriches (Struthio camelus), a member of the most basal group of living birds. We found that the brain activity of sleeping ostriches is unique. Episodes of REM sleep were delineated by rapid eye movements, reduced muscle tone, and head movements, similar to those observed in other birds and mammals engaged in REM sleep; however, during REM sleep in ostriches, forebrain activity would flip between REM sleep-like activation and SWS-like slow waves, the latter reminiscent of sleep in the platypus. Moreover, the amount of REM sleep in ostriches is greater than in any other bird, just as in platypuses, which have more REM sleep than other mammals. These findings reveal a recurring sequence of steps in the evolution of sleep in which SWS and REM sleep arose from a single heterogeneous state that became temporally segregated into two distinct states. This common trajectory suggests that forebrain activation during REM sleep is an evolutionarily new feature, presumably involved in performing new sleep functions not found in more basal animals.

Neurocognitive Dysfunction Associated With Sleep Quality and Sleep Apnea in Patients With Mild Cognitive Impairment

Abstract: Objectives Sleep apnea syndrome (SAS) is considered a risk factor for cognitive decline in the elderly. The specific neurocognitive decline has been suggested as a predictive factor for dementia in patients with mild cognitive impairment (MCI). The authors aim to illustrate the sleep characteristics related to the specific neurocognitive decline in the community-dwelling elderly including patients with MCI. Design Cross-sectional. Settings Center for sleep and chronobiology in Kangwon National University Hospital. Participants Thirty patients with MCI and 30 age- and sex-matched normal elderly subjects were selected. Measurements The authors administered seven tests in the Korean version of the Consortium to Establish A Registry of Alzheimer's Disease Neuropsychological battery and conducted nocturnal polysomnography. A p value below 0.05 was considered a statistical significance. Results There was no significant difference in sleep parameters between the MCI and normal comparison (NC) groups. Sleep efficiency was positively correlated with Constructional Recall (CR) scores in both NC and MCI groups (r = 0.393 and 0.391, respectively). The amount of slow wave sleep (SWS) was also positively correlated with Boston naming test (BNT) scores in both groups (r = 0.392, 0.470, respectively). Stepwise multiple regression models showed that SWS and the apnea index were significant independent variables associated with the BNT score (Δβ = 0.43 and −0.34, respectively; adjusted R 2 = 0.298) in the MCI group, and the amount of rapid eye movement sleep was a significant independent variable associated with the CR score (Δβ = 0.49; adjusted R 2 = 0.217) in the NC group. Conclusions Our results show that poor sleep quality and greater severity of SAS were associated with impaired language function reflecting frontal-subcortical pathology in patients with MCI. This suggests that vulnerability to a specific brain damage associated with SAS could increase the risk for dementia.

Melanin-concentrating hormone: a new sleep factor?

Abstract: Neurons containing the neuropeptide melanin-concentrating hormone (MCH) are mainly located in the lateral hypothalamus and the incerto-hypothalamic area, and have widespread projections throughout the brain. While the biological functions of this neuropeptide are exerted in humans through two metabotropic receptors, the MCHR1 and MCHR2, only the MCHR1 is present in rodents. Recently, it has been shown that the MCHergic system is involved in the control of sleep. We can summarize the experimental findings as follows: (1) The areas related to the control of sleep and wakefulness have a high density of MCHergic fibers and receptors. (2) MCHergic neurons are active during sleep, especially during rapid eye movement (REM) sleep. (3) MCH knockout mice have less REM sleep, notably under conditions of negative energy balance. Animals with genetically inactivated MCHR1 also exhibit altered vigilance state architecture and sleep homeostasis. (4) Systemically administered MCHR1 antagonists reduce sleep. (5) Intraventricular microinjection of MCH increases both slow wave sleep (SWS) and REM sleep; however, the increment in REM sleep is more pronounced. (6) Microinjection of MCH into the dorsal raphe nucleus increases REM sleep time. REM seep is inhibited by immunoneutralization of MCH within this nucleus. (7) Microinjection of MCH in the nucleus pontis oralis of the cat enhances REM sleep time and reduces REM sleep latency. All these data strongly suggest that MCH has a potent role in the promotion of sleep. Although both SWS and REM sleep are facilitated by MCH, REM sleep seems to be more sensitive to MCH modulation.

Sleep depth and fatigue: role of cellular inflammatory activation.

Abstract: Individuals with underlying inflammation present with a high prevalence of non-specific co-morbid symptoms including sleep disturbance and fatigue. However, the association between cellular expression of proinflammatory cytokines, alterations of sleep depth and daytime fatigue has not been concurrently examined. In healthy adults (24 – 61 years old), evening levels of monocyte intracellular proinflammatory cytokine production were assessed prior to evaluation of polysomonographic sleep and measures of fatigue the following day. Stimulated monocyte production of interleukin-6 (IL-6), but not tumor necrosis factor α (TNF- α), was negatively associated with slow wave sleep (ΔR2 =.17, p=.029). In contrast, stimulated monocyte production of IL-6 was positively associated with rapid-eye movement (REM) sleep duration during the first sleep cycle (ΔR2 = .26, p<.01). Moreover, evening stimulated production of IL-6 was associated with fatigue the following day (ΔR2 = .17, p=.05). Mediation analyses showed that slow wave sleep, but not REM sleep duration, mediated the relationship between evening levels of IL-6 production and daytime fatigue. These results indicate that increases in stimulated monocyte production of IL6 may be associated with changes in sleep architecture with decreases in slow wave sleep and increases in REM sleep duration. Relative loss of slow wave sleep may be one pathway through which cellular inflammation leads to daytime fatigue.