Showing papers on "Slow-wave sleep published in 2006"
TL;DR: It is shown that inducing slow oscillation-like potential fields by transcranial application of oscillating potentials during early nocturnal non-rapid-eye-movement sleep, enhances the retention of hippocampus-dependent declarative memories in healthy humans.
Abstract: Sleep is thought to enhance memory consolidation, since some tasks learned before a period of sleep are better remembered than those learned without. It now appears that this memory function of sleep can be enhanced electronically. By stimulating the scalp with a gentle electric current during sleep after learning, memory was enhanced by 8% in a word-learning task in volunteer medical students. There is compelling evidence that sleep contributes to the long-term consolidation of new memories1. This function of sleep has been linked to slow (<1 Hz) potential oscillations, which predominantly arise from the prefrontal neocortex and characterize slow wave sleep2,3,4. However, oscillations in brain potentials are commonly considered to be mere epiphenomena that reflect synchronized activity arising from neuronal networks, which links the membrane and synaptic processes of these neurons in time5. Whether brain potentials and their extracellular equivalent have any physiological meaning per se is unclear, but can easily be investigated by inducing the extracellular oscillating potential fields of interest6,7,8. Here we show that inducing slow oscillation-like potential fields by transcranial application of oscillating potentials (0.75 Hz) during early nocturnal non-rapid-eye-movement sleep, that is, a period of emerging slow wave sleep, enhances the retention of hippocampus-dependent declarative memories in healthy humans. The slowly oscillating potential stimulation induced an immediate increase in slow wave sleep, endogenous cortical slow oscillations and slow spindle activity in the frontal cortex. Brain stimulation with oscillations at 5 Hz—another frequency band that normally predominates during rapid-eye-movement sleep—decreased slow oscillations and left declarative memory unchanged. Our findings indicate that endogenous slow potential oscillations have a causal role in the sleep-associated consolidation of memory, and that this role is enhanced by field effects in cortical extracellular space.
1,615 citations
TL;DR: A brainstem flip–flop switch is proposed, consisting of mutually inhibitory REM-off and REM-on areas in the mesopontine tegmentum that contain GABA (γ-aminobutyric acid)-ergic neurons that heavily innervate the other.
Abstract: Rapid eye movement (REM) sleep consists of a dreaming state in which there is activation of the cortical and hippocampal electroencephalogram (EEG), rapid eye movements, and loss of muscle tone. Although REM sleep was discovered more than 50 years ago, the neuronal circuits responsible for switching between REM and non-REM (NREM) sleep remain poorly understood. Here we propose a brainstem flip–flop switch, consisting of mutually inhibitory REM-off and REM-on areas in the mesopontine tegmentum. Each side contains GABA (γ-aminobutyric acid)-ergic neurons that heavily innervate the other. The REM-on area also contains two populations of glutamatergic neurons. One set projects to the basal forebrain and regulates EEG components of REM sleep, whereas the other projects to the medulla and spinal cord and regulates atonia during REM sleep. The mutually inhibitory interactions of the REM-on and REM-off areas may form a flip–flop switch that sharpens state transitions and makes them vulnerable to sudden, unwanted transitions—for example, in narcolepsy. Rapid eye movement (REM) sleep is a dreaming state in which the brain is highly active. The mechanism responsible for switching between REM and non-REM sleep (also called slow-wave sleep, when cortical activity is slow) is poorly understood. Now, based on detailed anatomy and lesion experiments, Lu et al. have identified brainstem regions that control the transition from REM to non-REM sleep. The REM-off and REM-on areas are mutually inhibitory. This appears to produce a flip-flop switch relationship that could explain many of the properties of the abrupt switching into and out of REM states seen in sleep disorders such as narcolepsy.
1,073 citations
[...]
TL;DR: A central role for consolidating memories is played by the slow oscillation, that is, the oscillating field potential change dominating SWS, which synchronizes the occurrence of sharp wave ripples accompanying memory reactivations in the hippocampus with thalamocortical spindle activity.
Abstract: Recently, compelling evidence has accumulated that links sleep to learning and memory. Sleep has been identified as a state that optimizes the consolidation of newly acquired information in memory. Consolidation is an active process that is presumed to rely on the covert reactivation and reorganization of newly encoded representations. Hippocampus-dependent memories benefit primarily from slow-wave sleep (SWS), whereas memories not depending on the hippocampus show greater gains over periods containing high amounts of rapid eye movement sleep. One way sleep does this is by establishing different patterns of neurotransmitters and neurohormone secretion between sleep stages. Another central role for consolidating memories is played by the slow oscillation, that is, the oscillating field potential change dominating SWS. The emergence of slow oscillations in neocortical networks depends on the prior use of these networks for encoding of information. Via efferent pathways, they synchronize the occurrence of sharp wave ripples accompanying memory reactivations in the hippocampus with thalamocortical spindle activity. Thus, hippocampal memories are fed back into neocortical networks at a time when these networks are depolarized and, because of concurrent spindle activity, can most sensitively react to these inputs with plastic changes underlying the formation of long-term memory representations.
530 citations
TL;DR: Sleep patterns change with aging, independent of other factors, and include advanced sleep timing, shortened nocturnal sleep duration, increased frequency of daytime naps, increased number ofNocturnal awakenings and time spent awake during the night, and decreased slow wave sleep.
399 citations
TL;DR: Adenotonsillectomy yields improvements in respiratory abnormalities in children with obstructive sleep apnea syndrome, and comparison between the children who had AHI
368 citations
TL;DR: Following an intense period of simple motor procedural learning, the duration of Stage 2 sleep and spindle density increased, and the hypothesis that sleep spindles are involved in the off‐line reprocessing ofsimple motor procedural memory during Stage 2Sleep is supported.
Abstract: It has become increasingly clear that sleep is necessary for efficient memory consolidation. Recently, it has been found that Stage 2 sleep disruption impairs procedural memory performance, and that memory performance is correlated with the duration of Stage 2 sleep; but the mechanisms involved in synaptic plasticity for procedural memory during sleep have not been identified. The present study examined the learning-dependent changes in sleep, including Stage 2 sleep spindles. Following an intense period of simple motor procedural learning, the duration of Stage 2 sleep and spindle density increased. There were no changes observed in the duration of any other stage of sleep or in the density of rapid eye movements. These findings support the hypothesis that sleep spindles are involved in the off-line reprocessing of simple motor procedural memory during Stage 2 sleep.
336 citations
TL;DR: It is shown that, after a comparatively brief sleep episode, subjects that take a nap improve more on a declarative memory task than subjects that stay awake, but that improvement on a procedural memory task is the same regardless of whether subjects take aNap or remain awake.
316 citations
TL;DR: The results of this study show that cigarette smoking is independently associated with disturbances in sleep architecture, including a longer latency to sleep onset and a shift toward lighter stages of sleep.
Abstract: Cigarette smoking has been associated with a high prevalence of sleep-related complaints. However, its effects on sleep architecture have not been fully examined. The primary objective of this investigation was to assess the impact of cigarette smoking on sleep architecture. Polysomnography was used to characterize sleep architecture among 6,400 participants of the Sleep Heart Health Study (United States, 1994-1999). Sleep parameters included total sleep time, latency to sleep onset, sleep efficiency, and percentage of time in each sleep stage. The study sample consisted of 2,916 never smokers, 2,705 former smokers, and 779 current smokers. Compared with never smokers, current smokers had a longer initial sleep latency (5.4 minutes, 95% confidence interval (CI): 2.9, 7.9) and less total sleep time (14.0 minutes, 95% CI: 6.4, 21.7). Furthermore, relative to never smokers, current smokers also had more stage 1 sleep (relative proportion = 1.24, 95% CI: 1.14, 1.33) and less slow wave sleep (relative proportion = 0.86, 95% CI: 0.78, 0.95). Finally, no differences in sleep architecture were noted between former and never smokers. The results of this study show that cigarette smoking is independently associated with disturbances in sleep architecture, including a longer latency to sleep onset and a shift toward lighter stages of sleep. Nicotine in cigarette smoke and acute withdrawal from it may contribute to disturbances in sleep architecture.
297 citations
TL;DR: It is suggested that it is the synchronous termination of activity and occurrence of silent states of the neuronal network that makes the EEG picture during slow-wave sleep so characteristic, and the existence of a network mechanism is revealed.
Abstract: Slow-wave sleep is characterized by alternating periods of activity and silence in corticothalamic networks. Both activity and silence are stable network states, but the mechanisms of their alternation remain unknown. We show, using simultaneous multisite intracellular recordings in cats, that slow rhythm involves all neocortical neurons and that both activity and silence started almost synchronously in cells located up to 12 mm apart. Activity appeared predominantly at the area 5/7 border and spread in both anterior and posterior directions. The activity started earlier in fast-spiking cells and intrinsically bursting cells than in regular-spiking neurons. These results provide direct evidence for two mechanisms of active state generation: spread of activity from a local focus and synchronization of weaker activity, originating at multiple locations. Surprisingly, onsets of silent states were synchronized even more precisely than the onsets of activity, showing no latency bias for location or cell type. This most intriguing finding exposes a major gap in understanding the nature of state alternation. We suggest that it is the synchronous termination of activity and occurrence of silent states of the neuronal network that makes the EEG picture during slow-wave sleep so characteristic. Synchronous onset of silence in distant neurons cannot rely exclusively on properties of individual cells and synapses, such as adaptation of neuronal firing or synaptic depression; instead, it implies the existence of a network mechanism. Revealing this yet unknown large-scale mechanism, which switches network activity to silence, will aid our understanding of the origin of brain rhythms in normal function and pathology.
271 citations
TL;DR: The hypothesis that age-related changes in sleep are due to weaker circadian regulation of sleep and wakefulness is favored and manipulations of the circadian timing system, rather than the sleep homeostat, may offer a potential strategy to alleviate age‐related decrements in sleep and daytime alertness levels.
Abstract: The reduction of electroencephalographic (EEG) slow-wave activity (SWA) (EEG power density between 075-45 Hz) and spindle frequency activity, together with an increase in involuntary awakenings during sleep, represent the hallmarks of human sleep alterations with age It has been assumed that this decrease in non-rapid eye movement (NREM) sleep consolidation reflects an age-related attenuation of the sleep homeostatic drive To test this hypothesis, we measured sleep EEG characteristics (ie, SWA, sleep spindles) in healthy older volunteers in response to high (sleep deprivation protocol) and low sleep pressure (nap protocol) conditions Despite the fact that the older volunteers had impaired sleep consolidation and reduced SWA levels, their relative SWA response to both high and low sleep pressure conditions was similar to that of younger persons Only in frontal brain regions did we find an age-related diminished SWA response to high sleep pressure On the other hand, we have clear evidence that the circadian regulation of sleep during the 40 h nap protocol was changed such that the circadian arousal signal in the evening was weaker in the older study participants More sleep occurred during the wake maintenance zone, and subjective sleepiness ratings in the late afternoon and evening were higher than in younger participants In addition, we found a diminished melatonin secretion and a reduced circadian modulation of REM sleep and spindle frequency-the latter was phase-advanced relative to the circadian melatonin profile Therefore, we favor the hypothesis that age-related changes in sleep are due to weaker circadian regulation of sleep and wakefulness Our data suggest that manipulations of the circadian timing system, rather than the sleep homeostat, may offer a potential strategy to alleviate age-related decrements in sleep and daytime alertness levels
248 citations
TL;DR: The present study reports the first indication of learning-associated increase in spindle density in the rat, providing an animal model to study the role of brain oscillations in memory consolidation during sleep and substantially extend findings in humans.
Abstract: Non-rapid eye movement sleep has been strongly implicated in consolidation of both declarative and procedural memory in humans. Elevated sleep-spindle density in slow-wave sleep after learning has been shown recently in humans. It has been proposed that sleep spindles, 12-15 Hz oscillations superimposed on slow waves (<1 Hz), in concert with high-frequency hippocampal sharp waves/ripples, promote neural plasticity underlying remote memory formation. The present study reports the first indication of learning-associated increase in spindle density in the rat, providing an animal model to study the role of brain oscillations in memory consolidation during sleep. An odor-reward association task, analogous in many respects to human paired-associate learning, is rapidly learned and leads to robust memory in rats. Rats learned the task over 10 massed trials within a single session, and EEG was monitored for 3 h after learning. Learning-induced increase in spindle density is reliably reproduced in rats in two different learning situations, differing primarily in the behavioral component of the task. This increase in spindle density is also present after reactivation of remote memory and in situations when memory update is required; it is not observed after noncontingent exposure to reward and training context. The latter results substantially extend findings in humans. The magnitude of increase (approximately 25%) and the time window of maximal effect (approximately 1 h after sleep onset) were remarkably similar to human data, making this a valid rodent model to study network interactions through the use of simultaneous unit recordings and local field potentials during postlearning sleep.
TL;DR: A specific pattern of decreased brain activity during sleep is described and it is suggested that this pattern must be synchronized for establishing and maintaining sleep.
Abstract: Regional differences in sleep EEG dynamics indicate that sleep-related brain activity involves local brain processes with sleep stage specific activity patterns of neuronal populations. Macroscopically, it is not fully understood which cerebral brain regions are involved in the successive discontinuation of wakefulness. We simultaneously used EEG and functional MRI on 9 subjects (6 female: mean = 24.1 years, 3 male: mean = 26.0 years) and analyzed local blood oxygenation level dependent signal changes linked to the transition from wakefulness to different non-rapid eye movement (NREM) sleep stages (according to Rechtschaffen and Kales) of the first sleep cycles after 36 h of total sleep deprivation. Several brain regions throughout the cortex, the limbic lobe, the thalamus, the caudate nucleus, as well as midbrain structures, such as the mammillary body/hypothalamus, showed reduced activity during NREM sleep across all sleep stages. Additionally, we found deactivation patterns specific to NREM sleep stages compared with wakefulness suggesting that a synchronized sleeping state can be established only if these regions interact in a well-balanced way. Sleep stage 2, which is usually linked to the loss of self-conscious awareness, is associated with signal decreases comprising thalamic and hypothalamic regions, the cingulate cortex, the right insula and adjacent regions of the temporal lobe, the inferior parietal lobule and the inferior/middle frontal gyri. The hypothalamic region known to be of particular importance in the regulation of the sleep-wake cycle shows specific temporally correlated network activity with the cortex while the system is in the sleeping state, but not during wakefulness. We describe a specific pattern of decreased brain activity during sleep and suggest that this pattern must be synchronized for establishing and maintaining sleep.
TL;DR: Efficient overnight consolidation of declarative memory is associated with high amounts of SWS and low serum cortisol levels during the early part of the night, where SWS is decreased, REM sleep might play a partly compensatory role in the consolidation of DeclarativeMemory.
TL;DR: Investigating sleep with polysomnography and self-ratings and the diurnal pattern of sleepiness and fatigue in a group suffering from severe occupational burnout found impaired sleep may play a role in the development of fatigue or exhaustion in burnout.
Abstract: OBJECTIVES: The purpose of this study was to investigate sleep with polysomnography and self-ratings and the diurnal pattern of sleepiness and fatigue in a group suffering from severe occupational ...
TL;DR: The model of head-restrained rats and functional neuroanatomical studies confirmed that the SLD in rats contains the neurons responsible for the onset and maintenance of paradoxical sleep, and it was proposed that these GABAergic neurons also inhibit the GABAergic neuron of the DPMe atThe onset and during PS and are therefore responsible for a reciprocal inhibitory interaction.
Abstract: In the middle of the last century, Michel Jouvet discovered paradoxical sleep (PS), a sleep phase paradoxically characterized by cortical activation and rapid eye movements and a muscle atonia. Soon after, he showed that it was still present in "pontine cats" in which all structures rostral to the brainstem have been removed. Later on, it was demonstrated that the pontine peri-locus coeruleus alpha (peri-LCalpha in cats, corresponding to the sublaterodorsal nucleus, SLD, in rats) is responsible for PS onset. It was then proposed that the onset and maintenance of PS is due to a reciprocal inhibitory interaction between neurons presumably cholinergic specifically active during PS localized in this region and monoaminergic neurons. In the last decade, we have tested this hypothesis with our model of head-restrained rats and functional neuroanatomical studies. Our results confirmed that the SLD in rats contains the neurons responsible for the onset and maintenance of PS. They further indicate that (1) these neurons are non-cholinergic possibly glutamatergic neurons, (2) they directly project to the glycinergic premotoneurons localized in the medullary ventral gigantocellular reticular nucleus (GiV), (3) the main neurotransmitter responsible for their inhibition during waking (W) and slow wave sleep (SWS) is GABA rather than monoamines, (4) they are constantly and tonically excited by glutamate and (5) the GABAergic neurons responsible for their tonic inhibition during W and SWS are localized in the deep mesencephalic reticular nucleus (DPMe). We also showed that the tonic inhibition of locus coeruleus (LC) noradrenergic and dorsal raphe (DRN) serotonergic neurons during sleep is due to a tonic GABAergic inhibition by neurons localized in the dorsal paragigantocellular reticular nucleus (DPGi) and the ventrolateral periaqueductal gray (vlPAG). We propose that these GABAergic neurons also inhibit the GABAergic neurons of the DPMe at the onset and during PS and are therefore responsible for the onset and maintenance of PS.
TL;DR: Although the data to guide the perioperative management of patients with moderate-to-severe obstructive sleep apnea syndrome is scarce, heightened awareness is recommended, as the selected use of therapy with nasal continuous positive airway pressure before surgery and after extubation may be beneficial.
TL;DR: In this paper, the relationship between sleep and depression is examined at both clinical and neurobiologic levels, and the treatment implications of the disturbances are reviewed at both the clinical and neurological levels.
Abstract: This review examines the relationship between sleep and depression. Most depressive disorders are characterized by subjective sleep disturbances, and the regulation of sleep is intricately linked to the same mechanisms that are implicated in the pathophysiology of depression. After briefly reviewing the physiology and topography of normal sleep, the disturbances revealed in studies of sleep in depression using polysomnographic recordings and neuroimaging assessments are discussed. Next, treatment implications of the disturbances are reviewed at both clinical and neurobiologic levels. Most antidepressant medications suppress rapid eye movement (REM) sleep, although this effect is neither necessary nor sufficient for clinical efficacy. Effects on patients' difficulties initiating and maintaining sleep are more specific to particular types of antidepressants. Ideally, an effective antidepressant will result in normalization of disturbed sleep in concert with resolution of the depressive syndrome, although few interventions actually restore decreased slow-wave sleep. Antidepressants that block central histamine 1 and serotonin 2 tend to have stronger effects on sleep maintenance, but are also prone to elicit complaints of daytime sedation. Adjunctive treatment with sedative hypnotic medications--primarily potent, shorter-acting benzodiazepine and gamma-aminobutyric acid (GABA A)-selective compounds such as zolpidem--are often used to treat associated insomnia more rapidly. Cognitive behavioral therapy and other nonpharmacologic strategies are also helpful.
TL;DR: It is speculated that chronic primary insomnia with polysomnographically documented sleep impairments activates the production of IL-6 analogous to sleep deprivation studies in healthy subjects, which might also implicate a higher risk for inflammatory and cardiovascular diseases in patients with chronic insomnia.
Abstract: The aim of the present study was to investigate whether there is a difference in evening/nocturnal interleukin-6 (IL-6) serum excretion in patients with primary insomnia compared to controls. We hypothesized that in insomniac patients, the excretion of evening/nocturnal IL-6 is enhanced, like observed in aged adults and after sleep deprivation in healthy subjects. We studied IL-6 serum concentrations in 11 patients (two males and nine females) with primary insomnia and 11 age and gender-matched healthy controls. Sleep was monitored polysomnographically for three consecutive nights. The measurement of IL-6 (from 19:00 h to 09:00 h) in 2-h intervals were performed prior to and during the last laboratory night. Polysomnographically determined sleep parameters and subjective ratings of sleep demonstrated clear-cut impairments of sleep in the insomniac group. Nocturnal IL-6 secretion was significantly increased (p<.05) in insomniac patients for the whole measurement period (mean area under the curve+/-SD: 27.94+/-14.15 pg/ml x 2h) compared to controls (16.70+/-7.64 pg/ml x 2h). Total IL-6 secretion correlated inversely with subjectively perceived sleep quality and amount of slow wave sleep in the insomniac patients. Amount of Wake Time correlated positively with IL-6 excretion in insomniacs. The results of the present study demonstrate significantly increased nocturnal IL-6 secretion in insomniacs. It might be speculated that chronic primary insomnia with polysomnographically documented sleep impairments activates the production of IL-6 analogous to sleep deprivation studies in healthy subjects. This might also implicate a higher risk for inflammatory and cardiovascular diseases in patients with chronic insomnia.
TL;DR: The sleep and epidemiological literatures to assess AA sleep suggest that AAs sleep worse than Caucasian Americans, and these data support further research into ethnic differences in both normal and disturbed sleep.
Abstract: Researchers have not thoroughly assessed the sleep of African Americans (AAs) despite the recent increased attention to ethnic research. This article reviews the sleep and epidemiological literatures to assess AA sleep. Although the limited data were sometimes inconsistent, they suggest that AAs sleep worse than Caucasian Americans. AAs take longer to fall asleep, report poorer sleep quality, have more light and less deep sleep, and nap more often and longer. AAs have a higher prevalence of sleep-disordered breathing and exhibit more risk factors for poor sleep. These differences are concentrated in young- and middle-age adults. There are no sleep disorders treatment data for AAs. These data support further research into ethnic differences in both normal and disturbed sleep.
TL;DR: A short nap is favorable for consolidation of procedural memory and Females showed more improvement than males in the declarative memory tasks irrespective of nap or wake.
TL;DR: RBD is rare, but REM sleep without atonia is relatively fre-quent in patients with probable Alzheimer disease, a tauopathy.
Abstract: Study objective To determine the frequency of rapid eye movement (REM) sleep behavior disorder (RBD) and REM sleep without atonia among patients with Alzheimer disease and control subjects. Design Overnight polysomnography. Settings Sleep laboratory. Patients Fifteen patients with probable Alzheimer disease (mean age +/-SD, 70.2+/-5.6) and 15 age-matched healthy control subjects (mean age +/- SD, 67.9 +/-5.4). Intervention N/A. Results Four patients with Alzheimer disease presented REM sleep with-out atonia. One of these patients had all the polysomnographic features of RBD, including behavioral manifestations during REM sleep. Conclusion RBD is rare, but REM sleep without atonia is relatively fre-quent in patients with probable Alzheimer disease, a tauopathy.
TL;DR: The effects of sleep deprivation and caffeine on sustained attention and regional EEG power in waking and sleep were inversely related and suggest that adenosinergic mechanisms contribute to individual differences in waking-induced impairment of neurobehavioral performance and functional aspects of EEG topography associated with sleep deprivation.
Abstract: Large individual differences characterize the changes induced by sleep deprivation on neurobehavioral functions and rhythmic brain activity. To investigate adenosinergic mechanisms in these differences, we studied the effects of prolonged waking and the adenosine receptor antagonist caffeine on sustained vigilant attention and regional electroencephalogram (EEG) power in the ranges of theta activity (6.25–8.25 Hz) in waking and the slow oscillation (
TL;DR: It is proposed that hypoxic arousals may have a more severe impact on sleep architecture in patients with OSA than non-hypoxic arousal and caused overall deficits in the EEG delta power of NREMS and marked deficits inThe total amount of REMS.
TL;DR: It is demonstrated that drug-free patients with chronic undifferentiated type schizophrenia suffer from profound disturbances in sleep continuity and sleep architecture, which may relate to similar underlying structural brain abnormalities.
TL;DR: This work re‐examine the electrophysiological properties of dorsal raphe cells across the sleep–wake cycle in rats by the extracellular recording of a large sample of single units and identifies two major types of cells, which differ in spike waveform.
Abstract: Through their widespread projections to the entire brain, dorsal raphe cells participate in many physiological functions and are associated with neuropsychiatric disorders. In previous studies, the width of action potentials was used as a criterion to identify putative serotonergic neurons, and to demonstrate that cells with broad spikes were more active in wakefulness, slowed down their activity in slow wave sleep and became virtually silent during paradoxical sleep. However, recent studies reported that about half of these presumed serotonergic cells were not immunoreactive for tyrosine hydroxylase. Here, we re-examine the electrophysiological properties of dorsal raphe cells across the sleep–wake cycle in rats by the extracellular recording of a large sample of single units (n= 770). We identified two major types of cells, which differ in spike waveform: a first population characterized by broad, mostly positive spikes, and a second one displaying symmetrical positive–negative spikes with a large distribution of spike durations (0.6–3.2 ms). Although we found classical broad-spike cells that were more active in wakefulness, we also found that about one-third of these cells increased or did not change their firing rate during sleep compared with wakefulness. Moreover, 62% of the latter cells were active in paradoxical sleep when most of raphe cells were silent. Such a diversity in the neuronal firing behaviour is important in the light of the recent controversy regarding the neurochemical identity of dorsal raphe cells exhibiting broad spikes. Our results also suggest that the dorsal raphe contains subpopulations of neurons with reciprocal activity across the sleep–wake cycle.
TL;DR: CBD modulates waking via activation of neurons in the hypothalamus and DRD, both regions are apparently involved in the generation of alertness, and CBD increases DA levels as measured by microdialysis and HPLC procedures.
TL;DR: Five lines of evidence are reviewed which may be used to support the proposition that sleep homeostasis is altered in Primary Insomnia, including findings pertaining to Slow Wave Sleep density, level of daytime sleepiness, sleepiness following sleep deprivation, recovery sleep following sleep deprived, and response to sleep restriction therapy.
TL;DR: TST during a 24-h period is not reduced and delta activity is increased and may reflect age, drug, or a contributing metabolic process, and the effect of wakefulness in patients receiving chemical paralysis on recovery and weaning from mechanical ventilation is unknown.
TL;DR: In untreated schizophrenia, psychotic decompensation is associated with profound insomnia, one of the prodromal symptoms associated with psychotic relapse, but side effects may include sedation or residual insomnia.
TL;DR: The first quantitative analysis of sleep in a non‐mammalian taxon (birds) focusing on the daily amount of time spent in slow‐wave sleep (SWS) and rapid‐eye movement (REM) sleep as determined by electrophysiological methods suggests that further insight into the function of sleep across the animal kingdom may require an expansion of sleep research beyond the current mammalian paradigm.
Abstract: Quantitative comparative studies of sleep have focused exclusively on mammals. Such studies have repeatedly found strong relationships between the time spent in various sleep states and constitutive variables related to morphology, physiology, and life history. These studies influenced the development of several prominent hypotheses for the functions of sleep, but the applicability of these patterns and hypotheses to non-mammalian taxa is unclear. Here, we present the first quantitative analysis of sleep in a non-mammalian taxon (birds), focusing on the daily amount of time spent in slow-wave sleep (SWS) and rapid-eye movement (REM) sleep as determined by electrophysiological methods. We examined the relationships between constitutive and sleep variables in 23 avian species following earlier studies in mammals, but also considered an index of exposure to predators while asleep and controlled for shared evolutionary history among taxa. Overall, our results were very different from those obtained for mammals. Most remarkably, the relationships between both SWS time and REM sleep time and all constitutive variables were very weak and markedly non-significant, even though we had adequate power to detect correlations typical of the mammalian data. Only an index of exposure to predation during sleep was significantly related to sleep time, which is the only result common to both birds and mammals. Our results suggest that further insight into the function(s) of sleep across the animal kingdom may require an expansion of sleep research beyond the current mammalian paradigm.