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Showing papers on "Non-rapid eye movement sleep published in 2006"


Journal ArticleDOI
01 Jun 2006-Nature
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


Journal ArticleDOI
TL;DR: Experimental human and animal studies on the effects of sleep deprivation on pain processing suggest that sleep deprivation produces hyperalgesic changes, which can interfere with analgesic treatments involving opioidergic and serotoninergic mechanisms of action.

523 citations


Journal ArticleDOI
TL;DR: The authors describe the hypothalamic circuitry for the integration of photic and nonphotic environmental time cues and how this integration allows organisms to sculpt patterns of rest-activity and sleep-wake cycles that are optimally adaptive.
Abstract: This mini-review article presents the remarkable progress that has been made in the past decade in our understanding of the neural circuitry underlying the regulation of sleep-wake states and circa...

489 citations


Journal ArticleDOI
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


Journal ArticleDOI
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


Journal ArticleDOI
TL;DR: It is suggested that besides being involved in shaping neuronal networks after learning, sleep spindles do reflect important aspects of efficient cortical‐subcortical connectivity, and are thereby linked to cognitive‐ and memory‐related abilities alike.
Abstract: Stage 2 sleep spindles have been previously viewed as useful markers for the development and integrity of the CNS and were more currently linked to 'offline re-processing' of implicit as well as explicit memory traces. Additionally, it had been discussed if spindles might be related to a more general learning or cognitive ability. In the present multicentre study we examined the relationship of automatically detected slow ( 13 Hz) stage 2 sleep spindles with: (i) the Raven's Advanced Progressive Matrices (testing 'general cognitive ability'); as well as (ii) the Wechsler Memory scale-revised (evaluating memory in various subdomains). Forty-eight healthy subjects slept three times (separated by 1 week) for a whole night in a sleep laboratory with complete polysomnographic montage. Whereas the first night only served adaptation and screening purposes, the two remaining nights were preceded either by an implicit mirror-tracing or an explicit word-pair association learning or (corresponding) control task. Robust relationships of slow and fast sleep spindles with both cognitive as well as memory abilities were found irrespectively of whether learning occurred before sleep. Based on the present findings we suggest that besides being involved in shaping neuronal networks after learning, sleep spindles do reflect important aspects of efficient cortical-subcortical connectivity, and are thereby linked to cognitive- and memory-related abilities alike.

254 citations


Journal ArticleDOI
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


Journal ArticleDOI
TL;DR: The data suggest that individuals experience difficulty in withholding an inappropriate response during TSD, even when they are able to attend to the incoming stimuli and respond accurately to appropriate stimuli.
Abstract: This study examined the effects of two nights of total sleep deprivation (TSD) and two nights of recovery sleep on response inhibition. Thirty-eight young, healthy adults performed a Go-NoGo task at 14 : 00 after: (1) a normal night of sleep; (2) each of two consecutive nights of TSD; and (3) each of two consecutive nights of recovery sleep; they also performed the task at 05 : 00 during the first night of sleep deprivation. We hypothesized that TSD would lead to an impaired ability to withhold a response that would be reversed with recovery sleep. Subjects did experience a significant increase in false positive responses throughout all of TSD, errors of omission (i.e. missed 'go' targets) were not significant until after the second night of TSD. Both components (withholding a response and automatic responding) of the task returned to baseline levels after one night of recovery sleep. These data suggest that individuals experience difficulty in withholding an inappropriate response during TSD, even when they are able to attend to the incoming stimuli and respond accurately to appropriate stimuli.

246 citations


Journal ArticleDOI
01 Mar 2006-Brain
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.

234 citations


Journal ArticleDOI
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.

225 citations


Journal ArticleDOI
TL;DR: The results indicate that, like during nocturnal sleep, daytime sleep EEG oscillations including spindle activity are modified after declarative learning of word pairs, and demonstrate here that the nature of the learning material is a determinant factor for sleep-related alterations after declARative learning.
Abstract: Learning-dependent increases in sleep spindle density have been reported during nocturnal sleep immediately after the learning session Here, we investigated experience-dependent changes in daytime sleep EEG activity after declarative learning of unrelated word pairs At weekly intervals, 13 young male volunteers spent three 24 h sessions in the laboratory under carefully controlled homeostatic and circadian conditions At approximately midday, subjects performed either one of two word-pair learning tasks or a matched nonlearning control task, in a counterbalanced order The two learning lists differed in the level of concreteness of the words used, resulting in an easier and a more difficult associative encoding condition, as confirmed by performance at immediate cued recall Subjects were then allowed to sleep for 4 h; afterward, delayed cued recall was tested Compared with the control condition, sleep EEG spectral activity in the low spindle frequency range and the density of low-frequency sleep spindles (1125-1375 Hz) were both significantly increased in the left frontal cortex after the difficult but not after the easy encoding condition Furthermore, we found positive correlations between these EEG changes during sleep and changes in memory performance between pre-nap and post-nap recall sessions These results indicate that, like during nocturnal sleep, daytime sleep EEG oscillations including spindle activity are modified after declarative learning of word pairs Furthermore, we demonstrate here that the nature of the learning material is a determinant factor for sleep-related alterations after declarative learning

Journal ArticleDOI
TL;DR: These findings suggest that motor patterns are already written in the brain codes (central pattern generators) embraced with an automatic sequence of EEG-vegetative events, but require a certain degree of activation (arousal) to become visibly apparent.

Journal ArticleDOI
TL;DR: The results suggest that sleep fragmentation negatively impacts spatial learning, and loss of N‐methyl‐d‐aspartate receptor‐dependent LTP in the hippocampal CA1 region may be one mechanism involved in this deficit.
Abstract: Sleep fragmentation, a symptom in many clinical disorders, leads to cognitive impairments. To investigate the mechanisms by which sleep fragmentation results in memory impairments, rats were awakened once every 2 min via 30 s of slow movement on an automated treadmill. Within 1 h of this sleep interruption (SI) schedule, rats began to sleep in the 90-s periods without treadmill movement. Total non-rapid eye movement sleep (NREM) sleep time did not change over the 24 h of SI, although there was a significant decline in rapid eye movement sleep (REM) sleep and a corresponding increase in time spent awake. In the SI group, the mean duration of sleep episodes decreased and delta activity during periods of wake increased. Control rats either lived in the treadmill without movement (cage controls, CC), or had 10-min periods of movement followed by 30 min of non-movement allowing deep/continuous sleep (exercise controls, EC). EC did not differ from baseline in the total time spent in each vigilance state. Hippocampal long-term potentiation (LTP), a long-lasting change in synaptic efficacy thought to underlie declarative memory formation, was absent in rats exposed to 24 and 72 h SI. In contrast, LTP was normal in EC rats. However, long-term depression and paired-pulse facilitation were unaltered by 24 h SI. Twenty-four hour SI also impaired acquisition of spatial learning in the hippocampus-dependent water maze test. Twenty-four hour SI elevated plasma corticosterone (CORT) to levels previously shown to enhance LTP (125 ng/mL). The results suggest that sleep fragmentation negatively impacts spatial learning. Loss of N-methyl-D-aspartate (NMDA) receptor-dependent LTP in the hippocampal CA1 region may be one mechanism involved in this deficit.

Journal ArticleDOI
TL;DR: In this paper, the authors used the DSM-IV-TR definition of nightmares to distinguish idiopathic nightmares from posttraumatic nightmares, which are part of a posttraumatic stress reaction or disorder that may result from experiencing a traumatic event.

Journal ArticleDOI
TL;DR: Stepwise regression analysis suggested that loss of REM sleep underlies the effects of SD on hippocampal BDNF, Synapsin I and CREB mRNA levels, whereas loss of NREM sleep underlie the effects on CAMKII mRNA.
Abstract: Previous work shows that sleep deprivation impairs hippocampal-dependent learning and long-term potentiation (LTP). Brain-derived neurotrophic factor (BDNF), cAMP response-element-binding (CREB) and calcium–calmodulin-dependent protein kinase II (CAMKII) are critical modulators of hippocampal-dependent learning and LTP. In the present study we compared the effects of short- (8 h) and intermediate-term (48 h) sleep deprivation (SD) on the expression of BDNF and its downstream targets, Synapsin I, CREB and CAMKII in the neocortex and the hippocampus. Rats were sleep deprived using an intermittent treadmill system which equated total movement in the SD and control treadmill animals (CT), but permitted sustained periods of rest in CT animals. Animals were divided into SD (treadmill schedule: 3 s on/12 s off) and two treadmill control groups, CT1 (15 min on/60 min off) and CT2 (30 min on/120 min off – permitting more sustained sleep). Real-time Taqman RT-PCR was used to measure changes in mRNA; BDNF protein levels were determined using ELISA. In the hippocampus, 8 h treatments reduced BDNF, Synapsin I, CREB and CAMKII gene expression in both SD and control groups. Following 48 h of experimental procedures, the expression of all these four molecular markers of plasticity was reduced in SD and CT1 groups compared to the CT2 and cage control groups. In the hippocampus, BDNF protein levels after 8 h and 48 h treatments paralleled the changes in mRNA. In neocortex, neither 8 h nor 48 h SD or control treatments had significant effects on BDNF, Synapsin I and CAMKII mRNA levels. Stepwise regression analysis suggested that loss of REM sleep underlies the effects of SD on hippocampal BDNF, Synapsin I and CREB mRNA levels, whereas loss of NREM sleep underlies the effects on CAMKII mRNA.

Journal ArticleDOI
TL;DR: The hypothesis that chronotype can originate from differences in the dissipation of sleep pressure and that homeostatic and circadian processes influence the sleep schedule preference independently is supported.
Abstract: Morningness-eveningness has been associated with the entrained circadian phase. However, we recently identified morning and evening types having similar circadian phases. In this paper, we compared parameters of slow-wave activity (SWA) decay in non-rapid-eye-movement (NREM) sleep between these two subgroups to test the hypothesis that differences in the dynamics of nocturnal homeostatic sleep pressure could explain differences in sleep timing preference. Twelve morning-type subjects and 12 evening-type subjects with evening types (aged 19-34 years) selected using the Morningness-Eveningness Questionnaire were further classified according to the phase of their dim light melatonin onset (DLMO). The six morning types with the earliest DLMO were compared to the six evening types with the latest DLMO ('extreme' phases), and the six morning types with the latest DLMO were compared to the six evening types with the earliest DLMO ('intermediate' phases). Subjects slept according to their preferred sleep schedule. Spectral activity in four midline derivations (Fz, Cz, Pz, Oz) was calculated in NREM sleep and an exponential decay function was applied on SWA data averaged per sleep cycle. In the subjects with intermediate circadian phases, both initial level and decay rate of SWA in Fz were significantly higher in morning than in evening types. No difference appeared between chronotypes of extreme circadian phases. There was no correlation between individual estimates of SWA decay and DLMO. These results support the hypothesis that chronotype can originate from differences in the dissipation of sleep pressure and that homeostatic and circadian processes influence the sleep schedule preference independently.

Journal ArticleDOI
TL;DR: The results establish that proper alignment between sleepwakefulness and internal circadian time is crucial for enhancement of cognitive performance and demonstrate that exposure to dim light is sufficient to expand the range of entrainment in humans.
Abstract: Sleep---wake homeostatic and internal circadian timedependent brain processes interact to regulate human brain function so that alert wakefulness is promoted during the daytime and consolidated sleep is promoted at nighttime. The consequence of chronically altering the normal relationship between these processes for human brain function is largely unknown. We tested cognitive and vigilance performance while subjects lived in the laboratory for over a month. The subjects lived on either 24.0- or 24.6-hr day lengths. Half of the subjects tested maintained a normal relationship between sleep---wakefulness and internal circadian time (synchronized group), whereas the other half did not (nonsynchronized group). Levels of the sleep-promoting hormone melatonin were high during scheduled sleep in the synchronized group, whereas melatonin levels were high during scheduled wakefulness in the nonsynchronized group. Failure to adapt to the scheduled day length was dependent upon individual differences in intrinsic circadian period. Total sleep time was reduced, sleep latency and Rapid Eye Movement (REM) latency were shortened, and wakefulness after sleep onset was increased in the nonsynchronized group. Cognitive performance improved (i.e., learning) in the synchronized group, whereas learning was significantly impaired in the nonsynchronized group. Attention progressively declined in both groups, suggesting that 8 hr of scheduled sleep per night is insufficient to maintain brain vigilance even when sleep occurs at an appropriate biological time. Our results establish that proper alignment between sleep---wakefulness and internal circadian time is crucial for enhancement of cognitive performance. In addition, our results demonstrate that exposure to dim light (~25 lx) is sufficient to expand the range of entrainment in humans.

Journal ArticleDOI
TL;DR: It is concluded that NPAS2 plays a role in sleep homeostasis, most likely at the level of the thalamus and cortex, whereNPAS2 is abundantly expressed.
Abstract: Because the transcription factor neuronal Per-Arnt-Sim-type signal-sensor protein-domain protein 2 (NPAS2) acts both as a sensor and an effector of intracellular energy balance, and because sleep is thought to correct an energy imbalance incurred during waking, we examined NPAS2's role in sleep homeostasis using npas2 knockout (npas2−/−) mice. We found that, under conditions of increased sleep need, i.e., at the end of the active period or after sleep deprivation (SD), NPAS2 allows for sleep to occur at times when mice are normally awake. Lack of npas2 affected electroencephalogram activity of thalamocortical origin; during non-rapid eye movement sleep (NREMS), activity in the spindle range (10–15 Hz) was reduced, and within the delta range (1–4 Hz), activity shifted toward faster frequencies. In addition, the increase in the cortical expression of the NPAS2 target gene period2 (per2) after SD was attenuated in npas2−/− mice. This implies that NPAS2 importantly contributes to the previously documented wake-dependent increase in cortical per2 expression. The data also revealed numerous sex differences in sleep; in females, sleep need accumulated at a slower rate, and REMS loss was not recovered after SD. In contrast, the rebound in NREMS time after SD was compromised only in npas2−/− males. We conclude that NPAS2 plays a role in sleep homeostasis, most likely at the level of the thalamus and cortex, where NPAS2 is abundantly expressed.

Journal ArticleDOI
TL;DR: The results indicate that H(1)R is involved in the regulation of behavioral state transitions from NREM sleep to wakefulness and that the arousal effect of the H(3)R antagonist completely depends on the activation of histaminergic systems through H( 1)R.
Abstract: Histaminergic neurons play an important role in the regulation of sleep-wake behavior through histamine H(1) receptors (H(1)R). Blockade of the histamine H(3) receptor (H(3)R) is proposed to induce wakefulness by regulating the release of various wake-related transmitters, not only histamine. In the present study, we characterized sleep-wake cycles of H(1)R knockout (KO) mice and their arousal responses to an H(3)R antagonist. Under baseline conditions, H(1)R KO mice showed sleep-wake cycles essentially identical to those of WT mice but with fewer incidents of brief awakening (<16-sec epoch), prolonged durations of non-rapid eye movement (NREM) sleep episodes, a decreased number of state transitions between NREM sleep and wakefulness, and a shorter latency for initiating NREM sleep after an i.p. injection of saline. The H(1)R antagonist pyrilamine mimicked these effects in WT mice. When an H(3)R antagonist, ciproxifan, was administered i.p., wakefulness increased in WT mice in a dose-dependent manner but did not increase at all in H(1)R KO mice. In vivo microdialysis revealed that the i.p. application of ciproxifan increased histamine release from the frontal cortex in both genotypes of mice. These results indicate that H(1)R is involved in the regulation of behavioral state transitions from NREM sleep to wakefulness and that the arousal effect of the H(3)R antagonist completely depends on the activation of histaminergic systems through H(1)R.

Journal ArticleDOI
TL;DR: It is shown that retention of visuospatial memories over a 24-h period correlates with the total number of sleep spindles detected over parietal regions during the intervening night-time sleep, which provides further evidence for the association between sleep spindle activity and declarative memory consolidation.

Journal ArticleDOI
TL;DR: T-type Ca2+ channels constitute the single most crucial voltage-dependent conductance that permeates all activities of thalamic neurones during NREM sleep and should now move away from the simplistic, though historically significant, view of these channels as being responsible only for low thresholdCa2+ potentials.

Journal ArticleDOI
TL;DR: Particular emphasis is placed on the differentiation of nocturnal frontal lobe epilepsy from non–rapid eye movement (NREM) arousal disorders and other parasomnias, and the value of recording episodes with video EEG polysomnography is discussed.
Abstract: The diagnosis of paroxysmal events in sleep represents a significant challenge for the clinician, with the distinction of nocturnal epilepsy from nonepileptic sleep disorders often the primary concern. Diagnostic error or uncertainty is not uncommon in this situation, particularly with respect to nocturnal frontal lobe epilepsy (NFLE), which has a variable and often unusual presentation. Such errors can be minimized if the range of nonepileptic disorders with motor activity in sleep is fully appreciated. Here we review these disorders, before discussing the important clinical and electrographic features that allow their accurate differentiation from seizures. Particular emphasis is placed on the differentiation of nocturnal frontal lobe epilepsy from non-rapid eye movement (NREM) arousal disorders and other parasomnias. The value of recording episodes with video EEG polysomnography is discussed.

Journal ArticleDOI
TL;DR: The frequency-specific clustering of power maps suggests that distinct generators underlie EEG frequency bands and that basic topographic features appear to be state-independent.

Journal ArticleDOI
TL;DR: These findings define potential roles for MnPN and vlPOA GABAergic neurons in homeostatic aspects of sleep regulation and examine c-Fos protein immunoreactivity in these neurons under experimental conditions that dissociated homeostatics sleep pressure, sleep amount, and time of day.
Abstract: The median preoptic nucleus (MnPN) and the ventrolateral preoptic area (vlPOA) contain putative sleep-regulatory neurons that exhibit elevated discharge rates during sleep compared with waking. Expression of c-Fos protein immunoreactivity (IR) in GABAergic neurons in the MnPN and the vlPOA is high in spontaneously sleeping rats and in rats undergoing recovery sleep after sleep deprivation. However, it is unclear whether c-Fos-IR in these neurons is evoked by increases in sleep pressure or by increases in sleep amount. We examined c-Fos-IR in MnPN and vlPOA neurons under experimental conditions that dissociated homeostatic sleep pressure, sleep amount, and time of day. Groups of rats with strong diurnal rhythms in sleep-wake organization were killed after (1) spontaneous sleep in the light, (2) spontaneous sleep in the dark, (3) sleep deprivation (SLD) in the light and (4) recovery sleep after SLD in the light. Numbers of GABAergic neurons expressing c-Fos-IR in the MnPN were significantly higher after SLD in the light compared with spontaneous sleep and recovery sleep in the light. In contrast, Fos-IR in vlPOA GABAergic neurons was most prevalent after spontaneous sleep and recovery sleep in the light. No light-dark differences in Fos-IR were observed in the MnPN after SLD in groups of rats with weak or absent diurnal sleep-waking rhythms. Our findings define potential roles for MnPN and vlPOA GABAergic neurons in homeostatic aspects of sleep regulation.

Journal ArticleDOI
01 Jul 2006-Sleep
TL;DR: The presence of periodic limb movements during sleep and chewing activity, the reported efficacy of dopaminergic medications, and the compulsory food-seeking behavior all argue for a dopaminaergic dysfunction underlying the pathogenesis of sleep-related eating disorder.
Abstract: Study objectives To describe the clinical and videopolysomnographic characteristics of nocturnal eating episodes in sleep-related eating disorder. Design Descriptive study of outpatients prospectively enrolled in 2 sleep centers. Setting Videopolysomnographic recordings done in the sleep laboratory. Patients Thirty-five consecutive drug-free patients with nocturnal eating. Interventions N/A. Measurements and results Clinical interviews disclosed abnormal compulsory nocturnal eating episodes in all patients associated with a clinical report of sleepwalking (in 1), somniloquy (in 5), restless legs syndrome (in 8), and periodic limb movements during sleep (in 4). Videopolysomnography documented 45 episodes of nocturnal eating in 26 patients. Eating always occurred after complete awakenings from non-rapid eye movement sleep and only in 1 patient from REM sleep and was characterized by electroencephalographic alpha activity with no dissociated features of state-dependent sleep variables. Patients interviewed during the eating episodes were fully conscious and remembered the events the next day. Pathological periodic limb movements during sleep index was recorded in 22 and restless legs syndrome dyskinesias in 5 patients. Recurring chewing and swallowing movements during sleep were a feature in 29 patients, associated in about half of the events with electroencephalographic arousals. Conclusions In our patients, eating episodes occurred with normal consciousness and recall. Chewing or swallowing movements during sleep occurred frequently, resembling rhythmic masticatory-muscle activity in bruxism patients. The presence of periodic limb movements during sleep and chewing activity, the reported efficacy of dopaminergic medications, and the compulsory food-seeking behavior all argue for a dopaminergic dysfunction underlying the pathogenesis of sleep-related eating disorder.

Journal ArticleDOI
01 Oct 2006-Sleep
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.

Journal ArticleDOI
TL;DR: It is concluded that CA neurones promote wakefulness, participate in central respiratory chemoreception, stimulate breathing frequency, and minimize breathing variability in REM sleep.
Abstract: Brainstem catecholamine (CA) neurones have wide projections and an arousal-state-dependent activity pattern. They are thought to modulate the processing of sensory information and also participate in the control of breathing. Mice with lethal genetic defects that include CA neurones have abnormal respiratory control at birth. Also the A6 region (locus coeruleus), which contains CA neurones sensitive to CO2in vitro, is one of many putative central chemoreceptor sites. We studied the role of CA neurones in the control of breathing during sleep and wakefulness by specifically lesioning them with antidopamine β-hydroxylase–saporin (DBH-SAP) injected via the 4th ventricle. After 3 weeks there was a 73–84% loss of A5, A6 and A7 tyrosine hydroxylase (TH) immunoreactive (ir) neurones along with 56–60% loss of C1 and C2 phenyl ethanolamine-N-methyltransferase (PNMT)-ir neurones. Over the 3 weeks, breathing frequency decreased significantly during air and 3 or 7% CO2 breathing in both wakefulness and non-REM (NREM) sleep. The rats spent significantly less time awake and more time in NREM sleep. REM sleep time was unaffected. The ventilatory response to 7% CO2 was reduced significantly in wakefulness at 7, 14 and 21 days (−28%) and in NREM sleep at 14 and 21 days (−26%). Breathing variability increased in REM sleep but not in wakefulness or NREM sleep. We conclude that CA neurones (1) promote wakefulness, (2) participate in central respiratory chemoreception, (3) stimulate breathing frequency, and (4) minimize breathing variability in REM sleep.

Journal ArticleDOI
01 Jun 2006-Sleep
TL;DR: Children with ADHD showed a lower CAP rate and a lower number of CAP sequences; this supports the hypothesis of the existence of a hypoarousal state in these patients.
Abstract: Study objectives To evaluate non-rapid eye movement sleep instability (NREM), as measured by the cyclic alternating pattern (CAP), in a cohort of children with attention-deficit/hyperactivity disorder (ADHD) and normal controls. Design Prospective study. Settings Sleep laboratory. Participants Twenty consecutive outpatients with ADHD (18 boys and 2 girls; age range 6-13 years, mean age 9.3 years) and 20 normal children matched for age and socioeconomic status underwent polysomnographic recordings for 2 consecutive nights in a standard laboratory setting. Sleep was visually scored for sleep macrostructure and CAP, according to standard criteria. Measurements and results Children with ADHD showed significantly reduced sleep duration and increased rate of stage shifts. All children with ADHD had an apnea-hypopnea index less than 1. Those with ADHD presented lower total CAP rates and lower CAP rates during sleep stage 2 than did normal controls. Moreover, in children with ADHD, we found a lower number of CAP sequences and a reduced total A1 index, mainly in light sleep (sleep stages 1 and 2). We did not find differences in A subtype percentages, but there was a longer duration of A1 subtypes in children with ADHD. Conclusions Children with ADHD showed a lower CAP rate and a lower number of CAP sequences; this supports the hypothesis of the existence of a hypoarousal state in these patients.

Journal ArticleDOI
TL;DR: The olfactory deficit found in most idiopathic RBD patients shares similarities with that described in PD and may be a sign of a widespread neurodegenerative process.

Journal ArticleDOI
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 (