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Rapid Eye Movement (rapid + eye_movement)
Terms modified by Rapid Eye Movement Selected AbstractsHistamine-1 receptor is not required as a downstream effector of orexin-2 receptor in maintenance of basal sleep/wake statesACTA PHYSIOLOGICA, Issue 3 2010M. Hondo Abstract Aim:, The effect of orexin on wakefulness has been suggested to be largely mediated by activation of histaminergic neurones in the tuberomammillary nucleus (TMN) via orexin receptor-2 (OX2R). However, orexin receptors in other regions of the brain might also play important roles in maintenance of wakefulness. To dissect the role of the histaminergic system as a downstream mediator of the orexin system in the regulation of sleep/wake states without compensation by the orexin receptor-1 (OX1R) mediated pathways, we analysed the phenotype of Histamine-1 receptor (H1R) and OX1R double-deficient (H1R,/,;OX1R,/,) mice. These mice lack OX1R-mediated pathways in addition to deficiency of H1R, which is thought to be the most important system in downstream of OX2R. Methods:, We used H1R deficient (H1R,/,) mice, H1R,/,;OX1R,/, mice, OX1R and OX2R double-deficient (OX1R,/,;OX2R,/,) mice, and wild type controls. Rapid eye movement (REM) sleep, non-REM (NREM) sleep and awake states were determined by polygraphic electroencephalographic/electromyographic recording. Results:, No abnormality in sleep/wake states was observed in H1R,/, mice, consistent with previous studies. H1R,/,;OX1R,/, mice also showed a sleep/wake phenotype comparable to that of wild type mice, while OX1R,/,; OX2R,/, mice showed severe fragmentation of sleep/wake states. Conclusion:, Our observations showed that regulation of the sleep/wake states is completely achieved by OX2R-expressing neurones without involving H1R-mediated pathways. The maintenance of basal physiological sleep/wake states is fully achieved without both H1 and OX1 receptors. Downstream pathways of OX2R other than the histaminergic system might play an important role in the maintenance of sleep/wake states. [source] Sleep staging and respiratory events in refractory epilepsy patients: Is there a first night effect?EPILEPSIA, Issue 12 2008Linda M. Selwa Summary Purpose:, We performed this analysis of possible first night effects (FNEs) on sleep and respiratory parameters in order to evaluate the need for two serial night polysomnograms (PSGs) to diagnose obstructive sleep apnea (OSA) in epilepsy patients. Methods:, As part of a pilot multicenter clinical trial investigating the effects of treating sleep apnea in epilepsy, two nights of PSG recording were performed for 40 patients with refractory epilepsy and OSA symptoms. Sleep architecture was examined in detail, along with respiratory parameters including apnea/hypopnea index (AHI) and minimum oxygen saturation. Analysis included two-tailed t -tests, Wilcox sign rank analysis, and Bland Altman measures of agreement. Results:, Total sleep time differed between the two nights (night 1,363.8 min + 59.4 vs. 386.3 min + 68.6, p = 0.05). Rapid eye movement (REM) sleep and percentage of REM sleep were increased during night two (night 1: 12.3% + 5.9 vs. night 2: 15.5% + 6.2, p = 0.007), and the total minutes of slow-wave sleep (SWS) were increased (night 1: 35.6 + 60.7 vs. night 2: 46.4 + 68.1, p = 0.01). No other sleep or respiratory variables differed between the two nights. Given an AHI inclusion criterion of five apneas per hour, the first PSG identified all but one patient with OSA. Discussion:, Respiratory parameters showed little variability between the first and second nights. Sleep architecture was mildly different between the first and second PSG night. Performing two consecutive baseline PSGs to diagnose OSA may not be routinely necessary in this population. [source] Characterization of sleep,wake patterns in a novel transgenic mouse line overexpressing human prepro-orexin/hypocretinACTA PHYSIOLOGICA, Issue 3 2010K. A. Mäkelä Abstract Aim:, Orexin/hypocretin peptides are expressed in the lateral hypothalamus and involved in the regulation of autonomic functions, energy homeostasis and arousal states. The sleep disorder narcolepsy, which is characterized by excessive daytime sleepiness and occurrence of sudden rapid eye movement (REM) sleep, is associated with a loss of orexin neurones. Our study investigated the effects of orexins on sleep,wake patterns in a novel transgenic mouse line overexpressing the human prepro-orexin (hPPO) gene under the control of its endogenous promoter. Methods:, Orexin overexpression was investigated by PCR, Southern and Western blotting as well as immunohistochemistry. Polysomnographic recordings were performed for analyses of sleep,wake patterns and for electroencephalographic activity during 24 h baseline and during and after 6 h of sleep deprivation (SD). Results:, Transgenic hPPO mice had increased expression of human prepro-orexin (hPPO) and orexin-A in the hypothalamus. Transgene expression decreased endogenous orexin-2 receptors but not orexin-1 receptors in the hypothalamus without affecting orexin receptor levels in the basal forebrain, cortex or hippocampus. Transgenic mice compared with their wild type littermates showed small but significant differences in the amount of waking and slow wave sleep, particularly during the light,dark transition periods, in addition to a slight reduction in REM sleep during baseline and during recovery sleep after SD. Conclusion:, The hPPO-overexpressing mice show a small reduction in REM sleep, in addition to differences in vigilance state amounts in the light/dark transition periods, but overall the sleep,wake patterns of hPPO-overexpressing mice do not significantly differ from their wild type littermates. [source] Vagus Nerve Stimulation Therapy Induces Changes in Heart Rate of Children during SleepEPILEPSIA, Issue 5 2007Boubker Zaaimi Summary:,Purpose: This study analyzed changes in the heart rates of children receiving vagus nerve stimulation (VNS) therapy for pharmacoresistant epilepsy. Methods: Changes in the heart rates of ten children receiving VNS therapy for pharmacoresistant epilepsy were evaluated with polysomnographic recordings, including electrocardiogram (ECG), EEG, thoraco-abdominal distension, nasal airflow, and VNS artifacts. Measurements during stimulation were compared with those at baseline for each patient. Result: While the VNS therapy pulse generator was delivering stimulation, the heart rates of four children increased significantly (p < 0.01), decreased for one child, and increased at the end of the stimulation for one child. The heart rates of four children did not change. Changes in heart rate varied during VNS, within stimulation cycles for individual children and from one child to another. Changes in heart rate differed between rapid eye movement (REM) and non-REM (NREM) sleep states. Respiratory changes (increases in frequency and decreases in amplitude) were concomitant with the changes in heart rate. Conclusion: In this case series of children with pharmacoresistant epilepsy, cardiorespiratory variations occurred while the VNS therapy pulse generator was delivering stimulation. Understanding these variations may allow further optimization of VNS parameters. [source] Paroxysmal Motor Disorders of Sleep: The Clinical Spectrum and Differentiation from EpilepsyEPILEPSIA, Issue 11 2006Christopher P. Derry Summary:, 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. [source] Two-way active avoidance training-specific increases in phosphorylated cAMP response element-binding protein in the dorsal hippocampus, amygdala, and hypothalamusEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2005Subhash Saha Abstract Previous studies have demonstrated that the activation of pontine-wave (P-wave) generating cells in the brainstem during post-training rapid eye movement (REM) sleep is critical for the consolidation of memory for two-way active avoidance (TWAA) learning in the rat. Here, using immunocytochemistry, we investigated the spatio-temporal distribution of CREB phosphorylation within different parts of the dorsal hippocampus, amygdala, and hypothalamus following a session of TWAA training in the rat. We show that the TWAA training trials increased phosphorylation of CREB (p-CREB) in the dorsal hippocampus, amygdala, amygdalo-hippocampal junction (AHi), and hypothalamus. However, the time intervals leading to training-induced p-CREB activity were different for different regions of the brain. In the dorsal hippocampus, p-CREB activity was maximal at 90 min and this activity disappeared by 180 min. In the AHi, activity of the p-CREB peaked by 180 min and disappeared by 360 min. In the amygdala, the p-CREB activity peaked at 180 min and still remained higher than the control at the 360 min interval. In the hypothalamus, at 90 min p-CREB activity was present only in the ventromedial hypothalamus; however, by 180 min this p-CREB activity was also present in the dorsal hypothalamus, perifornical area, and lateral hypothalamus. By 360 min, p-CREB activity disappeared from the hypothalamus. This TWAA training trials-induced spatiotemporal characteristic of CREB phosphorylation, for the first time, suggests that REM sleep P-wave generator activation-dependent memory processing involves different parts of the dorsal hippocampus, amygdala, and hypothalamus. [source] Single neuron burst firing in the human hippocampus during sleepHIPPOCAMPUS, Issue 6 2002Richard J. Staba Abstract Although there are numerous non-primate studies of the single neuron correlates of sleep-related hippocampal EEG patterns, very limited hippocampal neuronal data are available for correlation with human sleep. We recorded human hippocampal single neuron activity in subjects implanted with depth electrodes required for medical diagnosis and quantitatively evaluated discharge activity from each neuron during episodes of wakefulness (Aw), combined stage 3 and 4 slow-wave sleep (SWS), and rapid eye movement (REM) sleep. The mean firing rate of the population of single neurons was significantly higher during SWS and Aw compared with REM sleep (p = 0.002; p < 0.0001). In addition, burst firing was significantly greater during SWS compared with Aw (p = 0.001) and REM sleep (p < 0.0001). The synchronized state of SWS and associated high-frequency burst discharge found in human hippocampus may subserve functions similar to those reported in non-primate hippocampus that require burst firing to induce synaptic modifications in hippocampal circuitry and in hippocampal projections to neocortical targets that participate in memory consolidation. Hippocampus 2002;12:724,734. © 2002 Wiley-Liss, Inc. [source] Rhythmic hippocampal slow oscillation characterizes REM sleep in humansHIPPOCAMPUS, Issue 6 2001Róbert Bódizs Abstract Hippocampal rhythmic slow activity (RSA) is a well-known electrophysiological feature of exploratory behavior, spatial cognition, and rapid eye movement (REM) sleep in several mammalian species. Recently, RSA in humans during spatial navigation was reported, but systematic data regarding human REM sleep are lacking. Using mesio-temporal corticography with foramen ovale electrodes in epileptic patients, we report the presence of a 1.5,3-Hz synchronous rhythmic hippocampal oscillation seemingly specific to REM sleep. This oscillation is continuous during whole REM periods, is clearly observable by visual inspection, and appears in tonic and phasic REM sleep episodes equally. Quantitative analysis proved that this 1.5,3-Hz frequency band significantly differentiates REM sleep from waking and slow-wake sleep (SWS). No other frequency band proved to be significant or showed this high rhythmicity. Even in temporo-lateral surface recordings, although visually much less striking, the relative power of the 1.5,3-Hz frequency band differentiates REM sleep from other states with statistical significance. This could mean that the 1.5,3-Hz hippocampal RSA spreads over other cortical areas in humans as in other mammals. We suggest that this oscillation is the counterpart of the hippocampal theta of mammalian REM sleep, and that the 1.5,3-Hz delta EEG activity is a basic neurophysiological feature of human REM sleep. Hippocampus 2001;11:747,753. © 2001 Wiley-Liss, Inc. [source] fMRI evidence for multisensory recruitment associated with rapid eye movements during sleepHUMAN BRAIN MAPPING, Issue 5 2009Charles Chong-Hwa Hong Abstract We studied the neural correlates of rapid eye movement during sleep (REM) by timing REMs from video recording and using rapid event-related functional MRI. Consistent with the hypothesis that REMs share the brain systems and mechanisms with waking eye movements and are visually-targeted saccades, we found REM-locked activation in the primary visual cortex, thalamic reticular nucleus (TRN), ,visual claustrum', retrosplenial cortex (RSC, only on the right hemisphere), fusiform gyrus, anterior cingulate cortex, and the oculomotor circuit that controls awake saccadic eye movements (and subserves awake visuospatial attention). Unexpectedly, robust activation also occurred in non-visual sensory cortices, motor cortex, language areas, and the ascending reticular activating system, including basal forebrain, the major source of cholinergic input to the entire cortex. REM-associated activation of these areas, especially non-visual primary sensory cortices, TRN and claustrum, parallels findings from waking studies on the interactions between multiple sensory data, and their ,binding' into a unified percept, suggesting that these mechanisms are also shared in waking and dreaming and that the sharing goes beyond the expected visual scanning mechanisms. Surprisingly, REMs were associated with a decrease in signal in specific periventricular subregions, matching the distribution of the serotonergic supraependymal plexus. REMs might serve as a useful task-free probe into major brain systems for functional brain imaging. Hum Brain Mapp 2009. © 2008 Wiley-Liss, Inc. [source] Impact of the novel antidepressant agomelatine on disturbed sleep,wake cycles in depressed patients,HUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 3 2010Maria-Antonia Quera-Salva Abstract Background Disturbance of sleep,wake cycles is common in major depressive disorder (MDD), usually as insomnia, but also as hypersomnia or reduced daytime alertness. Agomelatine, an MT1 and MT2 receptor agonist and 5-HT2C receptor antagonist, represents a novel approach in MDD, with proven antidepressant efficacy and a positive impact on the sleep,wake cycle. We review the effects of agomelatine 25/50,mg/day on objective and subjective measures of the sleep,wake cycle in MDD. Subjective measures Agomelatine improved all aspects of the sleep,wake cycle from as early as 1 week in randomized trials versus selective serotonin reuptake inhibitors and venlafaxine, particularly getting off to sleep and quality of sleep, with an improvement in daytime alertness. Objective measures Agomelatine's effect on sleep architecture in MDD has been measured by polysomnography (PSG). There were significant improvements in sleep efficiency, slow-wave sleep (SWS), and the distribution of delta activity throughout the night, but no change in amount or latency of rapid eye movement (REM) sleep. Furthermore, the slow-wave sleep was resynchronized to the first sleep cycle of the night. Conclusion Agomelatine, a novel antidepressant, improves disturbed sleep,wake cycles in MDD. The improvement of both nighttime sleep and daytime functioning with agomelatine are promising features of this antidepressant regarding the management of MDD. Copyright © 2010 John Wiley & Sons, Ltd. [source] Increased turnover of Na-K ATPase molecules in rat brain after rapid eye movement sleep deprivationJOURNAL OF NEUROSCIENCE RESEARCH, Issue 6 2003Sudipta Majumdar Abstract It has been shown that rapid eye movement (REM) sleep deprivation increases Na-K ATPase activity. Based on kinetic study, it was proposed that increased activity was due to enhanced turnover of enzyme molecules. To test this, anti-,1 Na-K ATPase monoclonal antibody (mAb 9A7) was used to label Na-K ATPase molecules. These labeled enzymes were quantified on neuronal membrane by two methods: histochemically on neurons in tissue sections from different brain areas, and by Western blot analysis in control and REM sleep-deprived rat brains. The specific enzyme activity was also estimated and found to be increased, as in previous studies. The results confirmed our hypothesis that after REM sleep deprivation, increased Na-K ATPase activity was at least partly due to increased turnover of Na-K ATPase molecules in the rat brain. © 2003 Wiley-Liss, Inc. [source] Sleep architecture in children with adenoidal hypertrophyJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 10 2006Xiao-Wen Zhang Aim: Adenoidal hypertrophy (AH) in children is associated with obstructive manifestations like mouth breathing, snoring. Unfortunately, little is known regarding sleep architecture of AH in children. The purpose of this study was therefore undertaken to investigate the polysomnographic variables in children with AH. Method: 47 children with AH and 11 controls underwent nocturnal polysomnography. Sleep was scored manually according to the standard set by Rechtschaffen. Results: In AH, stage 1 sleep percentage and rapid eye movement (REM) latency were increased significantly, while the sleep percentage of stage 2 and REM was decreased remarkably compared with that of controls. Arousal index in AH was much more higher than that in controls. Arousal index in REM sleep was higher than that in non-rapid eye movement (NREM) sleep in AH, but the number of arousals in REM sleep was lower than that in NREM sleep. Hypopnea events were the most common type of respiratory events, followed by obstructive events in AH and controls. Apnea/hypopnea index in AH was higher in comparison to controls. No significant difference was found between the children with AH and controls in SaO2 nadir (%) and base mean SaO2 (%). Apnea/hypopnea index was related to hypopnea arousal in REM sleep and hypoxemia arousal in NREM sleep. Conclusion: AH is predominantly characterised by a hypopnea with little obstruction in children. Our results clearly and for the first time demonstrated that sleep architecture was abnormal in children with AH. We therefore speculate that hypopnea arousal in REM sleep and hypoxemia arousal in NREM sleep may play an important role in the course of respiratory disturbance. [source] Acute sleep-promoting action of the melatonin agonist, ramelteon, in the ratJOURNAL OF PINEAL RESEARCH, Issue 2 2008Simon P. Fisher Abstract:, Insomnia, which is severe enough to warrant treatment, occurs in ,10% of the general population. It is associated with a range of adverse consequences for human health, economic productivity and quality of life. In animal and human studies, administration of melatonin has been reported to promote sleep, although there has been controversy regarding its effectiveness. The present study used a chronically implanted radiotelemetry transmitter to record electroencephalogram (EEG) and electromyogram (EMG) to enable discrimination of wake (W), nonrapid eye movement (NREM) sleep and rapid eye movement (REM) sleep in un-restrained rats. The acute action of melatonin and ramelteon, a melatonin agonist recently approved for long-term treatment of insomnia in the USA, was examined. Radioligand binding assays on recombinant human MT1/MT2 receptors showed that both the melatonin and ramelteon were both high affinity, nonsubtype selective ligands. Both compounds acted as potent full agonists on a cellular model of melatonin action, the pigment aggregation response in Xenopus laevis melanophores. Both melatonin and ramelteon (10 mg/kg, i/p), administered close to the mid-point of the dark phase of the L:D cycle, significantly reduced NREM sleep latency (time from injection to the appearance of NREM sleep). Both the drugs also produced a short-lasting increase in NREM sleep duration, but the NREM power spectrum was unaltered. Neither drug altered REM latency, REM sleep duration nor power spectrum during REM sleep. In conclusion, ramelteon administration, like melatonin, exerted an acute, short-lasting sleep-promoting effect in the rat, the model most commonly used to evaluate the activity of novel hypnotic drugs. [source] Disruptions in Sleep Time and Sleep Architecture in a Mouse Model of Repeated Ethanol WithdrawalALCOHOLISM, Issue 7 2006Lynn M. Veatch Background: Insomnia and other sleep difficulties are perhaps the most common and enduring symptoms reported by alcoholics undergoing detoxification, especially those alcoholics with a history of multiple detoxifications. While some studies have reported sleep disruptions in animal models after chronic ethanol exposure, the reports are inconsistent and few address sleep architecture across repeated ethanol exposures and withdrawals. The present study evaluated sleep time and architecture in a well-characterized mouse model of repeated chronic ethanol exposure and withdrawal. Methods: C57BL6/J mice were fitted with electrodes in frontal cortex, hippocampus, and nuchal muscle for collection of continuous electroencephalogram (EEG)/electromyogram (EMG) data. Baseline data were collected, after which mice received 4 cycles of 16-hour exposure to alcohol (ethanol: EtOH) vapor separated by 8-hour periods of withdrawal or similar handling in the absence of EtOH vapor. Ethanol-exposed mice attained a blood ethanol concentration of 165 mg%. Upon completion of vapor exposure, EEG/EMG data were again collected across 4 days of acute withdrawal. Data were subjected to automated analyses classifying 10-second epochs into wake, non,rapid eye movement (REM) sleep, or REM sleep states. Results: Mice in withdrawal after chronic EtOH exposure showed profound disruptions in the total time asleep, across the acute withdrawal period. Sleep architecture, the composition of sleep, was also disrupted with a reduction in non-REM sleep concomitant with a profound increase in REM sleep. While altered sleep time and non-REM sleep loss resolved by the fourth day of withdrawal, the increase in REM sleep ("REM rebound") persisted. Conclusions: These results mirror those reported for the human alcoholic and demonstrate that EtOH withdrawal,induced sleep disruptions are evident in this mouse model of alcohol withdrawal,induced sensitization. This mouse model may provide mechanisms to investigate fully the high correlation between unremitting sleep problems and increased risk of relapse documented clinically. [source] Effects of Alcohol on Sleep and the Sleep Electroencephalogram in Healthy Young WomenALCOHOLISM, Issue 6 2006Eliza Van Reen Background: Although the association between sleep and alcohol has been of interest to scientists for decades, the effects of alcohol on sleep and sleep electroencephalogram (EEG) have not been extensively studied in women. Our specific aim was to determine whether sleep stage variables and/or spectral characteristics of the sleep EEG are altered by alcohol administration in women. Methods: Changes of sleep and the sleep EEG were investigated after administration of a moderate dose of alcohol (0.49 g/kg) in the hour before bedtime compared with placebo in young healthy women. After approximately 2 weeks at home on a fixed 8.5- or 9-hour stabilization sleep schedule, sleep was continuously recorded by polysomnography for 3 consecutive nights [adaptation, placebo, alcohol (mean breath alcohol concentration 0.043 g/% before bedtime)] in the laboratory in 7 women (ages 22,25, mean=23.5, SD=1 year). Sleep stages were scored according to conventional criteria. Electroencephalogram power spectra of the bipolar derivations Fz/Cz (anterior) and Pz/Oz (posterior) were calculated using a fast Fourier transform routine. Results: Only few changes in sleep and the sleep EEG were observed. Across the entire night rapid eye movement (REM) sleep decreased, while minutes of stage 4 sleep were increased in the first 2-hour interval on alcohol nights compared with placebo nights. Spectral analysis of the EEG showed increased power in the , range (9,11 Hz) during all-night non-REM (NREM) sleep in anterior derivations after alcohol compared with placebo. Differences in spectral EEG power were also present in 2-hour intervals of NREM sleep; in particular, EEG power was increased on the alcohol night for frequency bins within the , range in anterior derivations and within the , range (3,4 Hz) in posterior derivations during the initial part of the night. Conclusions: A moderate dose of alcohol just before bedtime resulted in a short-lived increase in sleep intensity. A limitation of the study, however, was that only a single dose of alcohol was used to examine the effects of alcohol on sleep. [source] Sleep electroencephalogram in children with a parental history of alcohol abuse/dependenceJOURNAL OF SLEEP RESEARCH, Issue 1p2 2010LEILA TAROKH Summary We examined the sleep electroencephalogram (EEG) in 9- and 10-year-old children with (PH+) and without (PH,) a parental history of alcohol abuse/dependence to determine whether sleep disturbances associated with alcohol precede the onset of alcohol use. Participants slept on a fixed sleep schedule that ensured at least a 10-h time in bed for 1 week before an adaptation and baseline night. Data were collected in a four-bed sleep research laboratory. Thirty healthy boys and girls aged 9 or 10 years were classified as either PH+ or PH, based on DSM-IV criteria applied to structured parental interviews. All-night polysomnography was performed, sleep data were scored visually in 30-s epochs, and EEG power spectra were calculated for each epoch. All-night EEG spectra were calculated for rapid eye movement (REM) and non-REM (NREM) sleep, and cycle-by-cycle spectra were calculated for NREM sleep. The two groups did not differ on any sleep stage variable. All-night analyses revealed normalized power in the delta band and spindle range were lower in PH+ children. Within NREM sleep cycles PH+ children exhibited less normalized power in the delta band and spindle range compared with PH, children. This effect occurred in the first four cycles and was most pronounced in the first sleep cycle of the night. We found no signs of sleep disruption in sleep stages for PH+ children. Sleep EEG spectral differences, however, suggest that certain circuits responsible for ,protecting' sleep may be impaired in PH+ children, which may lead to disrupted sleep later in life. [source] Differential effects of lorazepam on sleep and activity in C57BL/6J and BALB/cJ strain miceJOURNAL OF SLEEP RESEARCH, Issue 3 2009XIANGDONG TANG Summary Compared to C57BL/6 mice, BALB/c mice exhibit greater ,anxiousness' on behavioural tests of anxiety, and can show significantly longer sleep disruptions after exposure to anxiogenic situations. Relative to C57BL/6 mice, BALB/c mice also have reduced benzodiazepine (BZ) receptor densities in the brain and fivefold less BZ receptor density in the amygdala, a region important in anxiety and in the control of arousal. Lorazepam is a BZ receptor full agonist and has been used to treat both anxiety and insomnia. Differences between C57BL/6 and BALB/c mice raise the question of whether BZ agonists would impact sleep and activity differentially in the two strains. We examined the effects of two doses of lorazepam (0.5 and 1.5 mg kg,1) or saline alone (0.2 mL) on sleep and activity in C57BL/6 (n = 8) and BALB/c (n = 7) mice. Compared to saline, both doses of lorazepam significantly increased non-rapid eye movement (NREM) and reduced activity in both strains. In C57BL/6 mice, rapid eye movement (REM) was increased at both doses. In BALB/c mice, the 0.5 mg kg,1 dose had no significant influence on REM, whereas REM was reduced significantly after the 1.5 mg kg,1 dose. The results demonstrate significant differences between C57BL/6 and BALB/c mice in the effects of lorazepam on REM, whereas the effects on NREM and activity were similar. Strain differences in the number of BZ receptors in the amygdala, but not other brain regions, suggests possible site specificity in the effects of lorazepam on REM. These differences in BZ-binding sites in the amygdala could be a significant factor in differences in the sleep response between C57 and BALB/c mice. [source] Differential localization of carbachol- and bicuculline-sensitive pontine sites for eliciting REM sleep-like effects in anesthetized ratsJOURNAL OF SLEEP RESEARCH, Issue 1 2009VICTOR B. FENIK Summary Carbachol, a cholinergic agonist, and GABAA receptor antagonists injected into the pontine dorsomedial reticular formation can trigger rapid eye movement (REM) sleep-like state. Data suggest that GABAergic and cholinergic effects interact to produce this effect but the sites where this occurs have not been delineated. In urethane-anesthetized rats, in which carbachol effectively elicits REM sleep-like episodes (REMSLE), we tested the ability of 10 nL microinjections of carbachol (10 mm) and bicuculline (0.5 or 2 mm) to elicit REMSLE at 47 sites located within the dorsal pontine reticular formation at the levels -8.00 to -10.80 from bregma (B) (Paxinos and Watson, The Rat Brain in Stereotaxic Coordinates, Academic Press, San Diego, 1997). At rostral levels, most carbachol and some bicuculline injections elicited REMSLE with latencies that gradually decreased from 242 to 12 s for carbachol and from 908 to 38 s for bicuculline for more caudal injection sites. As the latencies decreased, the durations of bicuculline-elicited REMSLE increased from 104 s to over 38 min, and the effect was dose dependent, whereas the duration of carbachol-elicited REMSLE changed little (104,354 s). Plots of REMSLE latency versus the antero-posterior coordinates revealed that both drugs were maximally effective near B-8.80. At levels caudal to B-8.80, carbachol was effective at few sites, whereas bicuculline-elicited REMSLE to at least B-9.30 level. Thus, the bicuculline-sensitive sites extended further caudally than those for carbachol and antagonism of GABAA receptors both triggered REMSLE and controlled their duration, whereas carbachol effects on REMSLE duration were small or limited by its concurrent REMSLE-opposing actions. [source] Changes in dreaming induced by CPAP in severe obstructive sleep apnea syndrome patientsJOURNAL OF SLEEP RESEARCH, Issue 4 2006EVA CARRASCO Summary To study dream content in patients with severe obstructive sleep apnea syndrome (OSAS) and its modification with Continuous Positive Airway Pressure (CPAP) therapy. We assessed twenty consecutive patients with severe OSAS and 17 healthy controls. Polysomnograms were recorded at baseline in patients and controls and during the CPAP titration night, 3 months after effective treatment and 2 years later in patients. Subjects were awakened 5,10 min after the beginning of the first and last rapid eye movement (REM) sleep periods and we measured percentage of dream recall, emotional content of the dream, word count, thematic units, sleep architecture and REM density. Dream recall in REM sleep was similar in patients at baseline and controls (51.5% versus 44.4% respectively; P = .421), decreased to 20% and 24.3% the first and third month CPAP nights, and increased to 39% 2 years later (P = 0.004). Violent/highly anxious dreams were only seen in patients at baseline. Word count was higher in patients than in controls. REM density was highest the first CPAP night. Severe OSAS patients recall dreams in REM sleep as often as controls, but their dreams have an increased emotional tone and are longer. Despite an increase in REM density, dream recall decreased the first months of CPAP and recovered 2 years later. Violent/highly anxious dreams disappeared with treatment. A dream recall decrease with CPAP is associated with normalization of sleep in OSAS patients. [source] Daytime sleepiness during Ramadan intermittent fasting: polysomnographic and quantitative waking EEG studyJOURNAL OF SLEEP RESEARCH, Issue 2 2003Rachida Roky Summary During the lunar month of Ramadan, Muslims abstain from eating, drinking and smoking from sunrise to sunset. We reported previously that Ramadan provokes a shortening in nocturnal total sleep time by 40 min, an increase in sleep latency, and a decrease in slow-wave sleep (SWS) and rapid eye movement (REM) sleep duration during Ramadan. During the same study, the effects of Ramadan intermittent fasting on daytime sleepiness were also investigated in eight healthy young male subjects using a quantitative waking electroencephalograph (EEG) analysis following the multiple sleep latency test (MSLT) procedure. This procedure was combined with subjective alertness and mood ratings and was conducted during four successive experimental sessions: (1) baseline (BL) 15 days before Ramadan, (2) beginning of Ramadan (R11) on the 11th day of Ramadan, (3) end of Ramadan (R25) on the 25th day of Ramadan, (4) recovery 2 weeks after Ramadan (AR). During each session, four 20-min nap opportunities (MSLTs) were given at 10:00, 12:00, 14:00 and 16:00 h and were preceded by rectal temperature readings. Nocturnal sleep was recorded before each daytime session. Subjective daytime alertness did not change in R25 but decreased in R11 at 12:00 h, and subjective mood decreased at 16:00 h, both in R11 and R25. During the MSLT, mean sleep latency decreased by an average of 2 min in R11 (especially at 10:00 and 16:00 h) and 6 min in R25 (especially at 10:00 and 12:00 h) compared with BL. There was an increase in the daily mean of waking EEG absolute power in the theta (5.5,8.5 Hz) frequency band. Significant correlations were found between sleep latency during the MSLT and the waking EEG absolute power of the fast alpha (10.5,12.5 Hz), sigma (11.5,15.5 Hz) and beta (12.5,30 Hz) frequency bands. Sleep latency was also related to rectal temperature. In conclusion, Ramadan diurnal fasting induced an increase in subjective and objective daytime sleepiness associated with changes in diurnal rectal temperature. [source] Rapid tryptophan depletion reverses phenelzine-induced suppression of REM sleepJOURNAL OF SLEEP RESEARCH, Issue 1 2003Hans-Peter Landolt SUMMARY Treatment with the monoamine oxidase inhibitor phenelzine completely suppressed rapid eye movement (REM) sleep in five depressed patients. Hypothesizing that increased serotonergic neurotransmission eliminated REM sleep, we administered a tryptophan-free amino acid drink (TFD) known to reduce plasma tryptophan and brain levels of serotonin. The TFD reversed the REM sleep suppression, while the control drink (TFD plus tryptophan) had virtually no effect on sleep. Neither TFD nor control drink affected mood, total sleep time, sleep efficiency or the all-night electroencephalogram power spectra in non-rapid eye movement (NREM) sleep. We report the first non-disruptive, double-blind method for studying human subjects overnight with and without REM sleep. It opens up a novel strategy for investigating the functions of REM sleep, and the roles of serotonin and REM sleep in the regulation of NREM sleep and mood. [source] Time course of EEG background activity level before spontaneous awakening in infantsJOURNAL OF SLEEP RESEARCH, Issue 4 2002Chiara Zampi SUMMARY This research aimed to investigate the time course of the cortical activity level preceding spontaneous awakening as a function of age and state. Two groups of infants (1,4 and 9,14 weeks of age) were continuously monitored by polygraphic recording and behavioural observation during the night. The electroencephalographic (EEG) activity recorded by the C3,O1 lead was analysed through an automatic analysis method which provides, for each 30-s epoch, a single measure, time domain based, of the EEG synchronization. The EEG parameter values were computed in the 6 min preceding each awakening out of non-rapid eye movement (NREM) sleep and out of rapid eye movement (REM) sleep. The EEG background activity level did not change in the minutes preceding awakening out of REM sleep. Awakening out of NREM sleep was preceded by a change of EEG activity level in the direction of higher activation with different time course according to the age. Both REM and NREM sleep results suggest that a high level of EEG activity is a prerequisite for the occurrence of a spontaneous awakening. [source] Short-term homeostasis of REM sleep assessed in an intermittent REM sleep deprivation protocol in the ratJOURNAL OF SLEEP RESEARCH, Issue 1 2002ADRIÁN OCAMPO-GARCÉS An intermittent rapid eye movement (REM) sleep deprivation protocol was applied to determine whether an increase in REM sleep propensity occurs throughout an interval without REM sleep comparable with the spontaneous sleep cycle of the rat. Seven chronically implanted rats under a 12 : 12 light,dark schedule were subjected to an intermittent REM sleep deprivation protocol that started at hour 6 after lights-on and lasted for 3 h. It consisted of six instances of a 10-min REM sleep permission window alternating with a 20-min REM sleep deprivation window. REM sleep increased throughout the protocol, so that total REM sleep in the two REM sleep permission windows of the third hour became comparable with that expected in the corresponding baseline hour. Attempted REM sleep transitions were already increased in the second deprivation window. Attempted transitions to REM sleep were more frequent in the second than in the first half of any 20-min deprivation window. From one deprivation window to the next, transitions to REM sleep changed in correspondence to the amount of REM sleep in the permission window in-between. Our results suggest that: (i) REM sleep pressure increases throughout a time segment similar in duration to a spontaneous interval without REM sleep; (ii) it diminishes during REM sleep occurrence; and (iii) that drop is proportional to the intervening amount of REM sleep. These results are consistent with a homeostatic REM sleep regulatory mechanism that operates in the time scale of spontaneous sleep cycle. [source] Prenatal protein malnourished rats show changes in sleep/wake behavior as adultsJOURNAL OF SLEEP RESEARCH, Issue 1 2000Subimal Datta SUMMARY Prenatal protein malnutrition significantly elevates brain levels of serotonin in rats, and these levels remain elevated throughout their lives. This biogenic amine is involved in the regulation of many physiological functions, including the normal sleep/wake cycle. The present study examined the effects of prenatal protein malnutrition on the sleep/wake cycle of freely moving adult rats. Six prenatally protein malnourished (6% casein) and 10 well-nourished (25% casein) male rats (90,120-day-old) were chronically implanted with a standard set of electrodes (to record cortical electroencephalogram, neck muscle electromyogram, electrooculogram, and hippocampal theta wave) to objectively measure states of sleep and wakefulness. Six-hour polygraphic recordings were made between 10.00 and 16.00 h; a time when the rats normally sleep. Prenatally malnourished rats spent 20% more time in slow wave sleep (SWS) compared to the well-nourished rats. The total percentage of time spent in rapid eye movement (REM) sleep was 61% less in prenatally malnourished rats compared to well-nourished control rats. These findings demonstrate the adverse consequences of prenatal protein malnutrition on the quality and quantity of adult sleep in rats. These sleep changes are potentially detrimental to normal social behavior and cognitive functions. Prenatally malnourished rats are an excellent animal model to study the role of endogenous serotonin in the regulation of the normal sleep/wake cycle. [source] Rhythmic movement disorder (head banging) in an adult during rapid eye movement sleepMOVEMENT DISORDERS, Issue 6 2006Kirstie N. Anderson MD Abstract Sleep-related rhythmic movements (head banging or body rocking) are extremely common in normal infants and young children, but less than 5% of children over the age of 5 years old exhibit these stereotyped motor behaviors. They characteristically occur during drowsiness or sleep onset rather than in deep sleep or rapid eye movement (REM) sleep. We present a 27-year-old man with typical rhythmic movement disorder that had persisted into adult life and was restricted to REM sleep. This man is the oldest subject with this presentation reported to date and highlights the importance of recognizing this nocturnal movement disorder when it does occur in adults. © 2006 Movement Disorder Society [source] Stages 1,2 non,rapid eye movement sleep behavior disorder associated with dementia: A new parasomnia?MOVEMENT DISORDERS, Issue 9 2005Isabelle Arnulf MD Abstract A 55-year-old woman with a progressive dementia and frontal syndrome was hospitalized because she was agitated every night after falling asleep (spoke, laughed, cried, tapped, kicked, walked, and fell down). She slept 5.5 hours during video polysomnography, but the theta rhythm electroencephalograph recording typical of sleep stages 1 to 2 and the spindles and K-complexes typical of sleep stage 2 contrasted with continuous muscular twitching, prominent rapid eye movements, vocalizations, and continuous, complex, purposeful movements typical of rapid eye movement (REM) sleep behavior disorder. This newly described stages 1,2 non-REM sleep behavior disorder suggests that central motor pattern generators were disinhibited during non-REM sleep. © 2005 Movement Disorder Society [source] Visual hallucinations as REM sleep behavior disorders in patients with Parkinson's diseaseMOVEMENT DISORDERS, Issue 7 2003Takashi Nomura MD Abstract To clarify whether visual hallucinations in patients with Parkinson's disease (PD) are related to rapid eye movement (REM) sleep, nocturnal polysomnographic variables were compared between a group with hallucinations (hallucinators, n = 14) and a group without hallucinations (nonhallucinators, n = 8). A multiple sleep latency test (MSLT) was performed on 3 hallucinators, and the content of dreams during daytime REM sleep was investigated. The efficacy of clonazepam, a standard treatment choice for REM sleep behavior disorders, was investigated in 8 hallucinators. Nocturnal polysomnograms of the hallucinators showed a higher amount of stage 1,REM sleep with tonic electromyogram (stage 1,REM) than the nonhallucinators, and the reported occurrences of nocturnal hallucinations corresponded with the periods of stage REM or stage 1,REM in most hallucinators. The frequency of sleep onset REM periods (SOREMP) on the MSLT were pathologically high in the hallucinators, and the content of the dreams during the MSLT period was quite similar to their hallucinations. During clonazepam treatment, the frequency of hallucinatory symptoms decreased in 5 of 8 hallucinators. These results indicate that visual hallucinations in PD are likely to be related to a REM sleep disorder manifested as the appearance of both stage 1,REM during the night and SOREMP in the daytime. © 2003 Movement Disorder Society [source] Site-specific Effects of Transcranial Direct Current Stimulation on Sleep and Pain in Fibromyalgia: A Randomized, Sham-controlled StudyPAIN PRACTICE, Issue 4 2007Suely Roizenblatt MD ,,Abstract Objective: To investigate whether active anodal transcranial direct current stimulation (tDCS) (of dorsolateral prefrontal cortex [DLPFC] and primary motor cortex [M1]) as compared to sham treatment is associated with changes in sleep structure in fibromyalgia. Methods: Thirty-two patients were randomized to receive sham stimulation or active tDCS with the anode centered over M1 or DLPFC (2 mA, 20 minutes for five consecutive days). A blinded evaluator rated the clinical symptoms of fibromyalgia. All-night polysomnography was performed before and after five consecutive sessions of tDCS. Results: Anodal tDCS had an effect on sleep and pain that was specific to the site of stimulation: such as that M1 and DLPFC treatments induced opposite effects on sleep and pain, whereas sham stimulation induced no significant sleep or pain changes. Specifically, whereas M1 treatment increased sleep efficiency (by 11.8%, P = 0.004) and decreased arousals (by 35.0%, P = 0.001), DLPFC stimulation was associated with a decrease in sleep efficiency (by 7.5%, P = 0.02), an increase in rapid eye movement (REM) and sleep latency (by 47.7%, P = 0.0002, and 133.4%, P = 0.02, respectively). In addition, a decrease in REM latency and increase in sleep efficiency were associated with an improvement in fibromyalgia symptoms (as indexed by the Fibromyalgia Impact Questionnaire). Finally, patients with higher body mass index had the worse sleep outcome as indexed by sleep efficiency changes after M1 stimulation. Interpretation: Our findings suggest that one possible mechanism to explain the therapeutic effects of tDCS in fibromyalgia is via sleep modulation that is specific to modulation of primary M1 activity.,, [source] Polysomnography in patients with post-traumatic stress disorderPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 3 2010Sinan Yetkin MD Aims:, The purpose of the present study was to investigate sleep structure in post-traumatic stress disorder (PTSD) patients with and without any psychiatric comorbidities. The relationship between sleep variables and measurements of clinical symptom severity were also investigated. Methods:, Sleep patterns of 24 non-medicated male PTSD patients and 16 age- and sex-matched normal controls were investigated on polysomnography on two consecutive nights. Six PTSD-only patients and 15 PTSD patients with major depressive disorder (MDD) were also compared to normal controls. Sleep variables were correlated with PTSD symptoms. Results:, Compared to the normal controls, the PTSD patients with MDD had difficulty initiating sleep, poor sleep efficiency, decreased total sleep time, decreased slow wave sleep (SWS), and a reduced rapid eye movement (REM) sleep latency. The PTSD patients without any comorbid psychiatric disorders had moderately significant disturbances of sleep continuity, and decreased SWS, but no abnormalities of REM sleep. REM sleep latency was inversely proportional to the severity of startle response. SWS was found to be inversely correlated with the severity of psychogenic amnesia. Conclusions:, PTSD patients have disturbance of sleep continuity, and SWS deficit, without the impact of comorbid depression on sleep. The relationship between SWS and the inability to recall an important aspect of trauma may indicate the role of sleep in the consolidation of traumatic memories. The relationship between the severity of the startle response and REM latency may suggest that REM sleep physiology shares common substrates with the symptoms of PTSD. [source] The neurochemistry of waking and sleeping mental activity: The disinhibition-dopamine hypothesisPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 4 2002CLAUDE GOTTESMANN Abstract This paper describes a hypothesis related to the neurochemical background of sleep-waking mental activity which, although associated with subcortical structures, is principally generated in the cerebral cortex. Acetylcholine, which mainly activates cortical neurons, is released at the maximal rate during waking and rapid eye movement (REM) sleep dreaming stage. Its importance in mental functioning is well-known. However, brainstem-generated monoamines, which mainly inhibit cortical neurons, are released during waking. Both kinds of influences contribute to the organized mentation of waking. During slow wave sleep, these two types of influence decrease in intensity but maintain a sufficiently high level to allow mental activity involving fairly abstract pseudo-thoughts, a mode of activity modelled on the diurnal pattern of which it is a poor reply. During REM sleep, the monoaminergic neurons become silent except for the dopaminergic ones. This results in a large disinhibition and the maintained dopamine influence may be involved in the familiar psychotic-like mental activity of dreaming. Indeed, in this original activation,disinhibition state, the increase of dopamine influence at the prefrontal cortex level could explain the almost total absence of negative symptoms of schizophrenia during dreaming, while an increase in the nucleus accumbens is possibly responsible for hallucinations and delusions, which are regular features of mentation during this sleep stage. [source] | |||||||||||||||||||||||||||||||