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Alexander A. Borbély - One of the best experts on this subject based on the ideXlab platform.
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Individual ‘Fingerprints’ in Human Sleep EEG Topography
Neuropsychopharmacology, 2001Co-Authors: Luca A Finelli, Peter Achermann, Alexander A. BorbélyAbstract:The Sleep EEG of eight healthy young men was recorded from 27 derivations during a baseline night and a recovery night after 40 h of waking. Individual power maps of the nonREM Sleep EEG were calculated for the delta, theta, alpha, sigma and beta range. The comparison of the normalized individual maps for baseline and recovery Sleep revealed very similar individual patterns within each frequency band. This high correspondence was quantified and statistically confirmed by calculating the Manhattan distance between all pairs of maps within and between individuals. Although prolonged waking enhanced power in the low-frequency range (0.75–10.5 Hz) and reduced power in the high-frequency range (13.25–25 Hz), only minor effects on the individual topography were observed. Nevertheless, statistical analysis revealed frequency-specific regional effects of Sleep deprivation. The results demonstrate that the pattern of the EEG power distribution in nonREM Sleep is characteristic for an individual and may reflect individual traits of functional anatomy.
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functional topography of the human nonREM Sleep electroencephalogram
European Journal of Neuroscience, 2001Co-Authors: Luca A Finelli, Alexander A. Borbély, Peter AchermannAbstract:The Sleep EEG of healthy young men was recorded during baseline and recovery Sleep after 40 h of waking. To analyse the EEG topography, power spectra were computed from 27 derivations. Mean power maps of the nonREM Sleep EEG were calculated for 1-Hz bins between 1.0 and 24.75 Hz. Cluster analysis revealed a topographic segregation into distinct frequency bands which were similar for baseline and recovery Sleep, and corresponded closely to the traditional frequency bands. Hallmarks of the power maps were the frontal predominance in the delta and alpha band, the occipital predominance in the theta band, and the sharply delineated vertex maximum in the sigma band. The effect of Sleep deprivation on EEG topography was determined by calculating the recovery/baseline ratio of the power spectra. Prolonged waking induced an increase in power in the low-frequency range (1-10.75 Hz) which was largest over the frontal region, and a decrease in power in the sigma band (13-15.75 Hz) which was most pronounced over the vertex. The topographic pattern of the recovery/baseline power ratio was similar to the power ratio between the first and second half of the baseline night. These results indicate that changes in Sleep propensity are reflected by specific regional differences in EEG power. The predominant increase of low-frequency power in frontal areas may be due to a high 'recovery need' of the frontal heteromodal association areas of the cortex.
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serotonin 2 receptors and human Sleep effect of a selective antagonist on eeg power spectra
Neuropsychopharmacology, 1999Co-Authors: Hans-peter Landolt, Peter Achermann, Viola Meier, Helen J Burgess, Luca A Finelli, Francoise Cattelin, Alexander A. BorbélyAbstract:To investigate the effect on the Sleep EEG, a 1-mg oral dose of SR 46349B, a novel 5-HT2 antagonist, was administered three hours before bedtime. The drug enhanced slow wave Sleep (SWS) and reduced stage 2 without affecting subjective Sleep quality. In nonREM Sleep (NREMS) EEG slow-wave activity (SWA; power within 0.75–4.5 Hz) was increased and spindle frequency activity (SFA; power within 12.25–15 Hz) was decreased. The relative NREMS power spectrum showed a bimodal pattern with the main peak at 1.5 Hz and a secondary peak at 6 Hz. A regional analysis based on bipolar derivations along the antero-posterior axis revealed significant ‘treatment’ × ‘derivation’ interactions within the 9–16 Hz range. In enhancing SWA and attenuating SFA, the 5-HT2 receptor antagonist mimicked the effect of Sleep deprivation, whereas the pattern of the NREMS spectrum differed.
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Effect of frequent brief awakenings from nonREM Sleep on the nonREM-REM Sleep cycle.
Psychiatry and Clinical Neurosciences, 1998Co-Authors: Takuro Endo, Corinne Roth, Hans-peter Landolt, Esther Werth, Daniel Aeschbach, Peter Achermann, Alexander A. BorbélyAbstract:In the framework of a selective Sleep deprivation study, eight young men were repeatedly awakened during 3 nights from nonREM Sleep (nonREMS). The mean number of awakenings per night was 27.4, 29.5 and 32.8. In order to avoid excessive suppression of slow wave Sleep, no awakening occurred in the first nonREMS episode. Compared to baseline, cycle 2 was significantly prolonged in all 3 nights, and cycle 3 in night 3 only. However, after subtracting the waking intervals, the differences from baseline was eliminated. The results show that the mechanisms underlying Sleep cycle control keep track of Sleep time and disregard epochs of waking.
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effect of age on the Sleep eeg slow wave activity and spindle frequency activity in young and middle aged men
Brain Research, 1996Co-Authors: Hans-peter Landolt, Peter Achermann, Derk-jan Dijk, Alexander A. BorbélyAbstract:The effect of age on Sleep and the Sleep EEG was investigated in middle-aged men (mean age: 62.0 years) and in young men (mean age: 22.4 years). Even though the older men reported a higher number of nocturnal awakenings, subjective Sleep quality did not differ. Total Sleep time, Sleep efficiency, and slow wave Sleep were lower in the middle-aged, while stage 1 and wakefulness after Sleep onset were higher. The differences in wakefulness within nonREM-REM Sleep cycles was most pronounced in the third and fourth cycle. In the older men, EEG power density in nonREM Sleep was reduced in frequencies below 14.0 Hz, whereas in REM Sleep age-related reductions were limited to he delta-theta (0.25-7.0 Hz) and low alpha (8.25-10.0 Hz) band. Slow-wave activity (SWA, power density in the 0.75-4.5 Hz range) decreased in the course of Sleep in both age groups. The between-group difference in SWA diminished in the course of Sleep, whereas the difference in activity in the frequency range of Sleep spindles (12.25-14.0 Hz) increased. It is concluded that frequency and state specific changes occur as a function of age, and that Sleep dependent decline in SWA and increase in Sleep spindle activity are attenuated with age.
Derk-jan Dijk - One of the best experts on this subject based on the ideXlab platform.
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age related increase in awakenings impaired consolidation of nonREM Sleep at all circadian phases
Sleep, 2001Co-Authors: Derk-jan Dijk, Jeanne F Duffy, Charles A CzeislerAbstract:Study objectives (1) To assess the circadian and Sleep-dependent regulation of the frequency and duration of awakenings in young and older people; (2) to determine whether age-related deterioration of Sleep consolidation is related to an increase in the frequency or duration of awakenings; (3) to determine whether pre-awakening Sleep structure is preferentially enriched by REM Sleep or nonREM Sleep and (4) to determine whether Sleep structure prior to awakenings is affected by age. Design Between age-group comparison of Sleep consolidation and Sleep structure preceding awakenings. Setting Environmental Scheduling Facility, General Clinical Research Center. Participants Eleven healthy young men (21-30 years) and 13 older healthy men (n=9) and women (n=4) (64-74 years). Interventions Forced desynchrony between the Sleep-wake cycle and circadian rhythms by scheduling of the rest-activity cycle to 28-h for 21-25 cycles. Measurements and results Circadian and Sleep-dependent regulation of the frequency and duration of awakenings and of Sleep structure preceding awakenings were assessed in 482 Sleep episodes (9h 20 min each). The circadian modulation of wakefulness within Sleep episodes was primarily related to a variation in the duration of awakenings. In contrast, the age-related reduction of Sleep consolidation was primarily related to an increase in the frequency of awakenings. Whereas in both young and older subjects pre-awakening Sleep contained more REM Sleep than overall Sleep, this enrichment of REM Sleep (i.e., the gating of wakefulness by REM Sleep) was diminished in older people. In older people, preawakening Sleep contained more nonREM Sleep and stage two Sleep in particular, than in young people. Conclusions At all circadian phases, the age-related reduction of Sleep consolidation is primarily related to a reduction in the consolidation of nonREM Sleep.
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age related increase in awakenings impaired consolidation of nonREM Sleep at all circadian phases Sleep and aging
2001Co-Authors: Derk-jan Dijk, Jeanne F Duffy, Charles A CzeislerAbstract:AGING IS ASSOCIATED WITH MAJOR CHANGES IN Sleep STRUCTURE, Sleep QUALITY AND Sleep TIMING. Decreases in stage 4 or EEG slow-wave activity are among the most pronounced and first age-related changes in Sleep structure to occur. Earlier timing of Sleep and wakefulness and reduced nocturnal Sleep consolidation and according to some studies, a reduction in REM Sleep, occur later in the aging process. Sleep disorders such as Sleep apnea and nocturnal myoclonus and other health problems can contribute to these changes in Sleep structure and quality in older people. These changes in Sleep quality and Sleep timing may lead to Sleep complaints and the associated use of hypnotics in older people.1-5 Two neurobiological processes, circadian rhythmicity and Sleep homeostasis, play a key role in the regulation of Sleep timing and Sleep structure.6-12 It has been hypothesized that changes in these two processes contribute to the age-related changes in Sleep timing and Sleep consolidation which occur in healthy people without Sleep complaints or Sleep disorders. We recently quantified the contribution of the circadian process in a forced desynchrony protocol in which the Sleep-wake cycles of healthy older men and women and healthy young men were scheduled to a 28-hour period while they were living in a time-free laboratory environment for approximately one month. Under these conditions the intrinsic period of the human circadian pacemaker, as indexed by the plasma melatonin and body temperature rhythm, was on average 24.18 h in both young and older adults.13 These data and data obtained in adolescents living under similar conditions14 challenge the notion that a systematic age-related reduction of the intrinsic period of the human circadian pacemaker is a major determinant of age-related changes in Sleep timing and Sleep consolidation. Analysis of the subjective perception of the duration of final awakening in this forced desynchrony protocol revealed that, even in the absence of knowledge about either clock time or circadian phase, older subjects report earlier awakening than young subjects, especially when the scheduled wake time occurs at or closely after the nadir of the temperature cycle.15 Analyses of polysomnographic recordings of these Sleep episodes have demonstrated that in both young and older people the propensity for wakefulness depends on a non-additive interaction of the time elapsed since start of Sleep episode (i.e., the Sleep homeostatic process) and circadian phase.16 Wakefulness in older people is at higher levels throughout the Sleep episode at all circadian phases and this increase in wakefulness as Sleep progresses occurs at a more rapid rate than in young people. Furthermore, the interaction between the circadian and homeostatic regulation of Sleep is changed such that there is an age-related phase advance of wake propensity relative to the endogenous circadian component of the body temperature and plasma melatonin rhythms. These analyses as well as other experiments,17-20 suggest that an age-related Study Objectives: (1) To assess the circadian and Sleep-dependent regulation of the frequency and duration of awakenings in young and older people; (2) to determine whether age-related deterioration of Sleep consolidation is related to an increase in the frequency or duration of awakenings; (3) to determine whether pre-awakening Sleep structure is preferentially enriched by REM Sleep or nonREM Sleep and (4) to determine whether Sleep structure prior to awakenings is affected by age. Design: Between age-group comparison of Sleep consolidation and Sleep structure preceding awakenings. Setting: Environmental Scheduling Facility, General Clinical Research Center. Participants: Eleven healthy young men (21—30 years) and 13 older healthy men (n=9) and women (n=4) (64—74 years). Interventions: Forced desynchrony between the Sleep-wake cycle and circadian rhythms by scheduling of the rest-activity cycle to 28-h for 21—25 cycles. Measurements and Results: Circadian and Sleep-dependent regulation of the frequency and duration of awakenings and of Sleep structure preceding awakenings were assessed in 482 Sleep episodes (9h 20 min each). The circadian modulation of wakefulness within Sleep episodes was primarily related to a variation in the duration of awakenings. In contrast, the age-related reduction of Sleep consolidation was primarily related to an increase in the frequency of awakenings. Whereas in both young and older subjects pre-awakening Sleep contained more REM Sleep than overall Sleep, this enrichment of REM Sleep (i.e., the gating of wakefulness by REM Sleep) was diminished in older people. In older people, preawakening Sleep contained more nonREM Sleep and stage two Sleep in particular, than in young people. Conclusions: At all circadian phases, the age-related reduction of Sleep consolidation is primarily related to a reduction in the consolidation of nonREM Sleep.
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effect of age on the Sleep eeg slow wave activity and spindle frequency activity in young and middle aged men
Brain Research, 1996Co-Authors: Hans-peter Landolt, Peter Achermann, Derk-jan Dijk, Alexander A. BorbélyAbstract:The effect of age on Sleep and the Sleep EEG was investigated in middle-aged men (mean age: 62.0 years) and in young men (mean age: 22.4 years). Even though the older men reported a higher number of nocturnal awakenings, subjective Sleep quality did not differ. Total Sleep time, Sleep efficiency, and slow wave Sleep were lower in the middle-aged, while stage 1 and wakefulness after Sleep onset were higher. The differences in wakefulness within nonREM-REM Sleep cycles was most pronounced in the third and fourth cycle. In the older men, EEG power density in nonREM Sleep was reduced in frequencies below 14.0 Hz, whereas in REM Sleep age-related reductions were limited to he delta-theta (0.25-7.0 Hz) and low alpha (8.25-10.0 Hz) band. Slow-wave activity (SWA, power density in the 0.75-4.5 Hz range) decreased in the course of Sleep in both age groups. The between-group difference in SWA diminished in the course of Sleep, whereas the difference in activity in the frequency range of Sleep spindles (12.25-14.0 Hz) increased. It is concluded that frequency and state specific changes occur as a function of age, and that Sleep dependent decline in SWA and increase in Sleep spindle activity are attenuated with age.
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effect of unilateral somatosensory stimulation prior to Sleep on the Sleep eeg in humans
Journal of Sleep Research, 1994Co-Authors: Herbert Kattler, Derk-jan Dijk, Alexander A. BorbélyAbstract:SUMMARY The hypothesis that local activation of brain regions during wakefulness affects the EEG recorded from these regions during Sleep was tested by applying vibratory stimuli to one hand prior to Sleep. Eight subjects slept in the laboratory for five consecutive nights. During a 6-h period prior to night 3, either the left or the right hand was vibrated intermittently (20 min on-8 min off), while prior to night 5 the same treatment was applied to the contralateral hand. The Sleep EEG was recorded from frontal, central, parietal and occipital derivations and subjected to spectral analysis. The interhemispheric asymmetry index (IAI) was calculated for spectral power in nonREM Sleep in the frequency range 0.25-25.0 Hz for 0.5-Hz or 1-Hz bins. In the first hour of Sleep following right-hand stimulation, the IAI of the central derivation was increased relative to baseline, which corresponds to a shift of power towards the left hemisphere. This effect was most prominent in the delta range, was limited to the first hour of Sleep and was restricted to the central derivation situated over the somatosensory cortex. No significant changes were observed following left-hand stimulation. Although the effect was small, it is consistent with the hypothesis that the activation of specific neuronal populations during wakefulness may have repercussions on their electrical activity pattern during subsequent Sleep.
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Sleep in a sitting position: effect of triazolam on Sleep stages and EEG power spectra
Psychopharmacology, 1994Co-Authors: Daniel Aeschbach, Derk-jan Dijk, Christian Cajochen, Irene Tobler, Alexander A. BorbélyAbstract:The effect of triazolam (0.25 mg) and placebo was investigated in healthy, male subjects who slept in a sitting position. After the intake of placebo, Sleep efficiency, rapid eye movement (REM) Sleep and subjective Sleep quality were lower than in the preceding Sleep episode in bed, while stage 1 and REM Sleep latency were higher. Triazolam did not prevent this impairment of Sleep. However, in comparison with the placebo condition, the percentage of slow wave Sleep was higher in the first third of the night, and in the morning Sleep was rated as more quite. EEG power density in nonREM Sleep was reduced in the frequency range of 1.25–10.0 Hz and enhanced in the range of Sleep spindles (12.25–13.0 Hz). These changes were still present in the last third of the night. In REM Sleep, triazolam reduced spectral activity in some frequency bins between 4.25 and 10.0 Hz. The sitting position itself affected the nonREM Sleep spectra, since the placebo level in the 2.25–21.0-Hz range exceeded the baseline level. We conclude that a 0.25 mg dose of triazolam does not effectively counteract a posture-induced Sleep disturbance, but induces changes in the EEG spectra which are typical for benzodiazepine receptor agonists.
Peter Achermann - One of the best experts on this subject based on the ideXlab platform.
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induced hyperammonemia may compromise the ability to generate restful Sleep in patients with cirrhosis
Hepatology, 2012Co-Authors: Alessia Bersagliere, Peter Achermann, Iolanda Daniela Raduazzo, Mariateresa Nardi, Sami Schiff, Angelo Gatta, Piero Amodio, Sara MontagneseAbstract:In patients with cirrhosis, hyperammonaemia and hepatic encephalopathy are common after a gastrointestinal bleeding and can be simulated by an amino acid challenge (AAC), or the administration of a mixture of amino acids mimicking the composition of haemoglobin. The aim of this study was to investigate the clinical, psychometric, wake-/Sleep-EEG correlates of induced hyperammonaemia. Ten patients with cirrhosis and ten matched healthy volunteers underwent: i) 8-day Sleep quality/timing monitoring; ii) neuropsychiatric assessment at baseline/after AAC; iii) hourly ammonia/subjective Sleepiness assessment for 8 hours after AAC; iv) Sleep EEG recordings (nap opportunity: 17:00-19:00) at baseline/after AAC. Neuropsychiatric performance was scored according to age-/education-adjusted Italian norms. Sleep stages were scored visually for 20-s epochs; power density spectra were calculated for consecutive 20-s epochs and average spectra determined for consolidated episodes of nonREM Sleep of minimal common length. The AAC resulted in: i) an increase in ammonia concentrations/subjective Sleepiness in both patients and healthy volunteers; ii) a worsening of neuropsychiatric performance (wake EEG slowing) in two (20%) patients and none of the healthy volunteers; iii) an increase in the length of nonREM Sleep in healthy controls [49.3(26.6) vs. 30.4(15.6) min; p=0.08]; iv) a decrease in the Sleep EEG beta power (fast activity) in the healthy volunteers; v) a decrease in the Sleep EEG delta power in patients. IN CONCLUSION: the AAC led to significant increase in daytime subjective Sleepiness and changes in the EEG architecture of a subsequent Sleep episode in patients with cirrhosis, pointing to a reduced ability to produce restorative Sleep. (HEPATOLOGY 2011.).
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Individual ‘Fingerprints’ in Human Sleep EEG Topography
Neuropsychopharmacology, 2001Co-Authors: Luca A Finelli, Peter Achermann, Alexander A. BorbélyAbstract:The Sleep EEG of eight healthy young men was recorded from 27 derivations during a baseline night and a recovery night after 40 h of waking. Individual power maps of the nonREM Sleep EEG were calculated for the delta, theta, alpha, sigma and beta range. The comparison of the normalized individual maps for baseline and recovery Sleep revealed very similar individual patterns within each frequency band. This high correspondence was quantified and statistically confirmed by calculating the Manhattan distance between all pairs of maps within and between individuals. Although prolonged waking enhanced power in the low-frequency range (0.75–10.5 Hz) and reduced power in the high-frequency range (13.25–25 Hz), only minor effects on the individual topography were observed. Nevertheless, statistical analysis revealed frequency-specific regional effects of Sleep deprivation. The results demonstrate that the pattern of the EEG power distribution in nonREM Sleep is characteristic for an individual and may reflect individual traits of functional anatomy.
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functional topography of the human nonREM Sleep electroencephalogram
European Journal of Neuroscience, 2001Co-Authors: Luca A Finelli, Alexander A. Borbély, Peter AchermannAbstract:The Sleep EEG of healthy young men was recorded during baseline and recovery Sleep after 40 h of waking. To analyse the EEG topography, power spectra were computed from 27 derivations. Mean power maps of the nonREM Sleep EEG were calculated for 1-Hz bins between 1.0 and 24.75 Hz. Cluster analysis revealed a topographic segregation into distinct frequency bands which were similar for baseline and recovery Sleep, and corresponded closely to the traditional frequency bands. Hallmarks of the power maps were the frontal predominance in the delta and alpha band, the occipital predominance in the theta band, and the sharply delineated vertex maximum in the sigma band. The effect of Sleep deprivation on EEG topography was determined by calculating the recovery/baseline ratio of the power spectra. Prolonged waking induced an increase in power in the low-frequency range (1-10.75 Hz) which was largest over the frontal region, and a decrease in power in the sigma band (13-15.75 Hz) which was most pronounced over the vertex. The topographic pattern of the recovery/baseline power ratio was similar to the power ratio between the first and second half of the baseline night. These results indicate that changes in Sleep propensity are reflected by specific regional differences in EEG power. The predominant increase of low-frequency power in frontal areas may be due to a high 'recovery need' of the frontal heteromodal association areas of the cortex.
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serotonin 2 receptors and human Sleep effect of a selective antagonist on eeg power spectra
Neuropsychopharmacology, 1999Co-Authors: Hans-peter Landolt, Peter Achermann, Viola Meier, Helen J Burgess, Luca A Finelli, Francoise Cattelin, Alexander A. BorbélyAbstract:To investigate the effect on the Sleep EEG, a 1-mg oral dose of SR 46349B, a novel 5-HT2 antagonist, was administered three hours before bedtime. The drug enhanced slow wave Sleep (SWS) and reduced stage 2 without affecting subjective Sleep quality. In nonREM Sleep (NREMS) EEG slow-wave activity (SWA; power within 0.75–4.5 Hz) was increased and spindle frequency activity (SFA; power within 12.25–15 Hz) was decreased. The relative NREMS power spectrum showed a bimodal pattern with the main peak at 1.5 Hz and a secondary peak at 6 Hz. A regional analysis based on bipolar derivations along the antero-posterior axis revealed significant ‘treatment’ × ‘derivation’ interactions within the 9–16 Hz range. In enhancing SWA and attenuating SFA, the 5-HT2 receptor antagonist mimicked the effect of Sleep deprivation, whereas the pattern of the NREMS spectrum differed.
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Effect of frequent brief awakenings from nonREM Sleep on the nonREM-REM Sleep cycle.
Psychiatry and Clinical Neurosciences, 1998Co-Authors: Takuro Endo, Corinne Roth, Hans-peter Landolt, Esther Werth, Daniel Aeschbach, Peter Achermann, Alexander A. BorbélyAbstract:In the framework of a selective Sleep deprivation study, eight young men were repeatedly awakened during 3 nights from nonREM Sleep (nonREMS). The mean number of awakenings per night was 27.4, 29.5 and 32.8. In order to avoid excessive suppression of slow wave Sleep, no awakening occurred in the first nonREMS episode. Compared to baseline, cycle 2 was significantly prolonged in all 3 nights, and cycle 3 in night 3 only. However, after subtracting the waking intervals, the differences from baseline was eliminated. The results show that the mechanisms underlying Sleep cycle control keep track of Sleep time and disregard epochs of waking.
Hans-peter Landolt - One of the best experts on this subject based on the ideXlab platform.
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Genotypedependent differences in Sleep, vigilance, and response to stimulants
2008Co-Authors: Hans-peter LandoltAbstract:Abstract: To better understand the neurobiology of Sleep disorders, detailed understanding of circadian and homeostatic Sleep-wake regulation in healthy volunteers is mandatory. Sleep physiology and the repercussions of experimentallyinduced Sleep deprivation on Sleep and waking electroencephalogram (EEG), vigilance and subjective state are highly variable, even in healthy individuals. Accumulating evidence suggests that many aspects of normal Sleep-wake regulation are at least in part genetically controlled. Current heritability estimates of Sleep phenotypes vary between approximately 20-40 % for habitual Sleep duration, to over 90 % for the spectral characteristics of the EEG in nonREM Sleep. The molecular mechanisms underlying the trait-like, inter-individual variation are virtually unknown, and the human genetics of normal Sleep is only at the beginning of being explored. The first studies identified distinct polymorphisms in genes contributing to the endogenous circadian clock and neurochemical systems previously implicated in Sleep-wake regulation, to modulate Sleep architecture and Sleep EEG, vulnerability to Sleep loss, and subjective and objective effects of caffeine on Sleep. These insights are reviewed here. They disclose molecular mechanisms contributing to normal Sleep-wake regulation in humans, and have potentially important implications for the neurobiology of Sleep-wake disorders and their pharmacological treatment
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Effect of Chronic Phenelzine Treatment on REM Sleep: Report of Three Patients
Neuropsychopharmacology, 2001Co-Authors: Hans-peter Landolt, Lieselotte Posthuma De BoerAbstract:Antidepressants belonging to the class of monoamine oxidase inhibitors (MAOI) such as phenelzine have long been known to drastically suppress REM Sleep. Sleep and the electroencephalogram (EEG) in Sleep and waking were studied in three depressed patients at regular time intervals before, during and after 6 to 18 months of phenelzine treatment. While REM Sleep was initially eliminated in all patients, short REM Sleep episodes reappeared after three to six months of medication. Total Sleep time and EEG slow-wave activity (SWA, spectral power within 0.75–4.5 Hz) in nonREM Sleep (stages 1–4) were not changed. In contrast, EEG theta frequency activity (TFA, power within 4.75–8.0 Hz) during a 5-min wake interval recorded prior to the Sleep episodes was initially enhanced, and tended to correlate negatively with the percentage of REM Sleep ( p = .06 ). This observation indicates that compensatory REM Sleep mechanisms may occur in wakefulness during chronic MAOI treatment.
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serotonin 2 receptors and human Sleep effect of a selective antagonist on eeg power spectra
Neuropsychopharmacology, 1999Co-Authors: Hans-peter Landolt, Peter Achermann, Viola Meier, Helen J Burgess, Luca A Finelli, Francoise Cattelin, Alexander A. BorbélyAbstract:To investigate the effect on the Sleep EEG, a 1-mg oral dose of SR 46349B, a novel 5-HT2 antagonist, was administered three hours before bedtime. The drug enhanced slow wave Sleep (SWS) and reduced stage 2 without affecting subjective Sleep quality. In nonREM Sleep (NREMS) EEG slow-wave activity (SWA; power within 0.75–4.5 Hz) was increased and spindle frequency activity (SFA; power within 12.25–15 Hz) was decreased. The relative NREMS power spectrum showed a bimodal pattern with the main peak at 1.5 Hz and a secondary peak at 6 Hz. A regional analysis based on bipolar derivations along the antero-posterior axis revealed significant ‘treatment’ × ‘derivation’ interactions within the 9–16 Hz range. In enhancing SWA and attenuating SFA, the 5-HT2 receptor antagonist mimicked the effect of Sleep deprivation, whereas the pattern of the NREMS spectrum differed.
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Effect of frequent brief awakenings from nonREM Sleep on the nonREM-REM Sleep cycle.
Psychiatry and Clinical Neurosciences, 1998Co-Authors: Takuro Endo, Corinne Roth, Hans-peter Landolt, Esther Werth, Daniel Aeschbach, Peter Achermann, Alexander A. BorbélyAbstract:In the framework of a selective Sleep deprivation study, eight young men were repeatedly awakened during 3 nights from nonREM Sleep (nonREMS). The mean number of awakenings per night was 27.4, 29.5 and 32.8. In order to avoid excessive suppression of slow wave Sleep, no awakening occurred in the first nonREMS episode. Compared to baseline, cycle 2 was significantly prolonged in all 3 nights, and cycle 3 in night 3 only. However, after subtracting the waking intervals, the differences from baseline was eliminated. The results show that the mechanisms underlying Sleep cycle control keep track of Sleep time and disregard epochs of waking.
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effect of age on the Sleep eeg slow wave activity and spindle frequency activity in young and middle aged men
Brain Research, 1996Co-Authors: Hans-peter Landolt, Peter Achermann, Derk-jan Dijk, Alexander A. BorbélyAbstract:The effect of age on Sleep and the Sleep EEG was investigated in middle-aged men (mean age: 62.0 years) and in young men (mean age: 22.4 years). Even though the older men reported a higher number of nocturnal awakenings, subjective Sleep quality did not differ. Total Sleep time, Sleep efficiency, and slow wave Sleep were lower in the middle-aged, while stage 1 and wakefulness after Sleep onset were higher. The differences in wakefulness within nonREM-REM Sleep cycles was most pronounced in the third and fourth cycle. In the older men, EEG power density in nonREM Sleep was reduced in frequencies below 14.0 Hz, whereas in REM Sleep age-related reductions were limited to he delta-theta (0.25-7.0 Hz) and low alpha (8.25-10.0 Hz) band. Slow-wave activity (SWA, power density in the 0.75-4.5 Hz range) decreased in the course of Sleep in both age groups. The between-group difference in SWA diminished in the course of Sleep, whereas the difference in activity in the frequency range of Sleep spindles (12.25-14.0 Hz) increased. It is concluded that frequency and state specific changes occur as a function of age, and that Sleep dependent decline in SWA and increase in Sleep spindle activity are attenuated with age.
H C Heller - One of the best experts on this subject based on the ideXlab platform.
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neonatal treatments with the serotonin uptake inhibitors clomipramine and zimelidine but not the noradrenaline uptake inhibitor desipramine disrupt Sleep patterns in adult rats
Brain Research, 1997Co-Authors: Marcos G. Frank, H C HellerAbstract:Chronic postnatal exposure to clomipramine (CMI), a monoamine uptake inhibitor, results in persistent alterations in adult rat REM Sleep. These effects have been ascribed to CMI's ability to block neonatal active Sleep (AS). However, these effects have not been obtained with other anti-depressants which also block neonatal AS. We compared the long-term effects on adult rat Sleep after postnatal treatments (P8-P21) with either CMI or zimelidine (ZMI, a selective serotonin uptake inhibitor) or desipramine (DMI, a selective noradrenaline uptake inhibitor). ZMI and CMI increased the frequency and decreased the duration of REM Sleep bouts, increased the number of nonREM-REM transitions, and increased sigma power in REM and nonREM Sleep EEGs in adulthood. In contrast, DMI had no effect on any adult Sleep parameters. Since ZMI, DMI and CMI all reduce AS to similar levels, these results suggest that neonatal AS suppression is not responsible for the Sleep deficits following CMI or ZMI treatment. However, since ZMI and CMI, but not DMI, increase synaptic concentrations of serotonin, elevated serotonin levels during development may instead be responsible for the long-lasting Sleep deficits.
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Stimulation of A1 adenosine receptors mimics the electroencephalographic effects of Sleep deprivation.
Brain research, 1995Co-Authors: J H Benington, S K Kodali, H C HellerAbstract:N6-Cyclopentyladenosine (CPA), an A1 adenosine receptor agonist, increased EEG slow-wave activity in nonREM Sleep when administered either systemically (0.1-3 mg/kg) or intracerebroventricularly (3.5-10 micrograms) in the rat. The power spectrum of EEG changes (as calculated by Fourier analysis) matched that produced by total Sleep deprivation in the rat. The effects of CPA on the nonREM-Sleep EEG were dose-dependent. These findings suggest that adenosine is an endogenous mediator of Sleep-deprivation induced increases in EEG slow-wave activity, and therefore that increased adenosine release is a concomitant of accumulation of Sleep need and may be involved in homeostatic feedback control of Sleep expression.
