Showing papers on "Slow-wave sleep published in 1993"
TL;DR: It is proposed that the specific loops give the content of cognition, and a nonspecific loop gives the temporal binding required for the unity of cognitive experience.
Abstract: Magnetic recording from five normal human adults demonstrates large 40-Hz coherent magnetic activity in the awake and in rapid-eye-movement (REM) sleep states that is very reduced during delta sleep (deep sleep characterized by delta waves in the electroencephalogram). This 40-Hz magnetic oscillation has been shown to be reset by sensory stimuli in the awake state. Such resetting is not observed during REM or delta sleep. The 40 Hz in REM sleep is characterized, as is that in the awake state, by a fronto-occipital phase shift over the head. This phase shift has a maximum duration of approximately 12-13 msec. Because 40-Hz oscillation is seen in wakefulness and in dreaming, we propose it to be a correlate of cognition, probably resultant from coherent 40-Hz resonance between thalamocortical-specific and nonspecific loops. Moreover, we proposed that the specific loops give the content of cognition, and a nonspecific loop gives the temporal binding required for the unity of cognitive experience.
940 citations
TL;DR: Findings show that the SCN influence the regulation of daily total wake and sleep times, and implicate an alternative sleep-wake regulatory model in which an SCN-dependent process actively facilitates the initiation and maintenance of wakefulness and opposes homeostatic sleep tendency during the subjective day in diurnal primates.
Abstract: Sleep and wakefulness are governed by both the suprachiasmatic nuclei of the hypothalamus (SCN), and a sleep homeostatic process; however, the interaction of these control systems is not well understood. From rodent studies it has been assumed that the SCN promote neither wake nor sleep but gate the homeostatic sleep-promoting process. Yet in humans sleep tendency is lowest during the later waking hours of the day, and sleep duration can be predicted because of the precise circadian timing of waking. Thus in primates, the SCN could assure sleep-wake cycle consolidation by actively promoting or facilitating wakefulness. To evaluate this hypothesis, we examined the sleep-wake and sleep-stage patterns of intact and SCN-lesioned (SCNx) squirrel monkeys maintained in constant light. This diurnal primate has consolidated sleep and wake patterns more similar to man than rodents. Sleep-wake, sleep stages, brain temperature, and drinking circadian rhythms were eliminated, and total sleep time was significantly increased (4.0 hr, P < 0.01) in SCNx monkeys. However, total times in deeper stages of non-rapid eye movement (non-REM; e.g., delta sleep) and REM sleep were not significantly affected by SCN lesions. Increased total sleep time was associated with a reduction in subjective day wake consolidation, as evidenced by substantially shorter wake bout lengths in SCNx monkeys (15 +/- 6 min) as compared to intact monkeys (223 +/- 10 min; P < 0.0001, ANOVA). These findings show that the SCN influence the regulation of daily total wake and sleep times, and implicate an alternative sleep-wake regulatory model in which an SCN-dependent process actively facilitates the initiation and maintenance of wakefulness and opposes homeostatic sleep tendency during the subjective day in diurnal primates.
646 citations
TL;DR: The simulations demonstrate that the concept of sleep homeostasis as proposed in the two-process model of sleep regulation can be refined to account in quantitative terms for empirical data and to predict the changes induced by the prolongation of waking or sleep.
425 citations
TL;DR: These data demonstrate that when averaged per sleep episode or non-REM sleep episode an inverse relationship between SWA and spindle activity exists but that in the initial and final part of non-Rapid-eye-movement sleep episodes the association between these two activities is positive.
324 citations
TL;DR: Evaluated the efficacy of bright light exposure in the treatment of sleep maintenance insomnia with the aim of finding an effective non‐drug alternative in the management of age‐related sleep Maintenance insomnia.
Abstract: Objective: Half of the population over 65 suffers from chronic sleep disturbance. As a consequence, almost 40% of hypnotic medications are prescribed to people over age 60. Yet, hypnotics are often of little benefit in this population. As such, an effective non-drug alternative could prove important in the management of age-related sleep maintenance insomnia. The current study sought to evaluate the efficacy of bright light exposure in the treatment of sleep maintenance insomnia.
Design: Following baseline sleep and circadian rhythms assessment, subjects with sleep-maintenance insomnia were treated with timed exposure to either bright white light or dim red light for 12 consecutive days. Sleep and circadian rhythms recordings were subsequently obtained and measures of sleep quality were compared to assess efficacy of the treatments.
Setting: Baseline and post-treatment sleep and circadian rhythms assessments took place in the Laboratory of Human Chronobiology, Department of Psychiatry, Cornell University Medical College. The treatment phase of the study was conducted in participants' homes.
Participants: Sixteen men and women between the ages of 62 and 81 years were studied. All subjects were free of hypnotic medication, and all had experienced sleep disturbance for at least 1 year prior to entering the study.
Results: Exposure to bright light resulted in substantial changes in sleep quality. Waking time within sleep was reduced by an hour, and sleep efficiency improved from 77.5% to 90%, without altering time spent in bed. Increased sleep time was in the form of Stage 2 sleep, REM sleep, and slow wave sleep. The effects were remarkably consistent across subjects.
Conclusions: The findings demonstrate the effectiveness of timed exposure to bright light in the treatment of age-related sleep maintenance insomnia. With further refinement of treatment regimens, this non-drug intervention may prove useful in a large proportion of sleep disturbed elderly.
292 citations
TL;DR: Activity in the upper delta band tended to gradually increase from night to night during the sleep restriction period, whereas after an initial increase, activity in the theta-alpha band changed in the opposite direction and progressive changes were also present in the EEG spectra of REM sleep and wakefulness.
Abstract: The effect of repeated partial sleep deprivation on sleep stages and electroencephalogram (EEG) power spectra during sleep and wakefulness was investigated in nine healthy young subjects. Three baseline nights of 8 hours (2300-0700 hours) were followed by four nights with 4 hours of sleep (2300-0300 hours) and three recovery nights of 8 hours (2300-0700 hours). Sleep restriction curtailed sleep stages 1 and 2 as well as rapid eye movement (REM) sleep, but left slow wave sleep largely unaffected. In the first two recovery nights, total sleep time and REM sleep were enhanced, and sleep latency was shortened. Slow wave sleep was increased only in the first recovery night. In accordance with the prediction of the two-process model of sleep regulation, slow wave activity (SWA; spectral power density in the 0.75-4.5-Hz range) in nonrapid eye movement (NREM) sleep increased by approximately 20% in the first night following sleep restriction, remained at this level in the subsequent 3 nights and decreased immediately after the first recovery night. In contrast to these immediate changes, progressive and more persistent changes were seen in the EEG activity of higher frequencies. Thus, activity in the upper delta band tended to gradually increase from night to night during the sleep restriction period, whereas after an initial increase, activity in the theta-alpha band changed in the opposite direction. The progressive changes were also present in the EEG spectra of REM sleep and wakefulness. Because the time course of these changes paralleled the cumulative deficit in REM sleep, they may represent a correlate of REM sleep pressure.
227 citations
TL;DR: The results were consistent with the notion that delta activity is an indicator of depth within NREM sleep, and Epochs with high delta power had increased arousal threshold relative to epochs with low arousal threshold.
Abstract: This study was designed to functionally validate earlier described criteria for visual sleep scoring with respect to acoustical stimulus threshold for arousal. A further objective was to explore the relation between electroencephalographic (EEG) power spectrum and acoustical stimulus threshold for arousal. After habituation to an acoustical stimulus (a 1,000-Hz sine tone, increasing 1.5 dB per second for 45 seconds), values for latency to arousal after acoustical stimulus onset were analyzed. Arousal was determined based on EEG and electromyographic (EMG) criteria. There was a significant effect of sleep stage, with slow wave sleep 2 (SWS-2) having higher arousal threshold than slow wave sleep 1 (SWS-1), rapid eye movement (REM) sleep and transition type sleep. This indicates that the subdivision of nonrapid eye movement (NREM) sleep in the rat into SWS-1 and SWS-2 had functional validity in this paradigm. Time of day also had a significant effect, with lower arousal threshold in the last 2 hours (ninth and tenth hour of the light period) of the 8-hour registration period. Furthermore, there was a significant effect of EEG delta power density. Epochs with high delta power had increased arousal threshold relative to epochs with low arousal threshold. The results were consistent with the notion that delta activity is an indicator of depth within NREM sleep.
203 citations
TL;DR: It is concluded that GHB is an effective and well-tolerated treatment for narcolepsy and tends to increase slow wave sleep.
Abstract: We treated 24 patients with narcolepsy for 4 weeks with gammahydroxybutyrate (GHB), 60 mg/kg/night, in a randomized double-blind placebo-controlled cross-over trial. Both clinical and polysomnographic criteria were used to assess the results. Compared to placebo, GHB reduced the daily number of hypnagogic hallucinations (from 0.87 to 0.28; p = 0.008), daytime sleep attacks (from 2.27 to 1.40; p = 0.001) and the severity of subjective daytime sleepiness (from 1.57 to 1.24 on a 0-4 scale; p = 0.028). The number of daily cataplexy attacks was reduced from 1.26 at baseline to 0.56 after 4 weeks of GHB intake. This reduction, however, was not statistically significantly different from the difference between baseline and placebo. GHB stabilized nocturnal rapid eye movement (REM) sleep, i.e. it reduced the percentage of wakefulness during REM sleep (p = 0.007) and the number of awakenings out of REM sleep (p = 0.016), and tended to increase slow wave sleep (p = 0.053). Adverse events were few and mild. We conclude that GHB is an effective and well-tolerated treatment for narcolepsy.
174 citations
TL;DR: HA-containing neurons unit activity changes dramatically as a function of behavioral state across the sleep-wakefulness continuum, from 2.3 spikes/sec during active waking to virtual silence during slow wave sleep and REM sleep.
160 citations
TL;DR: GHRH has sleep-promoting effects in young adults, particularly when given at a time of decreased sleep propensity, as well as in the absence of sleep deprivation.
Abstract: Growth hormone-releasing hormone (GHRH) promotes rapid-eye-movement (REM) and non-REM sleep in animals, but there is little direct evidence for a hypnogenic action of GHRH in humans. In the present study, the possible somnogenic effects of intravenous bolus injections of a dose of GHRH eliciting physiological elevations of GH secretion in healthy young men were investigated. GHRH (0.3 micrograms/kg body wt) was given in early sleep [i.e., 1st slow-wave (SW) period], late sleep (i.e., 3rd REM period), and early sleep after sleep deprivation until 0400 h (i.e., 1st SW period). In the absence of sleep deprivation, injection of GHRH in early sleep did not modify SW sleep but increased REM sleep. GHRH administration in the third REM period was followed by a marked decrease of wake and an almost 10-fold increase in SW sleep. When GHRH was administered during the first SW period after sleep deprivation until 0400 h, the duration of wake decreased. Thus GHRH has sleep-promoting effects in young adults, particularly when given at a time of decreased sleep propensity.
147 citations
TL;DR: Experimental evidence instigated several theories like the REM deprivation hypothesis, the 2‐process model and the reciprocal interaction model of nonREM‐REM sleep regulation to explain the deviant sleep pattern of depression.
Abstract: Abnormalities of REM sleep, i.e. shortening of REM latency, lengthening of the duration of the first REM period and heightening of REM density, which are frequently observed in patients with a major depressive disorder (MDD), have attracted considerable interest. Initial hopes that these aberrant patterns of sleep constitute specific markers for the primary/endogenous sub-type of depression have not been fulfilled. The specificity of REM sleep disinhibition for depression in comparison with other psychopathological groups is challenged as well. Demographic variables like age and sex exert strong influences on sleep physiology and must be controlled when searching for specific markers of depressed sleep. It is still an open question whether abnormalities of sleep are state- or trait-markers of depression. Beyond baseline studies, the cholinergic REM induction test (CRIT) indicated a heightened responsitivity of the REM sleep system to cholinergic challenge in depression compared with healthy controls and other psychopathological groups, with the exception of schizophrenia. A special role for REM sleep in depression is supported by the well-known REM sleep suppressing effect of most antidepressants. The antidepressant effect of selective REM deprivation by awakenings stresses the importance of mechanisms involved in REM sleep regulation for the understanding of the pathophysiology of depressive disorders. The positive effect of total sleep deprivation on depressive mood which can be reversed by daytime naps, furthermore emphasizes relationships between sleep and depression. Experimental evidence as described above instigated several theories like the REM deprivation hypothesis, the 2-process model and the reciprocal interaction model of nonREM-REM sleep regulation to explain the deviant sleep pattern of depression. The different models will be discussed with reference to empirical data gathered in the field.
TL;DR: The results showed that the timing of the sleep gate was significantly correlated with the onset of aMT6s secretion, and this is discussed in light of the possible role of melatonin in sleep-wake regulation.
Abstract: The present study investigated the relationship between the time of nocturnal onset of urinary 6-sulfatoxymelatonin (aMT6s) secretion, and the timing of the steepest increase in nocturnal sleepiness ("sleep gate"), as determined by an ultrashort sleep-wake cycle test (7 min sleep, 13 min wake). Twenty-nine men (mean age 23.8 +/- 2.7 years) participated. The ultrashort sleep-wake paradigm started at 0700 hr after a night of sleep deprivation and continued for 24 hr until 0700 hr the next day. Electrophysiological recordings were carried out during the 7-min sleep trials, which were then scored conventionally for sleep stages. Urinary aMT6s was measured every 2 hr. The results showed that the timing of the sleep gate was significantly correlated with the onset of aMT6s secretion. These results are discussed in light of the possible role of melatonin in sleep-wake regulation.
TL;DR: It is concluded that dilation of the anterior nares in patients without nasal pathology has a relatively weak effect on snoring, and routine use of nasal dilating appliances is not recommended for treatment of snoring.
Abstract: This study was designed to test the hypothesis that nasal dilation reduces snoring. To achieve this we performed nocturnal polysomnography, including measurement of snoring, in 15 patients without nasal pathology before and after insertion of a nasal dilator (NOZOVENT). Snoring was quantified for each sleep stage by recording the number of snores per minute of sleep, number of snores per minute of snoring time and nocturnal sound intensities (maximum, average and minimum). We found that nasal dilation had no effect on the number of apneas, hypopneas or oxygen saturation. Snoring parameters were unaffected by NOZOVENT during stages I, II and REM sleep, but were all significantly reduced during slow wave sleep. We conclude that dilation of the anterior nares in patients without nasal pathology has a relatively weak effect on snoring, and routine use of nasal dilating appliances is not recommended for treatment of snoring.
TL;DR: Correlations between occurrence of complex partial seizures and altered sleep duration were analyzed in a small but strongly homogeneous population of temporal lobe epilepsy patients, finding that relative sleep deprivation may have a seizure‐provoking effect, especially inporal lobe epilepsy.
Abstract: Correlations between occurrence of complex partial seizures and altered sleep duration were analyzed in a small but strongly homogeneous population of temporal lobe epilepsy patients. Sleep deprivation and oversleep were determined individually; 682 epileptic seizures occurring on 4,995 days were related to occasional alterations of night sleep duration. The seizure-inducing effect of an actual relative sleep deprivation was 67-100% in four cases and 49-64% in four cases. Oversleep had no consistent seizure-provoking effect. Relative sleep deprivation may have a seizure-provoking effect, especially in temporal lobe epilepsy. This information may be used to instruct epileptic patients concerning sleep hygiene which might improve the efficacy of antiepileptic drug (AED) treatment, even if no change is made in medication.
TL;DR: Findings provide initial support for the contention that exercise and fitness may have significant effects on the sleep of older men, however, results also suggest that high levels of body heating resulting from a single exercise challenge may have adverse effects.
Abstract: In the current study 12 aerobically fit and 12 sedentary older men underwent two nocturnal polysomnographic (PSG) studies. A control PSG was conducted following a day without aerobic activity, whereas a postexercise PSG study was conducted following an afternoon session of exhaustive aerobic exercise. In addition to deriving usual sleep parameters, a computer scoring program was used to count the number of individual electroencephalographic (EEG) slow waves in each PSG tracing. Multivariate and univariate analyses showed that the fit subjects had shorter sleep onset latencies, less wake time after onset, fewer discrete sleep episodes, fewer sleep stage shifts during the initial portion of the night, less stage 1 sleep, a higher sleep efficiency and more total slow waves during both PSGs than did the sedentary subjects. Although no main effects were found for the acute exercise challenge, post hoc analyses showed that high levels of body heating during exercise predicted increased sleep fragmentation for both fit and sedentary subjects. These findings provide initial support for the contention that exercise and fitness may have significant effects on the sleep of older men. However, results also suggest that high levels of body heating resulting from a single exercise challenge may have adverse effects. Implications of the study are discussed and suggestions for future research are provided.
TL;DR: There are no advantages realized on sleep inertia by waking up from sleep at specific times of day, and an extreme form of sleep inertia was observed, when the process of waking up during the period of the circadian body temperature trough became so traumatic that it created "sleep (nap) aversion."
Abstract: Sleep inertia is a brief period of inferior task performance and/or disorientation immediately after sudden awakening from sleep. Normally sleep inertia lasts < 5 min and has no serious impact on conducting routine jobs. This preliminary study examined whether there are best and worst times to wake up stemming from circadian effects on sleep inertia. Since the process of falling asleep is strongly influenced by circadian time, the reverse process of awakening could be similarly affected. A group of nine subjects stayed awake for a 64-h continuous work period, except for 20-min sleep periods (naps) every 6 h. Another group of 10 subjects stayed awake for 64 h without any sleep. The differences between these two groups in performance degradation are expected to show sleep inertia on the background of sleep deprivation. Sleep inertia was measured with Baddeley's logical reasoning task, which started within 1 min of awakening and lasted for 5 min. There appeared to be no specific circadian time when sleep inertia is either maximal or minimal. An extreme form of sleep inertia was observed, when the process of waking up during the period of the circadian body temperature trough became so traumatic that it created "sleep (nap) aversion." The findings lead to the conclusion that there are no advantages realized on sleep inertia by waking up from sleep at specific times of day.
TL;DR: Nocturnal plasma and secretory GH profiles of OSA patients were examined in relation to the quality and quantity of sleep, together with plasma glucose and insulin levels and individual GH plasma and secretion rates showed a tendency to correlate with the amount of SWS.
Abstract: The principal nocturnal GH peak normally coincides with the first episode of slow wave sleep (SWS). Obstructive sleep apnea (OSA) patients have low nocturnal GH levels which may be explained by their poor quality fragmented sleep but other factors are possibly involved. Obesity is frequently associated with OSA, and obese patients also manifest reduced GH secretion. The mechanisms reducing GH levels in obese subjects are not understood, but hyperinsulinaemia is a suggested factor. In this study nocturnal plasma and secretory GH profiles of OSA patients were examined in relation to the quality and quantity of sleep, together with plasma glucose and insulin levels. Eight OSA patients, (BMI 32.7 +/- 2.3 kg/m2), underwent 2 night studies. For one night no treatment was given and for the other continuous positive airway pressure (CPAP) treatment was administered for the first time. Blood was collected continuously throughout each night and plasma GH, insulin and glucose profiles established in 10 min interval samples. From the plasma data a deconvolution model was used to calculate GH secretion rates. Sleep was recorded during the studies. For the non-treatment night GH levels were low and increased significantly with treatment, p = 0.008 for plasma levels and p = 0.02 for secretion rates. Treatment significantly decreased the cumulative apnea duration and increased the quantity of SWS and Rapid Eye Movement (REM) sleep (p = 0.008), but the mean insulin and glucose profiles did not differ between the two nights. Individual GH plasma and secretion rates, on treatment, showed a tendency to correlate with the amount of SWS (p = 0.09).(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: The sleep/wake status of three patients with bilateral lesions involving the paramedian thalamic regions was investigated and subjects with such lesions do not present a 'hypersomnia' but a 'de-arousal' or 'subwakefulness' with inability to develop sleep outside the normal circadian boundaries for its appearance.
Abstract: SUMMARY The sleep/wake status of three patients with bilateral lesions involving the paramedian thalamic regions was investigated Long-term monitoring with infrared video camera and polygraphy were performed In spite of presenting a behavioural aspect of sleep with sleep posture, eyes closed and lack of activity for 15–17 h per day, these subjects did not develop the normal non-rapid eye movement (NREM) and rapid eye movement (REM) sleep states during the daytime The EEG indicated presence of a mixture of low amplitude, irregular, diffuse theta and alpha range frequencies during hours associated with this ‘sleep-like’ behaviour Multiple sleep latency tests performed some time after the acute insult gave varying results, but while stage 1 NREM sleep might have been noted for three to four epochs, other states of sleep never appeared Patients were apathetic and ‘drowsy’ but could develop sleep only during the normal circadian period for sleep, ie during the night Even several years later, in one of the subjects in whom follow-up recordings were obtained, apathetic behaviour and sleep ‘posturing’ were present during much of the day, even though the subject, if requested, could perform tasks adequately all day long Subjects with such lesions do not present a ‘hypersomnia’ but a ‘de-arousal’ or ‘subwakefulness’ with inability to develop sleep outside the normal circadian boundaries for its appearance However, these subjects, at least initially, also lacked full wakefulness They have a behavioural impairment with a compulsive sleep posture and are left in the transition between wakefulness and sleep
TL;DR: An inhibiting influence of sleep is demonstrated on stimulated ACTH and cortisol secretion during early nocturnal sleep, with this effect restricted to the early part of sleep.
Abstract: Twenty-four-hour profiles of pituitary-adrenocortical secretory activity in humans are characterized by a distinct decrease in hormone secretion after sleep onset and a strong increase during the early morning hours. It is a widely accepted notion that this pattern of hormone secretion is driven by intrinsic circadian oscillators, and the contributions of sleep and wakefulness have been greatly neglected. Here, we examined whether there is a sleep-dependent inhibition of stimulated ACTH and cortisol release during early nocturnal sleep, which is dominated by slow wave sleep (SWS). We administered human CRH (hCRH; 50 micrograms), the main corticotropin secretagogue, to 14 healthy men during the first SWS period after sleep onset and another time in the same night during a period of stage 2 sleep in the second half of sleeping time. To discriminate possible circadian influences from influences of sleep, on a second night another two injections of hCRH were administered at identical points during the night to the same subject, who was kept awake. Exclusively during sleep, but only during SWS in the beginning of sleep time, ACTH and cortisol responses to hCRH were blunted. The results demonstrate an inhibiting influence of sleep on stimulated ACTH and cortisol secretion, with this effect restricted to the early part of sleep.
TL;DR: The inhibition of spindle activity could provide a phasically improved thalamocortical sensory inflow after environmental stimuli and serve as a transitory stand-by state ready to reach higher arousal rapidly while maintaining the continuity of sleep.
TL;DR: The results demonstrate the importance of nap timing, suggesting a circadian variation of propensity to relapse into depression, and refute some of the current theories on the relationship between sleep and depressive symptomatology.
TL;DR: It is concluded that 12-h SDEP causes an intensification of sleep, as indicated by the enhanced SWA and the reduced nBA, whereas 12-H cold has only marginal effects.
TL;DR: It is concluded that the wide oscillations in upper airway resistance present during sleep in supine healthy elderly subjects produce a fluctuating mechanical limitation of ventilation, which may contribute to periodic breathing.
Abstract: Elderly subjects are known to be prone to periodic breathing in sleep. Because periodic breathing may be associated with changes in upper airway caliber, we hypothesized that oscillations in upper airway caliber contribute to the increased prevalence of sleep-related periodic breathing in the elderly. We tested this hypothesis by measuring upper airway resistance, ventilatory variables, and the pattern of variation of these variables in groups of body size-matched young and elderly healthy individuals during wakefulness and stage 2 non-rapid-eye-movement sleep. No major differences existed between the two groups during either wakefulness or sleep in mean upper airway resistance or ventilation values. However, ventilation was more variable during sleep in the elderly; this variability was oscillatory in the majority of elderly subjects at an average rate of 0.04 breaths/cycle or one cycle approximately every 24 s. Oscillations in upper airway resistance during sleep were associated with reciprocal oscillations in tidal volume and/or minute ventilation at the same frequency. Those subjects who had significant oscillations in upper airway resistance had more apneas and hypopneas than those subjects without such oscillations. Oscillations in resistance and ventilation occurred in the supine but not in the lateral body position. We conclude that the wide oscillations in upper airway resistance present during sleep in supine healthy elderly subjects produce a fluctuating mechanical limitation of ventilation, which may contribute to periodic breathing.
TL;DR: Following heating, non-rapid eye movement sleep 2 (NREMS2 or deep NREMS) was significantly increased during the first 2 h of the recovery period compared with baseline and sleep-matched control conditions and During the first hour compared with the totally sleep-deprived condition.
TL;DR: The data demonstrate that antidepressants exert distinct effects on sleep, however, these substances do not induce changes in sleep structure which persist after their withdrawal in remitted patients.
Abstract: 1. The sleep EEG and nocturnal hormone secretion were studied simultaneously in normal male controls and in male patients with major endogenous depression before treatment with tricyclics and after recovery and drug cessation. 2. Several studies were performed in normal male controls to investigate the effect of antidepressants (brofaromine, moclobemide, amitriptyline, clomipramine and trimipramine) and of neuropeptides (CRH and the ACTH(4–9) fragment analog ebiratide) on the sleep EEG and sleep-associated hormone secretion. 3. Elevated cortisol and blunted testosterone secretion are state markers of acute depression, whereas sleep EEG, GH and prolactin variables do not show marked differences between acute depression and recovery. Except for trimipramine, all antidepressants investigated suppress REM sleep. No systematic relationship between the sleep EEG and endocrine effects of antidepressants is detectable. Pulsatile application of CRH in controls mimicks some of the neurobiological symptoms of acute depression. More shallow sleep occurs under ebiratide, whereas hormonal secretion remains unchanged. 4. Our data demonstrate that antidepressants exert distinct effects on sleep. However, these substances do not induce changes in sleep structure which persist after their withdrawal in remitted patients. Pulsatile application of neuropeptides leads to specific effects on CNS activity which are not mediated by changes of peripheral hormone secretion. The view that CRH plays a key role in the pathophysiology of affective disorders is corroborated.
TL;DR: It is suggested that lower dimensional chaotic processes might be associated with an overloading of neuronal networks during sleep and therefore the psychopathology of schizophrenics might be due to impaired complexity of their EEG's dynamics.
Abstract: Deterministic chaos could be regarded as a healthy flexibility of the human brain necessary for correct neuronal operations. Several investigations have demonstrated that in healthy subjects the dimensionality of REM sleep is much higher than that of slow wave sleep (SWS). We investigated the sleep-EEG of schizophrenic patients with methods from nonlinear system theory in order to estimate the dynamic properties of CNS. We hypothesized that schizophrenics would reveal alterations of their dynamic EEG features indicating impaired information processing. In 11 schizophrenic patients, the EEG's dimensionality during sleep stages II and REM was reduced. We suggest that such lower dimensional chaotic processes might be associated with an overloading of neuronal networks during sleep and therefore the psychopathology of schizophrenics might be due to impaired complexity of their EEG's dynamics.
TL;DR: Although the slight down-regulation of Tb and metabolism that accompanies the transition from wakefulness to NREM sleep may have served as a pre adaptation for the evolution of hibernation among the mammals, increasing consideration must be given to the possibility that hibernation represents an arousal state distinct from any known normothermic arousal state.
Abstract: Evidence from electroencephalographic, thermoregulatory and cellular neurophysiological studies suggests that sleep and hibernation may be homologous adaptations for energy conservation. However, despite the similarities between non-rapid eye movement (NREM) sleep and hibernation, the restorative function normally associated with slow wave sleep appears not to occur during hibernation, perhaps because of the low body temperature (Tb). Cellular neurophysiological studies also suggest that a bout of hibernation is not exclusively NREM sleep but is punctuated by periods of wakefulness. The entrance to hibernation involves both an inhibition of cortical activity and activation of hypothalamic regions, whereas the arousal from hibernation is primarily a hypothalamic function. Multiple neurochemical systems are affected by the arousal state change that occurs in hibernation, and a serotonergic-opiatergic interaction, in particular, may be important in regulating these events. Among regulated physiological systems affected by arousal state changes, the episodic respiration evident in hibernation shows striking similarities to the apneas observed during sleep in both humans and other mammals. Although the slight down-regulation of Tb and metabolism that accompanies the transition from wakefulness to NREM sleep may have served as a preadaptation for the evolution of hibernation among the mammals, increasing consideration must be given to the possibility that hibernation represents an arousal state distinct from any known normothermic arousal state.
TL;DR: The data support the notion that guinea pigs exhibit only a weak circadian rest-activity rhythm, andigilance states, electroencephalogram (EEG) power spectra, and cortical temperature were obtained in nine guinea pig for 24 h in a 12-h light-dark schedule.
Abstract: Vigilance states, electroencephalogram (EEG) power spectra (0.25-25.0 Hz), and cortical temperature (TCRT) were obtained in nine guinea pigs for 24 h in a 12:12-h light-dark (LD 12:12) schedule. Sleep was markedly polyphasic and fragmented and amounted to 32% of recording time, which is a low value compared with sleep in other rodents. There was 6.8% more sleep in the light period than in the dark period. EEG power density in non-rapid eye movement (NREM) sleep showed no significant temporal trend within the light or the dark period. The homeostatic aspects of sleep regulation, as proposed in the two-process model, can account for the slow-wave activity (SWA) pattern also in the guinea pig: The small 24-h amplitude of the sleep-wakefulness pattern resulted in a small, 12% decline of SWA within the light period. In contrast to more distinctly nocturnal rodents, SWA in the dark period was not higher than in the light period. TCRT showed no difference between the light and the dark period. TCRT in REM sleep and waking was higher than TCRT in NREM sleep. TCRT increased after the transition from NREM sleep to either REM sleep or waking, and decreased in the last minute before the transition and after the transition from waking to NREM sleep. Motor activity measured in six animals for 11 days in constant darkness showed no apparent rhythm in three animals and a significant circadian rhythm in three others. Our data support the notion that guinea pigs exhibit only a weak circadian rest-activity rhythm.
TL;DR: Using electroencephalographic methods, rats learning or not learning a two‐way active avoidance task were found to differ significantly in the structure of sleep determined the day before training, which might reflect the existence of a genetic determinant independently conditioning the ability to learn.
Abstract: Using electroencephalographic methods, rats learning or not learning a two-way active avoidance task were found to differ significantly in the structure of sleep determined the day before training. The main differences concerned (i) synchronized sleep episodes followed by wakefulness, which were longer and fewer in learning rats; (ii) paradoxical sleep episodes, which were longer in learning rats. Significant correlations were present between the number and/or the average duration of synchronized sleep episodes followed by wakefulness or by paradoxical sleep and the number of avoidances or escapes scored in the training session. Power spectral analysis indicated that the relative output in the 6-7-Hz region was higher in learning rats, notably during short episodes of synchronized sleep followed by paradoxical sleep. As two-way active avoidance training induces comparable modifications in postacquisition sleep (Ambrosini et al., Physiol. Behav., 51, 217-226, 1992), the features of preacquisition sleep which prevail in learning rats might directly determine their capacity to learn. Alternatively, they might reflect the existence of a genetic determinant independently conditioning the ability to learn.