Slow-wave sleep

About: Slow-wave sleep is a research topic. Over the lifetime, 6543 publications have been published within this topic receiving 320663 citations. The topic is also known as: deep sleep.

High-frequency oscillations recorded in human medial temporal lobe during sleep.

Abstract: The presence of fast ripple oscillations (FRs, 200-500 Hz) has been confirmed in rodent epilepsy models but has not been observed in nonepileptic rodents, suggesting that FRs are associated with epileptogenesis. Although studies in human epileptic patients have reported that both FRs and ripples (80-200 Hz) chiefly occur during non-rapid eye movement sleep (NREM), and that ripple oscillations in human hippocampus resemble those found in nonprimate slow wave sleep, quantitative studies of these oscillations previously have not been conducted during polysomnographically defined sleep and waking states. Spontaneous FRs and ripples were detected using automated computer techniques in patients with medial temporal lobe epilepsy during sleep and waking, and results showed that the incidence of ripples, which are thought to represent normal activity in animal and human hippocampus, was similar between epileptogenic and nonepileptogenic temporal lobe, whereas rates of FR occurrence were significantly associated with epileptogenic areas. The generation of both FRs and ripples showed the highest rates of occurrence during NREM sleep. During REM sleep, ripple rates were lowest, whereas FR rates remained elevated and were equivalent to rates observed during waking. The predominance of FRs within the epileptogenic zone not only during NREM sleep, but also during epileptiform-suppressing desynchronized episodes of waking and REM sleep supports the view that FRs are the product of pathological neuronal hypersynchronization associated with seizure-generating areas.

Respiratory arousal from sleep: mechanisms and significance.

Abstract: The mechanisms by which respiratory stimuli induce arousal from sleep and the clinical significance of these arousals have been explored by numerous studies in the last two decades. Evidence to date suggests that the arousal stimulus in nonrapid eye movement sleep (NREM) is related to the level of inspiratory effort rather than the individual stimuli that contribute to ventilatory drive. A component of the arousal stimulus proportional to the level of inspiratory effort may originate in mechanoreceptors either in the upper airway or respiratory pump. Medullary centers responsible for ventilatory drive may also send a signal proportionate to the level of drive to higher centers in the brain which are responsible for arousal. Thus, the arousal stimulus may consist of multiple components, each increasing as inspiratory effort increases. The level of effort triggering arousal is an index of the arousability of the brain (arousal threshold). A deeper stage of sleep, central nervous system depressants, prior sleep fragmentation, and the presence of obstructive sleep apnea (OSA) have been observed to increase the arousal threshold to airway occlusion. Less information is available concerning the mechanisms of arousal from rapid eye movement (REM) sleep. While REM sleep is associated with the longest obstructive apneas in patients with OSA, normal human subjects appear to have a similar or lower arousal threshold to respiratory stimuli in REM compared to NREM sleep. Recent studies have challenged the assumption that the termination of all obstructive apnea is dependent on arousal from sleep. Improvements in methods to detect and quantitate changes in the cortical electroencephalogram (EEG) may better define the relationship between arousal and apnea termination. This may result in improved criteria for identifying EEG changes of clinical significance. While little is known concerning the mechanisms of arousal in central sleep apnea, arousal may play an important role in inducing this type of apnea in some patients.

Genetic variation in EEG activity during sleep in inbred mice

Abstract: The genetic variation in spontaneous rhythmic electroencephalographic (EEG) activity was assessed by the quantitative analysis of the EEG in six inbred mice strains. Mean spectral EEG profiles (0-25 Hz) over 24 h were obtained for paradoxical sleep (PS), slow-wave sleep (SWS), and wakefulness. A highly significant genotype-specific variation was found for theta peak frequency during both PS and SWS, which strongly suggests the presence of a gene with a major effect. The strain distribution of theta peak frequency during exploratory behavior differed from that during sleep. In SWS, the relative contributions of delta (1-4 Hz) and sigma (11-15) power to the EEG varied with genotype and power in both frequency bands was negatively correlated. In addition, the EEG dynamics at state transitions were analyzed with a 4-s resolution. The onset of PS, but not that of wakefulness, was preceded by a pronounced peak in high-frequency (>11 Hz) power. These findings are discussed in terms of the neurophysiological mechanisms underlying rhythm generation and their control and modulation by the brain stem reticular-activating system.

Sleep-deprivation: Effects on sleep and EEG in the rat

Abstract: 1. The vigilance states (waking, rapid eye movement (REM) sleep, and non-REM (NREM) sleep), motor activity, food intake and water intake were continuously recorded by telemetry in unrestrained rats. In addition, an amplitude measure and a frequency measure (number of zero-crossings (ZCR) per 10 s) of the telemetered EEG-signal was obtained. The animals were recorded during a control day, then subjected to 12-h or 24-h sleep-deprivation (SD) by means of a slowly rotating cylinder, and subsequently recorded for further 1–2 days. The EEG-parameters were recorded also during SD. 2. On the control day, the EEG-amplitude of NREM-sleep exhibited a decreasing trend in the 12-h light-phase (Figs. 3, 4). The occurence of slow wave sleep (SWS; defined as the NREM-sleep fraction with less than 40 ZCR/10 s) was practically limited to the first part of the light-phase (Figs. 2, 4). Cumulative plots of the zero-crossing bands (Fig. 2) revealed a prominent daily rhythm in the EEG-frequency distributionwithin NREM-sleep. 3. The percentage of NREM-sleep and REM-sleep was little affected by the 12-h SD, but the amount of SWS and the EEG-amplitude of NREM-sleep were increased (Figs. 4, 6). After a 24-h SD period terminating before light-onset, NREM-sleep was reduced and REM-sleep was markedly enhanced (Figs. 4, 6; Table 1). Both the duration and frequency of REM-sleep episodes were increased, and episodes of total sleep prolonged (Table 2). The amount of SWS was significantly more increased after 24-h SD than after 12-h SD, whereas the EEG-amplitude of NREM-sleep was enhanced to a similar extent after both SD-schedules (Tables 1, 3 Fig. 6). 4. After a 24-h SD period terminating before dark-onset, sleep (particularly REM-sleep) was enhanced in the first hours of the dark-phase, yet the usual high activity bouts prevailed in the later part of the dark-phase (Figs. 7, 8; Table 1). The extent and time-course of REM-sleep rebound was similar after the two 24-SD schedules, whereas SWS-rebound was different: SWS exhibited a one-stage rebound when recovery started in the light-phase, and a two-stage rebound when recovery started in the dark-phase (Fig. 9). 5. A comparison of the effects of 12-h SD performed with the usual and with the double cylinder rotation rate, showed only small differences, indicating that forced locomotion was a minor factor in comparison to sleep-deprivation (Fig. 10; Table 1). 6. The daily pattern of SWS on control days, and the marked increase of SWS after SD correspond to the results from other animal and human studies. It is proposed that due to the existence of an intensity dimension, NREM-sleep is finely regulated around its baseline level, and thus may be readily and accurately adjusted to current ‘needs’, whereas REM-sleep, lacking an apparent intensity gradient, is regulated around a level which is considerably below baseline. Thus, in contrast to NREM-sleep, REM-sleep compensation can occur only by an increase in the time devoted to this state, thereby curtailing the time available for other activities.

Long-lasting novelty-induced neuronal reverberation during slow-wave sleep in multiple forebrain areas.

Abstract: The discovery of experience-dependent brain reactivation during both slow-wave (SW) and rapid eye-movement (REM) sleep led to the notion that the consolidation of recently acquired memory traces requires neural replay during sleep. To date, however, several observations continue to undermine this hypothesis. To address some of these objections, we investigated the effects of a transient novel experience on the long-term evolution of ongoing neuronal activity in the rat forebrain. We observed that spatiotemporal patterns of neuronal ensemble activity originally produced by the tactile exploration of novel objects recurred for up to 48 h in the cerebral cortex, hippocampus, putamen, and thalamus. This novelty-induced recurrence was characterized by low but significant correlations values. Nearly identical results were found for neuronal activity sampled when animals were moving between objects without touching them. In contrast, negligible recurrence was observed for neuronal patterns obtained when animals explored a familiar environment. While the reverberation of past patterns of neuronal activity was strongest during SW sleep, waking was correlated with a decrease of neuronal reverberation. REM sleep showed more variable results across animals. In contrast with data from hippocampal place cells, we found no evidence of time compression or expansion of neuronal reverberation in any of the sampled forebrain areas. Our results indicate that persistent experience-dependent neuronal reverberation is a general property of multiple forebrain structures. It does not consist of an exact replay of previous activity, but instead it defines a mild and consistent bias towards salient neural ensemble firing patterns. These results are compatible with a slow and progressive process of memory consolidation, reflecting novelty-related neuronal ensemble relationships that seem to be context- rather than stimulus-specific. Based on our current and previous results, we propose that the two major phases of sleep play distinct and complementary roles in memory consolidation: pretranscriptional recall during SW sleep and transcriptional storage during REM sleep.