Topic
Non-rapid eye movement sleep
About: Non-rapid eye movement sleep is a research topic. Over the lifetime, 8661 publications have been published within this topic receiving 389465 citations. The topic is also known as: NREM.
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TL;DR: It is concluded that CA neurones promote wakefulness, participate in central respiratory chemoreception, stimulate breathing frequency, and minimize breathing variability in REM sleep.
Abstract: Brainstem catecholamine (CA) neurones have wide projections and an arousal-state-dependent activity pattern. They are thought to modulate the processing of sensory information and also participate in the control of breathing. Mice with lethal genetic defects that include CA neurones have abnormal respiratory control at birth. Also the A6 region (locus coeruleus), which contains CA neurones sensitive to CO2in vitro, is one of many putative central chemoreceptor sites. We studied the role of CA neurones in the control of breathing during sleep and wakefulness by specifically lesioning them with antidopamine β-hydroxylase–saporin (DBH-SAP) injected via the 4th ventricle. After 3 weeks there was a 73–84% loss of A5, A6 and A7 tyrosine hydroxylase (TH) immunoreactive (ir) neurones along with 56–60% loss of C1 and C2 phenyl ethanolamine-N-methyltransferase (PNMT)-ir neurones. Over the 3 weeks, breathing frequency decreased significantly during air and 3 or 7% CO2 breathing in both wakefulness and non-REM (NREM) sleep. The rats spent significantly less time awake and more time in NREM sleep. REM sleep time was unaffected. The ventilatory response to 7% CO2 was reduced significantly in wakefulness at 7, 14 and 21 days (−28%) and in NREM sleep at 14 and 21 days (−26%). Breathing variability increased in REM sleep but not in wakefulness or NREM sleep. We conclude that CA neurones (1) promote wakefulness, (2) participate in central respiratory chemoreception, (3) stimulate breathing frequency, and (4) minimize breathing variability in REM sleep.
121 citations
TL;DR: The data presented here suggest a unifying mechanism linking slow waves, plasticity and cortical information integration and suggest that TMS can be used as a nonpharmacological means to controllably induce slow waves in the human cerebral cortex.
Abstract: Sleep slow waves are the main phenomenon underlying NREM sleep. They are homeostatically regulated, they are thought to be linked to learning and plasticity processes and, at the same time, they are associated with marked changes in cortical information processing. Using transcranial magnetic stimulation (TMS) and high-density (hd) EEG we can measure slow waves, induce and measure plastic changes in the cerebral cortex and directly assess corticocortical information transmission. In this manuscript we review the results of recent experiments in which TMS with hd-EEG is used to demonstrate (i) a causal link between cortical plastic changes and sleep slow waves and (ii) a causal link between slow waves and the decreased ability of thalamocortical circuits to integrate information and to generate conscious experience during NREM sleep. The data presented here suggest a unifying mechanism linking slow waves, plasticity and cortical information integration; moreover, they suggest that TMS can be used as a nonpharmacological means to controllably induce slow waves in the human cerebral cortex.
121 citations
TL;DR: The electroencephalogram (EEG) is the most common tool used in sleep research and this unit describes the methods for recording and analyzing the EEG.
Abstract: The electroencephalogram (EEG) is the most common tool used in sleep research. This unit describes the methods for recording and analyzing the EEG. Detailed protocols describe recorder calibration, electrode application, EEG recording, and computer EEG analysis with power spectral analysis. Computer digitization of an analog EEG signal is discussed, along with EEG filtering and the parameters of fast Fourier transform (FFT) power spectral analysis. Sample data are provided for a typical night's analysis of EEG during NREM (non-REM) and REM sleep.
120 citations
TL;DR: It is demonstrated that a circadian process modulates sleep spindle characteristics and that the strength of this circadian modulation is reduced with age.
120 citations
TL;DR: It is shown that when stage 1 sleep is excluded from TST, a stronger relationship between TST and subsequent alertness and performance emerges – and the need to invoke ‘sleep continuity’ as a variable that contributes independently to recuperative sleep processes is obviated.
Abstract: SUMMARY Studies have shown that next-day performance and alertness are impaired by sleep fragmentation procedures even when total sleep time (TST) is unaffected. Based on these studies it has been hypothesized that both the duration and continuity of sleep determine its recuperative value. This review of the literature suggests that when sleep fragmentation procedures increase the relative amount of stage 1 sleep, next-day performance and alertness are impaired. Other studies suggest that stage 1 sleep has little or no recuperative value. Total sleep time, however, is typically defined as the sum of time spent in sleep stages 1, 2, 3, 4, and REM. In the present paper it is shown that when stage 1 sleep is excluded from TST, a stronger relationship between TST and subsequent alertness and performance emerges - and the need to invoke 'sleep continuity' as a variable that contributes independently to recuperative sleep processes is obviated. In the same way that partial or total sleep deprivation impairs alertness and performance, it is proposed that sleep disruption also impairs alertness and performance by reducing true recuperative sleep time.
120 citations