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.

Reactivation of Hippocampal Cell Assemblies: Effects of Behavioral State, Experience, and EEG Dynamics

Abstract: During slow wave sleep (SWS), traces of neuronal activity patterns from preceding behavior can be observed in rat hippocampus and neocortex. The spontaneous reactivation of these patterns is manifested as the reinstatement of the distribution of pairwise firing-rate correlations within a population of simultaneously recorded neurons. The effects of behavioral state [quiet wakefulness, SWS, and rapid eye movement (REM)], interactions between two successive spatial experiences, and global modulation during 200 Hz electroencephalographic (EEG) "ripples" on pattern reinstatement were studied in CA1 pyramidal cell population recordings. Pairwise firing-rate correlations during often repeated experiences accounted for a significant proportion of the variance in these interactions in subsequent SWS or quiet wakefulness and, to a lesser degree, during SWS before the experience on a given day. The latter effect was absent for novel experiences, suggesting that a persistent memory trace develops with experience. Pattern reinstatement was strongest during sharp wave-ripple oscillations, suggesting that these events may reflect system convergence onto attractor states corresponding to previous experiences. When two different experiences occurred in succession, the statistically independent effects of both were evident in subsequent SWS. Thus, the patterns of neural activity reemerge spontaneously, and in an interleaved manner, and do not necessarily reflect persistence of an active memory (i.e., reverberation). Firing-rate correlations during REM sleep were not related to the preceding familiar experience, possibly as a consequence of trace decay during the intervening SWS. REM episodes also did not detectably influence the correlation structure in subsequent SWS, suggesting a lack of strengthening of memory traces during REM sleep, at least in the case of familiar experiences.

Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men.

Abstract: ContextIn young adults, sleep affects the regulation of growth hormone (GH) and cortisol The relationship between decreased sleep quality in older adults and age-related changes in the regulation of GH and cortisol is unknownObjectiveTo determine the chronology of age-related changes in sleep duration and quality (sleep stages) in healthy men and whether concomitant alterations occur in GH and cortisol levelsDesign and SettingData combined from a series of studies conducted between 1985 and 1999 at 4 laboratoriesSubjectsA total of 149 healthy men, aged 16 to 83 years, with a mean (SD) body mass index of 241 (23) kg/m2, without sleep complaints or histories of endocrine, psychiatric, or sleep disordersMain Outcome MeasuresTwenty-four–hour profiles of plasma GH and cortisol levels and polygraphic sleep recordingsResultsThe mean (SEM) percentage of deep slow wave sleep decreased from 189% (13%) during early adulthood (age 16-25 years) to 34% (10%) during midlife (age 36-50 years) and was replaced by lighter sleep (stages 1 and 2) without significant increases in sleep fragmentation or decreases in rapid eye movement (REM) sleep The transition from midlife to late life (age 71-83 years) involved no further significant decrease in slow wave sleep but an increase in time awake of 28 minutes per decade at the expense of decreases in both light non-REM sleep (−24 minutes per decade; P<001) and REM sleep (−10 minutes per decade; P<001) The decline in slow wave sleep from early adulthood to midlife was paralleled by a major decline in GH secretion (−372 µg per decade; P<001) From midlife to late life, GH secretion further declined at a slower rate (−43 µg per decade; P<02) Independently of age, the amount of GH secretion was significantly associated with slow wave sleep (P<001) Increasing age was associated with an elevation of evening cortisol levels (+193 nmol/L per decade; P<001) that became significant only after age 50 years, when sleep became more fragmented and REM sleep declined A trend for an association between lower amounts of REM sleep and higher evening cortisol concentrations independent of age was detected (P<10)ConclusionsIn men, age-related changes in slow wave sleep and REM sleep occur with markedly different chronologies and are each associated with specific hormonal alterations Future studies should evaluate whether strategies to enhance sleep quality may have beneficial hormonal effects

Effect of SCN lesions on sleep in squirrel monkeys: evidence for opponent processes in sleep-wake regulation

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.