Human slow‐wave sleep and the cerebral cortex

Horne, Jim

doi:10.1111/j.1365-2869.1992.tb00023.x

Cited by 11 publications

(12 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…comm. ) Three-process model of the regulation of sleepiness/alertness (Akerstedt and Folkard 1990;Folkard and Akerstedt 1987, 1989, 1992 A: alertness; C: changes in alertness due to circadian factors; S: changes in alertness due to homeostatic factors; W: sleep inertia, wake up process; S; level of S at awakening; S,; level of S at retiring. Time t has different reference values: wake up for W a n d S during waking; sleep onset for S during sleep; midnight for C. Note: The time course of the homeostatic process is the inverse of the time course of Process S of the two-process model; it builds up during sleep and declines during waking.…”

Section: Discussionmentioning

confidence: 99%

“…Thus an increase in slow-wave sleep was observed after a hyperthermic episode several hours prior t o sleep as well as after a day of exposure to intense and varied environmental stimuli (see Horne 1988Horne , 1991Horne , 1992 for references). Horne (1992) argues that the common effect of these procedures is the increase in brain metabolism. The notion that sleep is promoted by a cumulative effect of heat load has been incorporated in the model of Nakao et al (1990aNakao et al ( , 1991.…”

Section: Rem Sleep Homeostasismentioning

confidence: 99%

“…In contrast to the original two-process model, the change of S. Three-process model of the regulaiion of sleepiness/alertness* (Folkard and Akerstcdt 1987, 1989, 1992Akerstedt and Folkard 1990) Sleepiness/alertness are simulated by the combined action of a homeostatic process. a circadian Process, and sleep inertia (Process W).…”

Section: Miscellaneous Models (Table 4)mentioning

confidence: 99%

“…Oualitativc simulation of ultradian slow-wave activity pattern. , 1989, 1992: Akerstedt and Folkard 1990 simulated the changes of daytime alertness by the combined action of a homeostatic process, a circadian process and ;I sleep inertia process. It is interesting that the time constants of their homeostatic process that have been derived from sleepiness ratings, and the time constants of Process S derived from the sleep EEG, are in a similar range.…”

mentioning

confidence: 99%

See 3 more Smart Citations

Concepts and models of sleep regulation: an overview

Borbély

Achermann

1992

Journal of Sleep Research

206

View full text Add to dashboard Cite

S U M M A R Y Various mathematical models have been proposed to account for circadian, ultradian and homeostatic aspects of sleep regulation. Most circadian models assume that multiple oscillators underlie the differences in period and entrainment properties of the sleep/wake cycle and other rhythms (e.g. body temperature).Interactions of the oscillators have been postulated to account for multimodal sleep/wake patterns. The ultradim models simulate the cyclic alternation of nonREM sleep and REM sleep by assuming a reciprocal interaction of two cell groups. The homeostatic models propose that a sleep/wake dependent process (Process S ) underlies the rise in sleep pressure during waking and its decay during sleep. The time course of this process has been derived from EEG slow-wave activity, an indicator of nonREM sleep intensity. The predictions of homeostatic models have been most extensively tested in experiments. The interaction of Process S with a single circadian process can account for multimodal sleep/wake patterns, internal desynchronization and the time course of daytime sleepiness. Close links have emerged between the processes postulated by the various models and specific brain mechanisms. Due to its recent quantitative elaboration and experimental validation, the modelling approach has become one of the potent research strategies in sleep science.KEYWORDS circadian, homeostatic, mathematical model, nap, ultradian O V E R V I E W OF T H E M O D E L SThree basic processes underlie sleep regulation: (1) A homeostatic process mediating the rise in 'sleep pressure' during waking and the dissipation of 'sleep pressure' during sleep; (2) a circadian process, a clock-like mechanism defining the alternation of periods with high and low sleep propensity and being basically independent of prior sleep and waking; and (3) an ultradian process occurring within sleep and represented by the alternation of the two basic sleep states nonREM sleep and REM sleep. The three processes are illustrated schematically in Fig. 1. The tables provide a synopsis of models that have been proposed to account for circadian, ultradian and homeostatic aspects of sleep regulation. The mathematical equations of the major models are compiled in the appendix. Models of circadian rhythms (Table 1)The main objectives of these models are (1) to simulate spontaneously occurring phenomena in free-running Correspondence: Professor A. Borbkly, Institute of Pharmacology, University of Zurich, Gloriastrasse 32, CH-8006 Zurich, Switzerland rhythms such as changing phase-relations between the sleep/wake cycle and the temperature rhythm, and the splitting of the rest-activity rhythm into two components; and (2) to account mainly for the effects of light, the major zeitgeber, on the phase, amplitude and period of circadian rhythms. The database of the models consists in general of records of rest and activity rather than of polygraphically recorded sleep and waking. Moreover, the models attempt to describe general features of the circadian system rathe...

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Rem Sleep Homeostasismentioning

confidence: 99%

Section: Miscellaneous Models (Table 4)mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Concepts and models of sleep regulation: an overview

Borbély

Achermann

1992

Journal of Sleep Research

206

View full text Add to dashboard Cite

show abstract

“…Local differences in slow-wave homeostasis have been described in both humans and rodents, with frontal regions showing an especially strong response to sleep deprivation [20,28]. Since frontal regions are especially susceptible to the effects of sleep deprivation, and may be working harder than other brain areas during wakefulness, a possible relationship to synaptic potentiation is at least conceivable [26]. Direct evidence linking brain activation with local sleep homeostasis has been sought in two studies employing a lateralized task, one in humans [29] and one in rats [52].…”

Section: Synaptic Potentiation and Slow-wave Homeostasismentioning

confidence: 99%

Sleep and synaptic homeostasis: a hypothesis

Tononi

Cirelli

2003

Brain Research Bulletin

981

701

View full text Add to dashboard Cite

During much of sleep, the cerebral cortex is rippled by slow waves, which appear in the electroencephalogram as oscillations between 0.5 and 4.5 Hz. Slow waves are regulated as a function of previous wakefulness, being maximal at the beginning of sleep and then progressively returning to a baseline level. This paper discusses a hypothesis about the significance of slow-wave activity and its homeostatic regulation. The hypothesis is as follows:1. Wakefulness is associated with synaptic potentiation in several cortical circuits; 2. Synaptic potentiation is tied to the homeostatic regulation of slow-wave activity;3. Slow-wave activity is associated with synaptic downscaling; 4. Synaptic downscaling is tied to the beneficial effects of sleep on performance.The hypothesized link between sleep and synaptic homeostasis is supported by several lines of evidence and leads to testable predictions.

show abstract