J Sleep Res. 1992 Jun;1(2):63-79. doi: 10.1111/j.1365-2869.1992.tb00013.x.
Journal of sleep research
Borbély, Achermann
PMID: 10607028 DOI: 10.1111/j.1365-2869.1992.tb00013.x
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 ultradian 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.
