Models of human sleep regulation

Non-REM sleep deprivation and REM sleep deprivation both lead to specific rebounds, suggesting that these states fulfil physiological needs. In view of impaired performance after sleep deprivation, a recovery function of sleep seems likely. The timing of this recovery is restricted to a narrow time interval within the 24 hour day, i.e. the night. Generally, nocturnal sleep in humans is considered a consequence of the impact of the circadian pacemaker in the hypothalamus on sleep propensity. The interaction between the homeostatic recovery process and the circadian pacemaker has been modelled in the two-process model of sleep regulation. This model is used as a starting point in the present review. A series of refinements and several alternative models are discussed, both with respect to the quality of fit of theory and data, as well as with respect to the concepts behind the models

Total and Partial Sleep Deprivation in Clomipramine-Treated Endogenous Depressives

Improvement in depression after total sleep deprivation (TSD) is, as a rule, followed by relapse after subsequent ad libitum sleep. This study is addressed to the question of how nocturnal partial sleep following TSD affects this relapse. Thirty endogenously depressed patients participated in the study. During the night after TSD, subjects were allowed sleep during one of three periods, i.e., unlimited sleep (11:00 p.m.-8:00 a.m.), early partial sleep (11:00 p.m.-3:00 a.m.), or late partial sleep (4:00 a.m.-8:00 a.m.). The hypothesis that partial sleep deprivation on the night following TSD prevents relapse has to be rejected. Relapse was inversely related to a drop in minimum rectal temperature during the night with unlimited or partial sleep, compared with minimum rectal temperature on the previous night.

Relations between depressed mood and vocal parameters before, during and after sleep deprivation: a circadian rhythm study

The mechanism underlying improvement after total sleep deprivation (TSD) was studied in 14 major depressed patients. The suggestions that (1) circadian processes and/or (2) dimensions of arousal may play a role in the response to TSD were investigated. Diurnal variation of depressed mood and of mood- and arousal-related vocal parameters was studied in relation to the effect of TSD on depressed mood and vocal parameters. During 3 baseline days, during TSD and 2 days after TSD vocal parameters and depressed mood were assessed 6 and 3 times daily respectively. The mean fundamental frequency (frequency of vocal fold vibration, F0) (presumably reflecting aspects of arousal) as well as the range of the F0 (proposed to reflect sadness) showed a clear circadian pattern with a peak at about 4.00 p.m. TSD affected the circadian organization of the mean F0 and advanced the peak of the curve. After one night of subsequent sleep this effect disappeared. In addition, improvement after TSD coincided with an increase of the mean F0. The diurnal variation of mood before TSD predicted the mood response to TSD, whereas diurnal variation of vocal parameters did not. Moreover, circadian changes in vocal parameters were not related to changes in depressed mood. These findings suggest that the diurnal variations in mood and vocal parameters are regulated by different mechanisms. Data support the presumption that circadian as well as arousal processes are involved in the mood response to TSD. Circadian changes in vocal parameters due to TSD are not likely to reflect changes in the biological clock.

Plasticity in the period of the circadian pacemaker induced by phase dispersion of its constituent cellular clocks

The mammalian circadian pacemaker is commonly thought to be a rigid oscillator that generates output under a variety of circumstances that differ only in phase, period, and/or amplitude. Yet the pacemaker is composed of many cells that each can respond to varying circumstances in different ways. Computer simulations demonstrate that networks of such pacemaker cells behave differently under a light-dark cycle compared with constant darkness. The differences demonstrate that the circadian pacemaker is plastic: The pacemaker shapes its properties in response to the circumstances. A consequence is that properties of a pacemaker under a light-dark cycle cannot be derived from studies of the same system in constant darkness. In this paper we show that the dispersion of phase in a network of coupled oscillators can influence ensemble period: For the considered type of coupling, it is demonstrated that the more synchronous the cells are, the longer is the ensemble period. This is consistent with various data sets obtained in mammals, and even with a data set from fruit flies, in which circadian variation in behavior is regulated in a distinctly differently way from that in mammals. We conclude that environmental circumstances such as photoperiod and exposure to light pulses in otherwise darkness modify the phase distribution of the network and, thereby, the period of the ensemble. Our study supports the view that such properties as circadian period are not solely determined by clock genes but are also determined by the genes that regulate the communication in cellular networks

Pacer cell response to periodic Zeitgebers

Almost all organisms show some kind of time periodicity in their behavior. Especially in mammals the neurons of the suprachiasmatic nucleus form a biological clock regulating the activity-inactivity cycle of the animal. This clock is stimulated by the natural 24-hour light-dark cycle. In our model of this system we consider each neuron as a so called phase oscillator, coupled to other neurons for which the light-dark cycle is a Zeitgeber. To simplify the model we first take an externally stimulated single phase oscillator. The first part of the phase interval is called the active state and the remaining part is the inactive state. Without external stimulus the oscillator oscillates with its intrinsic period. An external stimulus, be it from activity of neighboring cells or the periodic daylight cycle, acts twofold, it may delay the change form active to inactive and it may advance the return to the active state. The amount of delay and advance depends on the strength of the stimulus. We use a circle map as a mathematical model for this system. This map depends on several parameters, among which the intrinsic period and phase delay and advance. In parameter space we find Arnol'd tongues where the system is in resonance with the Zeitgeber. Thus already in this simplified system we find entrainment and synchronization. Also some other phenomena from biological experiments and observations can be related to the dynamical behavior of the circle map