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Background Aside from the homeostatic and circadian components, light has itself an important, direct as well as indirect role in sleep regulation. Light exerts indirect sleep effect by modulating the circadian rhythms. Exposure to short light-dark cycle (LD 1:1, 1:1 h light - dark) eliminates the circadian sleep regulatory component but direct sleep effect of light could prevail. The aim of the present study was to examine the interaction between the light and the homeostatic influences regarding sleep regulation in a rat model. Methods Spontaneous sleep–wake and homeostatic sleep regulation by sleep deprivation (SD) and analysis of slow waves (SW) were examined in Wistar rats exposed to LD1:1 condition using LD12:12 regime as control. Results Slow wave sleep (SWS) and REM sleep were both enhanced, while wakefulness (W) was attenuated in LD1:1. SWS recovery after 6-h total SD was more intense in LD1:1 compared to LD12:12 and SWS compensation was augmented in the bright hours. Delta power increment during recovery was caused by the increase of SW number in both cases. More SW was seen during baseline in the second half of the day in LD1:1 and after SD compared to the LD12:12. Increase of SW number was greater in the bright hours compared to the dark ones after SD in LD1:1. Lights ON evoked immediate increase in W and decrease in both SWS and REM sleep during baseline LD1:1 condition, while these changes ceased after SD. Moreover, the initial decrease seen in SWS after lights ON, turned to an increase in the next 6-min bin and this increase was stronger after SD. These alterations were caused by the change of the epoch number in W, but not in case of SWS or REM sleep. Lights OFF did not alter sleep–wake times immediately, except W, which was increased by lights OFF after SD. Conclusions Present results show the complex interaction between light and homeostatic sleep regulation in the absence of the circadian component and indicate the decoupling of SW from the homeostatic sleep drive in LD1:1 lighting condition.

Sleep is homeostatically regulated suggesting a restorative function. Sleep deprivation is compensated by an increase in length and intensity of sleep. In this study, suppression of sleep was induced pharmacologically by drugs related to different arousal systems. All drugs caused non-rapid eye movement (NREM) sleep loss followed by different compensatory processes. Apomorphine caused a strong suppression of sleep followed by an intense recovery. In the case of fluoxetine and eserine, recovery of NREM sleep was completed by the end of the light phase due to the biphasic pattern demonstrated for these drugs first in the present experiments. Yohimbine caused a long-lasting suppression of NREM sleep, indicating that either the noradrenergic system has the utmost strength among the examined systems, or that restorative functions occurring normally during NREM sleep were not blocked. Arousal systems are involved in the regulation of various wakefulness-related functions, such as locomotion and food intake. Therefore, it can be hypothesized that activation of the different systems results in qualitatively different waking states which might affect subsequent sleep differently. These differences might give some insight into the homeostatic function of sleep in which the dopaminergic and noradrenergic systems may play a more important role than previously suggested.

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