[Chronic sleep restriction in rats leads to a weakening of compensatory reactions in response to acute sleep deprivation]. / Khronicheskoe ogranichenie sna u krys privodit k oslableniyu kompensatornykh reaktsii v otvet na ostruyu deprivatsiyu sna.

OBJECTIVE: To identify features in the compensatory mechanisms of sleep regulation in response to acute sleep deprivation after chronic sleep restriction in rats. MATERIAL AND METHODS: Male Wistar rats 7-8 months old underwent 5-day sleep restriction: 3 h of sleep deprivation and 1 h of sleep opportunity repeating throughout each day. Six-hour acute total sleep deprivation was performed at the beginning of daylight hours on the 3rd day after sleep restriction. Polysomnogramms were recorded throughout the day before chronic sleep restriction, on the 2nd recovery day after chronic sleep restriction and after acute sleep deprivation. The control group was not subjected to chronic sleep restriction. RESULTS: The animals after chronic sleep restriction had the compensatory increase in total sleep time in response to acute sleep deprivation weaker than in control animals. Animals after sleep restriction had the compensatory increase in the time of slow-wave sleep (SWS) only in the first 6 hours after acute sleep deprivation, whereas in control animals the period of compensation of SWS lasted 12 hours. A compensatory increase in slow-wave activity (SWA) was observed in both groups of animals, but in animals experiencing chronic sleep restriction the amplitude of SWA after acute sleep deprivation was less than in control animals. A compensatory increase in REM sleep in sleep restricted animals occurred immediately after acute sleep deprivation and coincides with a compensatory increase in SWS and SWA, whereas in control conditions these processes are spaced in time. CONCLUSION: Compensatory reactions in response to acute sleep deprivation (sleep homeostasis) are weakened in animals subjected to chronic sleep restriction, as the reaction time and amplitude are reduced.

[Modeling of chronic sleep restriction for translational studies]. / Sozdanie modeli khronicheskogo nedosypaniya dlya translyatsionnykh issledovanii.

OBJECTIVE: To develop of a chronic sleep restriction model in rats by repeated sleep deprivation using an orbital shaker and to determine whether this model leads to disturbances in sleep homeostatic mechanisms. MATERIAL AND METHODS: Male Wistar rats (7-8 months old) underwent sleep restriction for five consecutive days: 3 h of sleep deprivation and 1 h of sleep opportunity repeating throughout each day. Polysomnograms were recorded telemetrically throughout the day before sleep restriction (baseline), on the 1st, 3rd, 5th day of sleep restriction and 2 days after the end of sleep restriction (recovery period). RESULTS: During the period of sleep restriction, the total amount of slow-wave sleep (SWS) and rapid eye movement (REM) sleep decreased by 61% and 55%, respectively, compared to baseline. On the first day of recovery, amount of SWS increased mainly in the dark (active) phase of the day, while REM sleep increased in both light and dark phases; there was no marked rebound of daily SWS amount, while REM sleep increased by 30% from baseline. On the first day of recovery, an elevation of EEG beta and sigma power in sleep states was observed mainly in the light phase of the day. The loss of deep SWS throughout the sleep restriction period increased from 50% on 1st day to 75% on 5th day. The level of deep SWS remained below the baseline by 15-20% on the two subsequent days of recovery. The findings suggest that homeostatic mechanisms of SWS are persistently impaired after 5-day chronic sleep restriction. Besides, a decline of wakefulness accompanied by an increase of SWS in the active phase of the recovery period indicates a disruption in circadian rhythm. CONCLUSION: The proposed model leads to the disruption of sleep homeostatic mechanisms, which, in turn, impede compensation of SWS loss caused by chronic insufficient sleep.