Repeated sleep restriction in rats leads to homeostatic and allostatic responses during recovery sleep.

Recent studies indicate that chronic sleep restriction can have negative consequences for brain function and peripheral physiology and can contribute to the allostatic load throughout the body. Interestingly, few studies have examined how the sleep-wake system itself responds to repeated sleep restriction. In this study, rats were subjected to a sleep-restriction protocol consisting of 20 h of sleep deprivation (SD) followed by a 4-h sleep opportunity each day for 5 consecutive days. In response to the first 20-h SD block on day 1, animals responded during the 4-h sleep opportunity with enhanced sleep intensity [i.e., nonrapid eye movement (NREM) delta power] and increased rapid eye movement sleep time compared with baseline. This sleep pattern is indicative of a homeostatic response to acute sleep loss. Remarkably, after the 20-h SD blocks on days 2-5, animals failed to exhibit a compensatory NREM delta power response during the 4-h sleep opportunities and failed to increase NREM and rapid eye movement sleep times, despite accumulating a sleep debt each consecutive day. After losing approximately 35 h of sleep over 5 days of sleep restriction, animals regained virtually none of their lost sleep, even during a full 3-day recovery period. These data demonstrate that the compensatory/homeostatic sleep response to acute SD does not generalize to conditions of chronic partial sleep loss. We propose that the change in sleep-wake regulation in the context of repeated sleep restriction reflects an allostatic process, and that the allostatic load produced by SD has direct effects on the sleep-wake regulatory system.

Recovery from sleep deprivation occurs during propofol anesthesia.

BACKGROUND: Some neurophysiologic similarities between sleep and anesthesia suggest that an anesthetized state may reverse effects of sleep deprivation. The effect of anesthesia on sleep homeostasis, however, is unknown. To test the hypothesis that recovery from sleep deprivation occurs during anesthesia, the authors followed 24 h of sleep deprivation in the rat with a 6-h period of either ad libitum sleep or propofol anesthesia, and compared subsequent sleep characteristics. METHODS: With animal care committee approval, electroencephalographic/electromyographic electrodes and intrajugular cannulae were implanted in 32 rats. After a 7-day recovery and 24-h baseline electroencephalographic/electromyographic recording period, rats were sleep deprived for 24 h by the disk-over-water method. Rats then underwent 6 h of either propofol anesthesia (n = 16) or ad libitum sleep with intralipid administration (n = 16), followed by electroencephalographic/electromyographic monitoring for 72 h. RESULTS: In control rats, increases above baseline in non-rapid eye movement sleep, rapid eye movement sleep, and non-rapid eye movement delta power persisted for 12 h after 24 h of sleep deprivation. Recovery from sleep deprivation in anesthetized rats was similar in timing to that of controls. No delayed rebound effects were observed in either group for 72 h after deprivation. CONCLUSION: These data show that a recovery process similar to that occurring during naturally occurring sleep also takes place during anesthesia and suggest that sleep and anesthesia share common regulatory mechanisms. Such interactions between sleep and anesthesia may allow anesthesiologists to better understand a potentially important source of variability in anesthetic action and raise the possibility that anesthetics may facilitate sleep in environments where sleep deprivation is common.

Baseline and post-deprivation recovery sleep in SCN-lesioned rats.

In humans, advancing age alters sleep patterns, reducing high voltage NREM sleep, sleep bout length, and delta power during NREM sleep. Although the mechanism by which these alterations occur is unknown, age-related changes in normal circadian processes may play a role. Increased age produces histological and functional changes in the suprachiasmatic nucleus (SCN), and alters the amplitude and phase of circadian rhythms. To examine the relationship between SCN function and age-related changes in sleep, we produced radiofrequency (RF) lesions of the SCN in rats of different ages and examined sleep behavior before and after sleep deprivation. Three-, 12- and 18-month-old rats received RF or sham lesions of the SCN. After verifying loss of circadian rhythm, 24-h EEG/EMG/temperature recordings were made in dim light before and after 24 h of sleep deprivation using the disk-over-water method. Age-related changes in NREM sleep, sleep bout length, and delta EEG power persisted despite SCN lesions. SCN lesions in all age groups increased baseline NREM sleep by 4% and NREM delta power by 15%, and decreased REM sleep by 10%. Although SCN lesions initially produced more REM and NREM sleep during recovery, 24-h values did not differ. Deteriorating SCN function is unlikely to cause the characteristic changes in sleep that occur with age. Our data also imply that an intact SCN slightly inhibits NREM sleep in the rat. Changes in NREM sleep and delta EEG power during recovery in lesioned rats suggest that the SCN may influence homeostatic regulation.

Increases in amino-cupric-silver staining of the supraoptic nucleus after sleep deprivation.

Sleep deprived rats undergo a predictable sequence of physiological changes, including changes in skin condition, increased energy expenditure, and altered thermoregulation. Amino-cupric-silver staining was used to identify sleep deprivation related changes in the brain. A significant increase in staining was observed in the supraoptic nucleus (SON) of the hypothalamus of rats with high sleep loss (>45 h) vs. their yoked controls. Follow-up experiments showed that staining was not significantly different in rats sleep deprived for less than 45 h, suggesting that injurious sleep deprivation-related processes occur above a threshold quantity of sleep loss. These anatomical changes suggest that the effects of sleep deprivation may be related to protein metabolism in certain brain regions.

Sleep deprivation in the rat: X. Integration and discussion of the findings. 1989.

The results of a series of studies on total and selective sleep deprivation in the rat are integrated and discussed. These studies showed that total sleep deprivation, paradoxical sleep deprivation, and disruption and/or deprivation of non-rapid eye movement (NREM) sleep produced a reliable syndrome that included death, debilitated appearance, skin lesions, increased food intake, weight loss, increased energy expenditure, decreased body temperature during the late stages of deprivation, increased plasma norepinephrine, and decreased plasma thyroxine. The significance of this syndrome for the function of sleep is not entirely clear, but several changes suggested that sleep may be necessary for effective thermoregulation.