This study assessed a proposed sleep-preserving role for sleep spindles by evaluating variations in this activity as a function of factors, both naturally occurring and experimentally induced, known to affect and effect arousal from sleep. These factors included age, auditory stimulation, and experimentally induced arousal from sleep. Analyses were based on data from 84 males (5-49 yrs. old) from normal and clinical (hyperactive, enuretic, and chronic pain) populations who had participated in sleep auditory arousal threshold studies involving adaptation and 1-2 experimental nights. Spindles on experimental nights were visually analyzed and incidence determined for the two minutes preceding and throughout all Stage 2 arousal attempts. Prestimulation spindle occurrence in 39 preadolescent subjects with two experimental nights did not vary significantly from night-to-night, and prestimulation period comparisons between clinical groups and their respective controls were also non-significant. Anticipated relationships between spindle activity and indices of arousal-either inverse with respect to known variations in arousal threshold, i.e., decreases with age and across the night, or direct with respect to stimulus intensity particularly on trials when arousal did not occur-were not observed. Instead, all age groups showed significant decreases in spindle density as an increasing negative function of stimulus intensity. These findings suggest that to the extent to which sleep spindles can be considered to play a role in sleep preservation by inhibiting or attenuating potentially arousing stimuli, these effects appear to be restricted to endogenously generated stimuli and are passive rather than reactive in nature.

Sleep Research Online

Night sleepiness in two groups of student volunteers who stayed awake for one night was assessed at standardized time (22:00, 01:00, 04:00, 07:00) by the Stanford Sleepiness Scale (SSS). One group (N=21) chewed the chewing gum from midnight until the end of the experiment in the morning, while the other group (N=43) was not chewing at all. The results show that both groups at the initial assessment at 22:00 were not sleepy, with similar SSS scores. Sleepiness in both groups appeared after midnight, worsening towards the morning. The students who were chewing from midnight assessed their sleepiness as lower than the students who were not chewing, which was more marked at 01:00 and 04:00. In the group of medical professionals, nurses and technicians, sleepiness was assessed by SSS in a routine night shift when they, according to their own experience, had the most difficulty overcoming it. Immediately after the assessment they chewed the chewing gum (N=60) or stood/walked (N=27) for 15 minutes. At the end of the fifteenth minute, they assessed their sleepiness again. After 15 minutes of treatment both groups of medical professionals assessed their sleepiness as relieved, with a lower SSS score, more markedly in the chewing group. The obtained results seem to indicate that chewing may alleviate sleepiness in professionals and nonprofessionals who stayed awake through the night.

Sleep Research Online

It is a common belief that sleep deprivation increases the susceptibility to diseases. In order to evaluate the effects of sleep deprivation on immune profile in humans, peripheral venous blood was obtained from sixteen healthy young male volunteers. Ten of the volunteers underwent 48 hours of sleep deprivation and the other six maintained their regular sleep schedule and acted as controls. The first blood samples were taken at the end of the first polysomnographic recording at 8:00 a.m. After this sampling, ten subjects were sleep deprived for 48 hours in sedentary conditions. The second and third blood samples were taken at the 24^th and 48^th hours. The subjects were recorded again to verify rebound effects of sleep deprivation after the third blood sampling. In this second polysomnographic recording, all sleep-deprived subjects showed slow wave and REM sleep rebound. The last blood samples were taken at the 72^nd hour of study at 8:00 a.m. CD4, CD8, CD5, CD16, CD19 surface antigen positive lymphocyte subsets, serum IgG, IgM, and cortisol levels were assessed in all samples. Our results showed that the proportion of NK cells were decreased during sleep deprivation and returned to normal values after recovery sleep. In the control group, we did not observe any changes in the same direction as the sleep-deprived group.

Sleep Research Online

Orexin (hypocretin)-containing neurons of the hypothalamus project to brainstem sites that are involved in the neural control of REM sleep, including the locus coeruleus, the dorsal raphe nucleus, the cholinergic zone of the mesopontine tegmentum, and the pontine reticular formation (PRF). Orexin knockout mice exhibit narcolepsy/cataplexy, and a mutant and defective gene for the orexin type II receptor is present in dogs with an inherited form of narcolepsy/cataplexy. However, the physiological systems mediating these effects have not been described. We reasoned that, since the effector neurons for the majority of REM sleep signs, including muscle atonia, were located in the PRF, this region was likely implicated in the production of these orexin-related abnormalities. To test this possibility, we used microdialysis perfusion of orexin type II receptor antisense in the PRF of rats. Ten to 24 hours after antisense perfusion, REM sleep increased two- to three-fold during both the light period (quiescent phase) and the dark period (active phase), and infrared video showed episodes of behavioral cataplexy. Moreover, preliminary data indicated no REM-related effects following perfusion with nonsense DNA, or when perfusion sites were outside the PRF. More work is needed to provide precise localization of the most effective site of orexin-induced inhibition of REM sleep phenomena.

Sleep Research Online