Background: We have previously reported that the expression of circadian clock-genes increases in the cerebral cortex after sleep deprivation (SD) and that the sleep rebound following SD is attenuated in mice deficient for one or more clock-genes. We hypothesized that besides generating circadian rhythms, clock-genes also play a role in the homeostatic regulation of sleep. Here we follow the time course of the forebrain changes in the expression of the clock-genesperiod(per)-1, per2, and of the clock-controlled genealbumin D-binding protein(dbp) during a 6 h SD and subsequent recovery sleep in three inbred strains of mice for which the homeostatic sleep rebound following SD differs. We reasoned that if clock genes are functionally implicated in sleep homeostasis then the SD-induced changes in gene expression should vary according to the genotypic differences in the sleep rebound.Results: In all three strainsperexpression was increased when animals were kept awake but the rate of increase during the SD as well as the relative increase inperafter 6 h SD were highest in the strain for which the sleep rebound was smallest; i.e., DBA/2J (D2). Moreover, whereas in the other two strainsper1andper2reverted to control levels with recovery sleep,per2expression specifically, remained elevated in D2 mice.dbpexpression increased during the light period both during baseline and during SD although levels were reduced during the latter condition compared to baseline. In contrast toper2,dbpexpression reverted to control levels with recovery sleep in D2 only, whereas in the two other strains expression remained decreased.Conclusion: These findings support and extend our previous findings that clock genes in the forebrain are implicated in the homeostatic regulation of sleep and suggest that sustained, high levels ofper2expression may negatively impact recovery sleep.

Background: A number of benefits from meditation have been claimed by those who practice various traditions, but few have been well tested in scientifically controlled studies. Among these claims are improved performance and decreased sleep need. Therefore, in these studies we assess whether meditation leads to an immediate performance improvement on a well validated psychomotor vigilance task (PVT), and second, whether longer bouts of meditation may alter sleep need. Methods: The primary study assessed PVT reaction times before and after 40 minute periods of mediation, nap, or a control activity using a within subject cross-over design. This study utilized novice meditators who were current university students (n = 10). Novice meditators completed 40 minutes of meditation, nap, or control activities on six different days (two separate days for each condition), plus one night of total sleep deprivation on a different night, followed by 40 minutes of meditation. A second study examined sleep times in long term experienced meditators (n = 7) vs. non-meditators (n = 23). Experienced meditators and controls were age and sex matched and living in the Delhi region of India at the time of the study. Both groups continued their normal activities while monitoring their sleep and meditation times. Results: Novice meditators were tested on the PVT before each activity, 10 minutes after each activity and one hour later. All ten novice meditators improved their PVT reaction times immediately following periods of meditation, and all but one got worse immediately following naps. Sleep deprivation produced a slower baseline reaction time (RT) on the PVT that still improved significantly following a period of meditation. In experiments with long-term experienced meditators, sleep duration was measured using both sleep journals and actigraphy. Sleep duration in these subjects was lower than control non-meditators and general population norms, with no apparent decrements in PVT scores. Conclusions: These results suggest that meditation provides at least a short-term performance improvement even in novice meditators. In long term meditators, multiple hours spent in meditation are associated with a significant decrease in total sleep time when compared with age and sex matched controls who did not meditate. Whether meditation can actually replace a portion of sleep or pay-off sleep debt is under further investigation.

The basic functions of sleep are still unclear, however, recent advances in genomics and proteomics have begun to contribute to our understanding of both normal and pathological sleep. In this review, we focus primarily on normal sleep and wake that have been studied in model organisms such as mice. Mice have been especially valuable since many different inbred strains exist that differ in sleep-related traits, and genes can be altered by either mutagenesis or targeted approaches. Advances in QTL (Quantitative Trait Loci) analysis have also helped to identify important sleep related genes, and several other QTLs have been mapped as a first step toward finding the genes that underlie basic sleep traits. In addition to more traditional genetic approaches, the abundance of different mRNAs across sleep and wake can now be studied and compared in different brain regions much more thoroughly using microarray methods. Progress at the protein level has been more difficult, but a few studies have begun to investigate changes in proteins during sleep and wake, and we present some of our own preliminary data in this area. A knowledge of which genes and proteins control or respond to changes in sleep will not only help answer fundamental questions, but may also suggest novel drug targets for improving multiple aspects of sleep and wake.

Most published sleep studies use three species: human, house mouse, or Norway rat. The degree to which data from these species captures variability in mammalian sleep remains unclear. To gain insight into mammalian sleep diversity, we examined sleep architecture in the spiny basal murid rodentAcomys cahirinus. First, we used a piezoelectric system validated forMus musculusto monitor sleep in both species. We also included wildM. musculusto control for alterations generated by laboratory-reared conditions forM. musculus. Using this comparative framework, we found thatA. cahirinus, labM. musculus,and wildM. musculuswere primarily nocturnal, but exhibited distinct behavioral patterns. Although the activity ofA. cahirinusincreased sharply at dark onset, it decreased sharply just two hours later under group and individual housing conditions. To further characterize sleep patterns and sleep-related variables, we set up EEG/EMG and video recordings and found thatA. cahirinussleep significantly more thanM. musculus, exhibit nearly three times more REM, and sleep almost exclusively with their eyes open. The observed differences inA. cahirinussleep architecture raise questions about the evolutionary drivers of sleep behavior.

Dairy cows that are restricted from lying down have a reduced ability to sleep. In other species, sleep loss is a key risk factor for disease, mediated by changes in metabolic and inflammatory responses. The cumulative effect of lying and sleep deprivation on cow health is unknown. The objective was to determine the effects of lying and sleep deprivation on metabolic and inflammatory responses of dairy cows. Data were collected from 8 multiparous and 4 primiparous lactating cows (199 ± 44 d in milk, 77 ± 30 d pregnant; mean ± standard deviation) enrolled in a study using a crossover design. Each cow was exposed to 2 treatments meant to induce sleep loss: (1) human disturbance (imposed by researchers making noise or physical contact when the cow's posture suggested sleep) and (2) lying deprivation (imposed by a wooden grid placed on the pen floor). Cows experienced a 24-h baseline period (d -1) followed by a 24-h treatment period (d 0), with a 12-d washout period between treatments. Baseline and treatment periods were imposed from 2100 to 2059 h. Cows were housed in individual pens during the acclimation period (d -3 and -2), d -1, and d 0. Nonesterified fatty acid and glucose concentrations were measured at 0300, 0900, 1500, and 2059 h on d -1 and 0. Proinflammatory cytokine mRNA [tumor necrosis factor (TNF), interleukin-1B (IL1B), and interleukin-6 (IL6)] abundance in whole-blood leukocytes, both nonstimulated and stimulated with lipopolysaccharide, were assessed at 2059 h on d -1 (end of baseline) and d 0 (end of treatment). Nonesterified fatty acids and glucose varied by time of day but were not affected by treatment or day. The abundances of TNF and IL1B from both stimulated and nonstimulated cells were higher following 24 h of lying deprivation (d 0) compared with baseline (d -1). Abundance of IL6 was increased in nonstimulated cells after lying deprivation compared with baseline. In contrast, human disturbance for 24 h did not alter TNF, IL1B, or IL6 abundance relative to baseline levels. These results suggest that a short period of lying deprivation generally increases inflammatory responses but not metabolic responses.

Study Objective:. We have previously established that CAST/EiJ (CAST) mice differ from normal mice, such as C57BL/6J (B6), in the timing of wheel-runni