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Sleep Regulation (sleep + regulation)
Selected AbstractsPuberty-Dependent Sleep Regulation and Alcohol Use in Early AdolescentsALCOHOLISM, Issue 9 2010Sara Pieters Background:, Research has shown a bi-directional relation between alcohol use and sleep regulation in adults. Much less is known about this association in early adolescents, while profound puberty-dependent transitions regarding sleep patterns take place in early adolescence. Moreover, puberty has been associated with an increase in alcohol use of adolescents. Methods:, In this study, we investigated the associations between pubertal development, sleep preference, sleep problems, and alcohol use in 431 early adolescents (mean age: 13.66). Second, it was studied whether the associations changed when controlling for adolescent internalizing and externalizing problems. Furthermore, we included gender as a moderator on all the associations. Results:, Results showed that pubertal development was positively associated with sleep problems and more evening-type tendencies (e.g., favoring later bedtimes), which in turn were positively related to alcohol use. Underlying psychopathology, gender and educational level did not change these relationships. Conclusions:, From this study, it can be concluded that both puberty and sleep regulation are important factors in explaining alcohol use in early adolescence. [source] Homeostatic sleep regulation is preserved in mPer1 and mPer2 mutant miceEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2002Caroline Kopp Abstract A limited set of genes, Clock, Bmal1, mPer1, mPer2, mCry1 and mCry2, has been shown to be essential for the generation of circadian rhythms in mammals. It has been recently suggested that circadian genes might be involved in sleep regulation. We investigated the role of mPer1 and mPer2 genes in the homeostatic regulation of sleep by comparing sleep of mice lacking mPER1 (mPer1 mutants) or a functional mPER2 (mPer2 mutants), and wild-type controls (WT) after 6 h of sleep deprivation (SD). Our main result showed that after SD, all mice displayed the typical increase of slow-wave activity (SWA; EEG power density between 0.75 and 4 Hz) in nonREM sleep, reflecting the homeostatic response to SD. This increase was more prominent over the frontal cortex as compared to the occipital cortex. The genotypes did not differ in the effect of SD on the occipital EEG, while the effect on the frontal EEG was initially diminished in both mPer mutants. Differences between the genotypes were seen in the 24-h distribution of sleep, reflecting especially the phase advance of motor activity onset observed in mPer2 mutants. While the daily distribution of sleep was modulated by mPer1 and mPer2 genes, sleep homeostasis reflected by the SWA increase after 6-h SD was preserved in the mPer mutants. The results provide further evidence for the independence of the circadian and the homeostatic components underlying sleep regulation. [source] Cytokines and Cognition,The Case for A Head-to-Toe Inflammatory ParadigmJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 12 2002Craig J. Wilson MBBS The brain is not only immunologically active of its own accord, but also has complex peripheral immune interactions. Given the central role of cytokines in neuroimmmunoendocrine processes, it is hypothesized that these molecules influence cognition via diverse mechanisms. Peripheral cytokines penetrate the blood-brain barrier directly via active transport mechanisms or indirectly via vagal nerve stimulation. Peripheral administration of certain cytokines as biological response modifiers produces adverse cognitive effects in animals and humans. There is abundant evidence that inflammatory mechanisms within the central nervous system (CNS) contribute to cognitive impairment via cytokine-mediated interactions between neurons and glial cells. Cytokines mediate cellular mechanisms subserving cognition (e.g., cholinergic and dopaminergic pathways) and can modulate neuronal and glial cell function to facilitate neuronal regeneration or neurodegeneration. As such, there is a growing appreciation of the role of cytokine-mediated inflammatory processes in neurodegenerative diseases such as Alzheimer's disease and vascular dementia. Consistent with their involvement as mediators of bidirectional communication between the CNS and the peripheral immune system, cytokines play a key role in the hypothalamic-pituitary-adrenal axis activation seen in stress and depression. In addition, complex cognitive systems such as those that underlie religious beliefs, can modulate the effects of stress on the immune system. Indirect means by which peripheral or central cytokine dysregulation could affect cognition include impaired sleep regulation, micronutrient deficiency induced by appetite suppression, and an array of endocrine interactions. Given the multiple levels at which cytokines are capable of influencing cognition it is plausible that peripheral cytokine dysregulation with advancing age interacts with cognitive aging. [source] Delta sleep-inducing peptide (DSIP): a still unresolved riddleJOURNAL OF NEUROCHEMISTRY, Issue 2 2006Vladimir M. Kovalzon Abstract Delta sleep-inducing peptide (DSIP) was isolated from rabbit cerebral venous blood by Schoenenberger-Monnier group from Basel in 1977 and initially regarded as a candidate sleep-promoting factor. However, the link between DSIP and sleep has never been further characterized, in part because of the lack of isolation of the DSIP gene, protein and possible related receptor. Thus the hypothesis regarding DSIP as a sleep factor is extremely poorly documented and still weak. Although DSIP itself presented a focus of study for a number of researchers, its natural occurrence and biological activity still remains obscure. DSIP structure is different from any other known representative of the various peptide families. In this mini-review we hypothesize the existence of a DSIP-like peptide(s) that is responsible (at least partly) for DSIP-like immunoreactivity and DSIP biological activity. This assumption is based on: (i) a highly specific distribution of DSIP-like immunoreactivity in the neurosecretory hypothalamic nuclei of various vertebrate species that are not particularly relevant for sleep regulation, as revealed by the histochemical studies of the Geneva group (Charnay et al.); (ii) a large spectrum of DSIP biological activity revealed by biochemical and physiological studies in vitro; (iii) significant slow-wave sleep (SWS) promoting activity of certain artificial DSIP structural analogues (but not DSIP itself!) in rabbits and rats revealed by our early studies; and (iv) significant SWS-promoting activity of a naturally occurring dermorphin-decapeptide that is structurally similar to DSIP (in five of the nine positions) and the sleep-suppressing effect of its optical isomer, as revealed in rabbits. Potential future studies are outlined, including natural synthesis and release of this DSIP-like peptide and its role in neuroendocrine regulation. [source] Sleep and Rest Regulation in Young and Old Oestrogen-Deficient Female MiceJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2006V. V. Vyazovskiy The effect of circulating oestrogen deficiency on sleep regulation and locomotor activity was investigated in aromatase cytochrome P450 deficient mice (ArKO) and wild-type (WT) controls. Sleep was recorded in 3-month old mice during a 24-h baseline day, 6-h sleep deprivation (SD) and 18-h recovery, and activity was recorded at the age of 3, 9 and 12 months. In mice deficient of oestrogen, the total amount of sleep per 24 h was the same as in WT controls. However, in ArKO mice, sleep was enhanced in the dark period at the expense of sleep in the light phase, and was more fragmented than sleep in WT mice. This redistribution of sleep resulted in a damped amplitude of slow-wave activity (SWA; power between 0.75,4.0 Hz) in non-rapid eye movement sleep across 24 h. After SD, the rebound of sleep and SWA was similar between the genotypes, suggesting that oestrogen deficiency does not affect the mechanisms maintaining the homeostatic balance between the amount of sleep and its intensity. Motor activity decreased with age in both genotypes and was lower in ArKO mice compared to WT at all three ages. After SD, the amount of rest in 3-month old WT mice increased above baseline and was more consolidated. Both effects were less pronounced in ArKO mice, reflecting the baseline differences between the genotypes. The results indicate that despite the pronounced redistribution of sleep and motor activity in oestrogen deficient mice, the basic homeostatic mechanisms of sleep regulation in ArKO mice remain intact. [source] Puberty-Dependent Sleep Regulation and Alcohol Use in Early AdolescentsALCOHOLISM, Issue 9 2010Sara Pieters Background:, Research has shown a bi-directional relation between alcohol use and sleep regulation in adults. Much less is known about this association in early adolescents, while profound puberty-dependent transitions regarding sleep patterns take place in early adolescence. Moreover, puberty has been associated with an increase in alcohol use of adolescents. Methods:, In this study, we investigated the associations between pubertal development, sleep preference, sleep problems, and alcohol use in 431 early adolescents (mean age: 13.66). Second, it was studied whether the associations changed when controlling for adolescent internalizing and externalizing problems. Furthermore, we included gender as a moderator on all the associations. Results:, Results showed that pubertal development was positively associated with sleep problems and more evening-type tendencies (e.g., favoring later bedtimes), which in turn were positively related to alcohol use. Underlying psychopathology, gender and educational level did not change these relationships. Conclusions:, From this study, it can be concluded that both puberty and sleep regulation are important factors in explaining alcohol use in early adolescence. [source] Role of Wake-Promoting Basal Forebrain and Adenosinergic Mechanisms in Sleep-Promoting Effects of EthanolALCOHOLISM, Issue 6 2010Mahesh M. Thakkar Background:, Ethanol intake has significant impact on sleep. However, the cellular substrates responsible for sleep promotion following ethanol intake are unknown. The purine nucleoside, adenosine, is responsible for mediating many neuronal and behavioral responses to ethanol. Studies performed in cell cultures suggest that ethanol inhibits equilibrative nucleoside transporter 1 to block the reuptake of adenosine resulting in increased extracellular adenosine. Adenosine also has a pivotal role in sleep regulation. Adenosine acts via A1 receptor to inhibit the wake-promoting neurons of the basal forebrain (BF) resulting in the promotion of sleep. Is ethanol-induced sleep associated with the inhibition of the BF wake-promoting neurons? Do adenosinergic mechanisms in the BF have a role in sleep-promoting effects of ethanol? Methods:, To address these questions, we performed 3 experiments in Sprague,Dawley rats. First, we verified the effect of ethanol on sleep promotion. Second, we evaluated the effect of ethanol on c-Fos expression (a marker of neuronal activation) in the BF wake-promoting neurons and third we monitored the effects of A1 receptor blockade in the BF on ethanol-induced sleep. Results:, Significant increase in non-rapid eye movement (NREM) sleep with a concomitant decrease in wakefulness was observed during the first 12 hours postethanol. REM sleep remained unaffected. Ethanol administration caused a significant decrease in the number of BF wake-promoting neurons with c-Fos immunoreactivity. Bilateral microinjections of a selective A1R receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine into the BF significantly attenuated sleep-promoting effects of ethanol. Conclusion:, These results suggest that the inhibition of BF wake-promoting neurons by adenosinergic mechanism may be responsible for the sleep promoting effects of ethanol. We believe our study is the first to investigate the cellular mechanisms responsible for the somnogenic effects of ethanol. [source] Individualized and time-variant model for the functional link between thermoregulation and sleep onsetJOURNAL OF SLEEP RESEARCH, Issue 2 2006STIJN QUANTEN Summary This study makes use of control system model identification techniques to examine the relationship between thermoregulation and sleep regulation. Specifically, data-based mechanistic (DBM) modelling is used to formulate and experimentally test the hypothesis, put forth by Gilbert et al. [Sleep Med. Rev.8 (2004) 81], that there exists a connection between distal heat loss and sleepiness. Six healthy sleepers each spent three nights and the following day in the sleep laboratory: an adaptation, a cognitive arousal and a neutral testing day. In the cognitive arousal condition, a visit of a television camera crew took place and subjects were asked to be interviewed. During each of the three 25-min driving simulator tasks per day, the distal-to-proximal gradient and the electroencephalogram are recorded. It is observed from these experimental data that there exists a feedback connection between thermoregulation and sleep. In addition to providing experimental evidence in support of the Gilbert et al. (2004) hypothesis, the authors propose that the nature of the feedback connection is determined by the nature of sleep/wake state (i.e. NREM sleep versus unwanted sleepiness in active subjects). Besides this, an individualized and time-variant model for the linkage between thermoregulation and sleep onset is presented. This compact model feeds on real-time data regarding distal heat loss and sleepiness and contains a physically meaningful parameter that delivers an individual- and time-depending quantification of a well known biological features in the field of thermoregulation: the thermoregulatory error signal Thypo(t),Tset(t). A validation of these physical/biological features emphasizes the reliability and power of DBM in describing individual differences related to the sleep process. [source] Investigating the interaction between the homeostatic and circadian processes of sleep,wake regulation for the prediction of waking neurobehavioural performanceJOURNAL OF SLEEP RESEARCH, Issue 3 2003Hans P. A. Van Dongen Summary The two-process model of sleep regulation has been applied successfully to describe, predict, and understand sleep,wake regulation in a variety of experimental protocols such as sleep deprivation and forced desynchrony. A non-linear interaction between the homeostatic and circadian processes was reported when the model was applied to describe alertness and performance data obtained during forced desynchrony. This non-linear interaction could also be due to intrinsic non-linearity in the metrics used to measure alertness and performance, however. Distinguishing these possibilities would be of theoretical interest, but could also have important implications for the design and interpretation of experiments placing sleep at different circadian phases or varying the duration of sleep and/or wakefulness. Although to date no resolution to this controversy has been found, here we show that the issue can be addressed with existing data sets. The interaction between the homeostatic and circadian processes of sleep,wake regulation was investigated using neurobehavioural performance data from a laboratory experiment involving total sleep deprivation. The results provided evidence of an actual non-linear interaction between the homeostatic and circadian processes of sleep,wake regulation for the prediction of waking neurobehavioural performance. [source] The association between pubertal status and sleep duration and quality among a nationally representative sample of U. S. AdolescentsAMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 4 2005Kristen L. Knutson Many hormones play important roles in both pubertal development and sleep regulation. Because of the possible consequences of impaired sleep, including impaired health and cognition, it is important to examine whether an association between pubertal stage and sleep exists. The aim of this analysis is to examine the association between sleep and adolescent growth and developmental stage in a large sample of adolescents ages 12,16 years from a nationally representative longitudinal study. This analysis used the public-use data set of the National Longitudinal Study of Adolescent Health, an extensive survey of health and behavior among adolescents in the United States. The study included two interviews approximately 1 year apart. Pubertal development, sleep variables, and height are self-reported. Pubertal development scores were calculated by summing responses to three questions for each sex. The sleep variables include sleep duration, frequent insomnia (once/week or more), frequently waking tired (once/week or more), and insufficient sleep. The results indicate a sex difference in the association between sleep problems and pubertal development. Among females, there was a significant increase in sleep problems with increasing pubertal development score, but not among males. The negative association between sleep duration and pubertal development score, however, was significant in both males and females. There is no association between sleep duration and height velocity (inches/year) in this sample. The results, which are based on a large sample size, warrant further examination with more objective measures into the association between sleep and growth and development among adolescents. Am. J. Hum. Biol. 17:418,424, 2005.© 2005 Wiley-Liss, Inc. [source] | |||||||||||||