Sleep Cycle Regulation Research Articles

Recent advances in sleep cycle regulation and hormonal imbalance: a comprehensive review

A vital physiological function, sleep is necessary for general health and wellbeing. It is essential for several body processes, including as metabolism, immunological response, emotional control, and cognitive function. A complicated mechanism involving intricate connections between brain circuits, neurotransmitters, and hormone cues governs the sleep-wake cycle. Scientific research has recently made significant progress in understanding the mechanisms behind the control of the sleep cycle and how it relates to hormone imbalance. The goal of this thorough review is to examine the most recent research in this area, with a particular emphasis on the interaction between hormone variations and sleep regulation.

Exploring the aperiodic nature of parasympathetic activity during sleep in idiopathic gastroparesis.

The parasympathetic nervous system is necessary to regulate both sleep and digestion. Investigating abnormalities during the controlled setting of sleep can shed light on digestion, specifically for patients with idiopathic gastroparesis. In this study, we specifically investigate heartbeat-derived parasympathetic activity during sleep at very low frequencies, relevant to sleep cycle regulation. To do this, we adapt a method that extracts both periodic and aperiodic information from the power spectral density and recognize that the aperiodic activity may contain information relevant to very low frequencies. After testing on both synthetic noise data (pink and white) and overnight data from seven healthy controls and idiopathic gastroparetics, we find that the healthy controls' low-frequency aperiodic activity reflects pink noise structure, while the majority of the patients' aperiodic activity reflects white noise structure. At these low frequencies, these differences suggest differences in autonomic sleep cycle regulation.Clinical Relevance- This methodology can be optimized to track the health of the parasympathetic nervous system and suggest whether individual disease etiology is autonomic-related.

Fluoride exposure and sleep patterns among older adolescents in the United States: a cross-sectional study of NHANES 2015\u20132016

BackgroundFluoride from environmental sources accumulates preferentially in the pineal gland which produces melatonin, the hormone that regulates the sleep-wake cycle. However, the effects of fluoride on sleep regulation remain unknown. This population-based study examined whether chronic low-level fluoride exposure is associated with sleep patterns and daytime sleepiness among older adolescents in the United States (US).MethodThis cross-sectional study utilized data from the National Health and Nutrition Examination Survey (2015–2016). We analyzed data from adolescents who had plasma fluoride (n = 473) and water fluoride (n = 419) measures and were not prescribed medication for sleep disorders. Relationships between fluoride exposure and self-reported sleep patterns or daytime sleepiness were examined using survey-weighted linear, binomial logistic or multinomial logistic regression after covariate adjustment. A Holm-Bonferroni correction accounted for multiple comparisons.ResultsThe average age of adolescents was 17 years (range = 16–19). Median (IQR) water and plasma fluoride concentrations were 0.27 (0.52) mg/L and 0.29 (0.19) μmol/L respectively. An IQR increase in water fluoride was associated with 1.97 times higher odds of reporting symptoms suggestive of sleep apnea (95% CI: 1.27, 3.05; p = 0.02), a 24 min later bedtime (B = 0.40, 95% CI: 0.10, 0.70; p = 0.05), a 26 min later morning wake time (B = 0.43, 95% CI: 0.13, 0.73; p = 0.04), and among males, a 38% reduction in the odds of reporting snoring (95% CI: 0.45, 0.87, p = 0.03).ConclusionsFluoride exposure may contribute to changes in sleep cycle regulation and sleep behaviors among older adolescents in the US. Additional prospective studies are warranted to examine the effects of fluoride on sleep patterns and determine critical windows of vulnerability for potential effects.

Inadequate sleep and unhealthy food habits in portuguese adolescents

Adolescence is a unique stage of life time that often promotes changes in sleep habits, meals frequency and body composition, reflecting on the physical, mental and social well-being. The aim of this study was to analyze sleep quality and food habits in adolescents of both sexes. And to determine whether the food consumed favor the regulation of sleep cycle in accordance with its nutritional properties. 143 Portuguese adolescents (15.6 ± 2.71 years old): 73 girls (15.16 ± 1.02 years old) and 70 boys (15.20 ± 1.10 years old) were evaluated by a questionnaire, which collected: anthropometric data (weight, height and body mass index-BMI); food habits from a semi-quantitative questionnaire and; sleep assessed by the Epworth Sleepiness Scale and the Pittsburgh Sleep Quality Index. Descriptive linear regression analysis and Pearson correlation coefficients were used. The significance level was 5%. Data was analyzed using SPSS, version 18.0. Most adolescents presented poor sleep quality ( n = 72;50.3%) and severe somnolence ( n = 52;36.4%). Adolescents consumed more macronutrients than recommended. On the other hand, skipping meals was very frequent ( n = 89;62.4%), as well as the consumption of snacks rich in fat and soft drinks. Adolescents with higher levels of energy intake showed poorest sleep quality and more daytime somnolence ( p < 0.05). Snacks and soft drinks consumption were associated to a high BMI (>30 Kg/m 2 ). Poor sleep quality and quantity can influence energy intake in adolescents and BMI. Energy balance was altered, which can compromises adolescents health and daily behaviors.

Short sleep duration heralds essential tremor: A prospective, population‐based study

Lewy bodies have been described in the locus coeruleus of some patients with essential tremor (ET), and this brainstem nucleus plays an important role in sleep cycle regulation. Despite this, no studies have investigated the relationship between daily sleep duration and the risk of ET. We determined whether baseline daily sleep duration was associated with an increased risk of incident ET. In this prospective, population-based study of individuals > 65 years of age (the Neurological Disorders in Central Spain [NEDICES] cohort), participants were evaluated at baseline and 3 years later. At baseline, participants indicated their daily sleep duration as the sum of nighttime sleep and daytime napping. The average daily total sleep duration was grouped into four categories: ≤ 5 hours (short sleepers), 6 hours, 7 to 8 hours (reference), and ≥ 9 hours (long sleepers) hours. In total, 3,303 participants had a median duration of follow-up of 3.3 years. There were 76 incident ET cases at follow-up. The relative risks for short sleepers and for long sleepers were 2.25 (95% confidence interval [CI], 1.21-4.16; P = 0.01) and 0.74 (95% CI, 0.41-1.32; P = 0.31), respectively. After adjustment for potential confounders, including age, sex, educational level, current smoker, current drinker, and depressive symptoms or antidepressant use, the risk remained significantly increased for short sleepers (relative risk, 1.95; 95% CI, 1.03-3.70; P = 0.04]). The results indicated that short daily sleep duration may be a pre-motor marker for ET. Additional prospective studies are needed to confirm these results, and the biological basis for this association merits additional investigation.

The role of visual cortex acetylcholine in learning to discriminate temporally modulated visual stimuli

Cholinergic neurons in the basal forebrain innervate discrete regions of the cortical mantle, bestowing the cholinergic system with the potential to dynamically modulate sub-regions of the cortex according to behavioral demands. Cortical cholinergic activity has been shown to facilitate learning and modulate attention. Experiments addressing these issues have primarily focused on widespread cholinergic depletions, extending to areas involved in general cognitive processes and sleep cycle regulation, making a definitive interpretation of the behavioral role of cholinergic projections difficult. Furthermore, a review of the electrophysiological literature suggests that cholinergic modulation is particularly important in representing the fine temporal details of stimuli, an issue rarely addressed in behavioral experimentation. The goal of this work is to understand the role of cholinergic projections, specific to the sensory cortices, in learning to discriminate fine differences in the temporal structure of stimuli. A novel visual Go/No-Go task was developed to assess the ability of rats to learn to discriminate fine differences in the temporal structure of visual stimuli (lights flashing at various frequencies). The cholinergic contribution to this task was examined by selective reduction of acetylcholine projections to visual cortex (VCx) (using 192 IgG-saporin), either before or after discrimination training. We find that in the face of compromised cholinergic input to the VCx, the rats' ability to learn to perform fine discriminations is impaired, whereas their ability to perform previously learned discriminations remains unaffected. These results suggest that acetylcholine serves the role of facilitating plastic changes in the sensory cortices that are necessary for an animal to refine its sensitivity to the temporal characteristics of relevant stimuli.

P.1.c.028 Systemically and spinally administered etanercept, a TNF-alpha antagonist, blocks allodynia in diabetic mice

The original aims of our study have been to investigate in sleep-deprived mice, the effects of modafinil administration on spatial working memory, in parallel with the evaluation of neural activity level, as compared to non-sleep-deprived animals. For this purpose, an original sleep deprivation apparatus was developed and validated with continuous electroencephalography recording. Memory performance was evaluated using spontaneous alternation in a T-maze, whereas the neural activity level was estimated by the quantification of the c-Fos protein in various cerebral zones. This study allowed altogether:First, to evidence that a diurnal 10-h sleep deprivation period induced an impairment of spatial working memory.Second, to observe a decrease in c-Fos expression after sleep deprivation followed by a behavioural test, as compared to non-sleep-deprived mice. This impairment in neural activity was evidenced in areas involved in wake–sleep cycle regulation (anterior hypothalamus and supraoptic nucleus), but also in memory (frontal cortex and hippocampus) and emotions (amygdala).Finally, to demonstrate that modafinil 64 mg/kg is able to restore on the one hand memory performance after a 10-h sleep deprivation period, and on the other hand, the neural activity level in the very same brain areas where it was previously impaired by sleep deprivation and cognitive task.

Modafinil restores memory performance and neural activity impaired by sleep deprivation in mice

The original aims of our study have been to investigate in sleep-deprived mice, the effects of modafinil administration on spatial working memory, in parallel with the evaluation of neural activity level, as compared to non-sleep-deprived animals. For this purpose, an original sleep deprivation apparatus was developed and validated with continuous electroencephalography recording. Memory performance was evaluated using spontaneous alternation in a T-maze, whereas the neural activity level was estimated by the quantification of the c-Fos protein in various cerebral zones. This study allowed altogether: First, to evidence that a diurnal 10-h sleep deprivation period induced an impairment of spatial working memory. Second, to observe a decrease in c-Fos expression after sleep deprivation followed by a behavioural test, as compared to non-sleep-deprived mice. This impairment in neural activity was evidenced in areas involved in wake–sleep cycle regulation (anterior hypothalamus and supraoptic nucleus), but also in memory (frontal cortex and hippocampus) and emotions (amygdala). Finally, to demonstrate that modafinil 64 mg/kg is able to restore on the one hand memory performance after a 10-h sleep deprivation period, and on the other hand, the neural activity level in the very same brain areas where it was previously impaired by sleep deprivation and cognitive task.

Muscarinic and GABAA receptors modulate acetylcholine release in feline basal forebrain

Acetylcholine (ACh) release within the basal forebrain changes significantly as a function of sleep and wakefulness, hence identifying the neurochemical modulators of basal forebrain ACh release will contribute to a mechanistic understanding of sleep cycle regulation. This study tested the hypothesis that muscarinic and gamma aminobutyric acid(A) (GABAA) receptors modulate basal forebrain ACh release. Cats were anaesthetized with halothane to hold arousal state constant and a microdialysis probe was aimed stereotaxically for the substantia innominata region of the basal forebrain. Four concentrations of the muscarinic antagonist scopolamine (0.1, 0.3, 1.0, and 10 nm) and five concentrations of the GABAA antagonist bicuculline (3, 10, 30, 100, and 300 micro m) were delivered by reverse dialysis from the same probes used to collect ACh. These results are based on 27 experiments in nine animals. Scopolamine and bicuculline each caused a concentration dependent enhancement of ACh release. Scopolamine increased ACh by 118% above control levels whereas bicuculline was more effective, causing a 287% increase in ACh release. Scopolamine was more potent (EC50 = 0.16 nm) than bicuculline (EC50 > or = 90 micro m) for increasing ACh release. The results support the hypothesis that substantia innominata ACh release is modulated by muscarinic autoreceptors and inhibited by GABAA receptors. These findings are consistent with the interpretation that inhibition of basal forebrain cholinergic neurotransmission by GABA contributes to the generation of sleep.

Serotonin neurons and sleep. II. Time course of dorsal raphe discharge, PGO waves, and behavioral states.

This study documents the time course profiles for simultaneous measures of: the electrographic signs of sleep and wakefulness, ponto-geniculo-occipital (PGO) waves, and extracellular discharge potentials for single cells in the dorsal raphe nucleus (DRN). These measures were obtained from intact, undrugged cats across 177 sleep cycles. Ninety-one of these sleep cycles were recorded with no prior forced activity. Forced activity previously has been shown to powerfully alter the temporal organization of sleep by shortening the duration of both the sleep cycle and the ultradian rhythm of DRN discharge. The present paper evaluated the hypothesis that DRN discharge time course might regulate the sleep cycle. These experiments documented the phase relationship between the time course of DRN discharge and the electrographic signs of sleep. These phase relationship were examined by determining whether forced locomotor activity could dissociate the time course profile for behavioral states, PGO waves, and DRN discharge. The results revealed that the time course of DRN discharge and PGO waves were always phase-locked to the time course of the ultradian sleep cycle. Furthermore, the results show that changes in DRN discharge consistently precede changes in PGO waves, and behavioral state. Since a cause must precede an effect, these data are consistent with the hypothesis that the DRN may be causally involved in sleep cycle regulation. These temporal data also provide parameter values for the continued evaluation of cellularly based, mathematical models of sleep cycle control.

Serotonin neurons and sleep. I. Long term recordings of dorsal raphe discharge frequency and PGO waves.

Brain stem transection studies suggest that pontine neurons play a key role in regulating the mammalian sleep cycle. The serotonin (5-HT) hypothesis originally postulated that pontine 5-HT containing neurons directly initiated and maintained synchronized or NREM sleep and "primed" rapid eye movement (REM) sleep. Contrary to the predictions of this hypothesis, single unit recordings from the serotonergic dorsal raphe nucleus (DRN) have uniformly shown that DRN discharge rate is positively correlated with behavioral arousal but negatively correlated with both the NREM and REM phases of sleep. These findings required revision of the original 5-HT hypothesis and suggested instead that DRN discharge may influence the maintenance of behavioral arousal and, by ceasing to discharge, may contribute to the generation of NREM and REM sleep. The purpose of this paper was to quantitatively assess the strength of the correlation between DRN discharge, REM sleep, and PGO waves following the experimental perturbations of the sleep cycle. Since forced locomotor activity is known to powerfully alter the timing of sleep and wakefulness, the present experiments used forced activity in an attempt to dissociate DRN discharge from the sleep cycle. It was hypothesized that such dissociations would suggest DRN discharge is not involved in sleep cycle regulation. Contrastingly, preserved correlations would support the hypothesis of a possible causal relationship between DRN discharge, PGO waves activity, and the timing of sleep and wakefulness. Extracellular recordings were obtained from single cells in the DRN of intact, undrugged cats across greater than 300 sleep cycles with durations ranging from about 8 to 80 mins. Forced activity significantly reduced the amount of time spent in wakefulness and increased the number but not the duration of REM sleep epochs. The results revealed that DRN discharge rate was altered as a function of sleep cycle duration. In no case, however, was forced activity able to completely dissociate the characteristic DRN discharge rates from PGO waves or the ultradian sleep cycle. The inability of forced activity to disrupt the faithful relationships between DRN discharge, PGO waves, and sleep cycle phase thus provides a new form of correlative evidence consistent with the hypothesis that the DRN is involved in sleep cycle regulation.