Epidemiological investigations have indicated that insufficient sleep is prevalent among adolescents, posing a globally underestimated health risk. Sleep fragmentation and sleep loss during adolescence have been linked to concurrent emotional dysregulation and an increase in impulsive, risk-taking behaviors, including a higher likelihood of substance abuse. Among the most widely used substances, alcohol stands as the primary risk factor for deaths and disability among individuals aged 15-49 worldwide.
View Article and Find Full Text PDFChronic sleep restriction (CSR) is a prevalent issue in modern society that is associated with several pathological states, ranging from neuropsychiatric to metabolic diseases. Despite its known impact on metabolism, the specific effects of CSR on the molecular mechanisms involved in maintaining metabolic homeostasis at the level of white adipose tissue (WAT) remain poorly understood. Therefore, this study aimed to investigate the influence of CSR on sirtuin 1 (SIRT1) and the peroxisome proliferator-activated receptor γ (PPARγ) signaling pathway in the WAT of young male mice.
View Article and Find Full Text PDFREM sleep is critical for memory, emotion, and cognition. Manipulating brain activity during REM could improve our understanding of its function and benefits. Earlier studies have suggested that auditory stimulation in REM might modulate REM time and reduce rapid eye movement density.
View Article and Find Full Text PDFInsufficient sleep is a serious public health problem in modern society. It leads to increased risk of chronic diseases, and it has been frequently associated with cellular oxidative damage and widespread low-grade inflammation. Probiotics have been attracting increasing interest recently for their antioxidant and anti-inflammatory properties.
View Article and Find Full Text PDFBackground: Prolonged cellular activity may overload cell function, leading to high rates of protein synthesis and accumulation of misfolded or unassembled proteins, which cause endoplasmic reticulum (ER) stress and activate the unfolded protein response (UPR) to re-establish normal protein homeostasis. Previous molecular work has demonstrated that sleep deprivation (SD) leads to ER stress in neurons, with a number of ER-specific proteins being upregulated to maintain optimal cellular proteostasis. It is still not clear which cellular processes activated by sleep deprivation lead to ER- stress, but increased cellular metabolism, higher request for protein synthesis, and over production of oxygen radicals have been proposed as potential contributing factors.
View Article and Find Full Text PDFMultiple evidence in rodents shows that the strength of excitatory synapses in the cerebral cortex and hippocampus is greater after wake than after sleep. The widespread synaptic weakening afforded by sleep is believed to keep the cost of synaptic activity under control, promote memory consolidation, and prevent synaptic saturation, thus preserving the brain's ability to learn day after day. The cerebellum is highly plastic and the Purkinje cells, the sole output neurons of the cerebellar cortex, are endowed with a staggering number of excitatory parallel fiber synapses.
View Article and Find Full Text PDFModern life poses many threats to good-quality sleep, challenging brain health across the lifespan. Curtailed or fragmented sleep may be particularly damaging during adolescence, when sleep disruption by delayed chronotypes and societal pressures coincides with our brains preparing for adult life via intense refinement of neural connectivity. These vulnerabilities converge on the prefrontal cortex, one of the last brain regions to mature and a central hub of the limbic-cortical circuits underpinning decision-making, reward processing, social interactions and emotion.
View Article and Find Full Text PDFApelin (APLN) is an adipokine mainly produced by adipose tissue and related to an individual's nutritional status as well as digestive apparatus functions. In this work, APLN and its receptor (APLNR) were investigated, by immunohistochemistry, in the abomasum and duodenum of 15 Comisana × Appenninica adult sheep reared in a semi-natural pasture. Organ samples were collected after maximum pasture flowering (M × F group) and after maximum pasture dryness (M × D group); the experimental group (E × p group) received a feed supplementation of 600 grams/day/head of barley and corn in addition to M × D group feeding.
View Article and Find Full Text PDFSleep spindles of non-REM sleep are transient, waxing-and-waning 10-16 Hz EEG oscillations, whose cortical synchronization depends on the engagement of thalamo-cortical loops. However, previous studies in animal models lacking the corpus callosum due to agenesis or total callosotomy and in humans with agenesis of the corpus callosum suggested that cortico-cortical connections may also have a relevant role in cortical (inter-hemispheric) spindle synchronization. Yet, most of these works did not provide direct quantitative analyses to support their observations.
View Article and Find Full Text PDFPerisynaptic astrocytic processes (PAPs) carry out several different functions, from metabolite clearing to control of neuronal excitability and synaptic plasticity. All these functions are likely orchestrated by complex cellular machinery that resides within the PAPs and relies on a fine interplay between multiple subcellular components. However, traditional transmission electron microscopy (EM) studies have found that PAPs are remarkably poor of intracellular organelles, failing to explain how such a variety of PAP functions are achieved in the absence of a proportional complex network of intracellular structures.
View Article and Find Full Text PDFA good quality and amount of sleep are fundamental to preserve cognition and affect. New evidence also indicates that poor sleep is detrimental to brain myelination. In this study, we test the hypothesis that sleep quality and/or quantity relate to variability in cognitive and emotional function via the mediating effect of interindividual differences in proxy neuroimaging measures of white matter integrity and intracortical myelination.
View Article and Find Full Text PDFSleep-dependent synaptic plasticity is crucial for optimal cognition. However, establishing the direction of synaptic plasticity during sleep has been particularly challenging since data in support of both synaptic potentiation and depotentiation have been reported. This review focuses on structural synaptic plasticity across sleep and wake and summarizes recent developments in the use of 3-dimensional electron microscopy as applied to this field.
View Article and Find Full Text PDFThe slow waves of non-rapid eye movement (NREM) sleep reflect experience-dependent plasticity and play a direct role in the restorative functions of sleep. Importantly, slow waves behave as traveling waves, and their propagation is assumed to occur through cortico-cortical white matter connections. In this light, the corpus callosum (CC) may represent the main responsible for cross-hemispheric slow-wave propagation.
View Article and Find Full Text PDFIn adolescent and adult brains several molecular, electrophysiological, and ultrastructural measures of synaptic strength are higher after wake than after sleep [1, 2]. These results support the proposal that a core function of sleep is to renormalize the increase in synaptic strength associated with ongoing learning during wake, to reestablish cellular homeostasis and avoid runaway potentiation, synaptic saturation, and memory interference [2, 3]. Before adolescence however, when the brain is still growing and many new synapses are forming, sleep is widely believed to promote synapse formation and growth.
View Article and Find Full Text PDFSleep has been hypothesized to rebalance overall synaptic strength after ongoing learning during waking leads to net synaptic potentiation. If so, because synaptic strength and size are correlated, synapses on average should be larger after wake and smaller after sleep. This prediction was recently confirmed in mouse cerebral cortex using serial block-face electron microscopy (SBEM).
View Article and Find Full Text PDFMyelin plasticity is gaining increasing recognition as an essential partner to synaptic plasticity, which mediates experience-dependent brain structure and function. However, how neural activity induces adaptive myelination and which mechanisms are involved remain open questions. More than two decades of transcriptomic studies in rodents have revealed that hundreds of brain transcripts change their expression in relation to the sleep-wake cycle.
View Article and Find Full Text PDFSeveral neurodegenerative disorders, namely Parkinson's disease dementia, dementia with Lewy bodies, and Alzheimer's disease, share common pathophysiological features, such as (1) cognitive deficits, (2) glutamatergic hyperactivity-related excitotoxicity, and (3) deposition of α-synuclein (α-syn) and β-amyloid (Aβ). Ceftriaxone (CEF) is a well-tested and safe drug that has been used as an antibiotic for several decades. Recent studies have demonstrated the following effects of CEF: (1) increasing glutamate transporter-1 expression and glutamate reuptake and suppressing excitotoxicity, (2) binding well with α-syn and inhibition of α-syn polymerization, (3) modulating expression of genes related to Aβ metabolism, and (4) enhancing neurogenesis and recovery of neuronal density.
View Article and Find Full Text PDFFront Cell Neurosci
September 2018
Astrocytic glycogen represents the only form of glucose storage in the brain, and one of the outcomes of its breakdown is the production of lactate that can be used by neurons as an alternative energetic substrate. Since brain metabolism is higher in wake than in sleep, it was hypothesized that glycogen stores are depleted during wake and replenished during sleep. Furthermore, it was proposed that glycogen depletion leads to the progressive increase in adenosine levels during wake, providing a homeostatic signal that reflects the buildup of sleep pressure.
View Article and Find Full Text PDFBy identifying endogenous molecules in brain extracellular fluid metabolomics can provide insight into the regulatory mechanisms and functions of sleep. Here we studied how the cortical metabolome changes during sleep, sleep deprivation and spontaneous wakefulness. Mice were implanted with electrodes for chronic sleep/wake recording and with microdialysis probes targeting prefrontal and primary motor cortex.
View Article and Find Full Text PDFStudy Objectives: Previous studies found that sleep loss can suppress the expression of genes implicated in myelination and can have adverse effects on oligodendrocyte precursor cells. On the other hand, sleep may favor myelination by promoting the expression of genes involved in its formation and maintenance. Albeit limited, these results suggest that sleep loss can have detrimental effects on the formation and maintenance of myelin.
View Article and Find Full Text PDFDuring non-rapid eye-movement (NREM) sleep, cortical and thalamic neurons oscillate every second or so between ON periods, characterized by membrane depolarization and wake-like tonic firing, and OFF periods, characterized by membrane hyperpolarization and neuronal silence. Cortical slow waves, the hallmark of NREM sleep, reflect near-synchronous OFF periods in cortical neurons. However, the mechanisms triggering such OFF periods are unclear, as there is little evidence for somatic inhibition.
View Article and Find Full Text PDFWe previously found that and its ligand , astrocytic genes involved in phagocytosis, are upregulated after acute sleep deprivation. These results suggested that astrocytes may engage in phagocytic activity during extended wake, but direct evidence was lacking. Studies in humans and rodents also found that sleep loss increases peripheral markers of inflammation, but whether these changes are associated with neuroinflammation and/or activation of microglia, the brain's resident innate immune cells, was unknown.
View Article and Find Full Text PDFIntroduction: Sleep-dependent consolidation of motor learning has been extensively studied in humans, but it remains unclear why some, but not all, learned skills benefit from sleep.
Aims And Methods: Here, we compared 2 different motor tasks, both requiring the mice to run on an accelerating device. In the rotarod task, mice learn to maintain balance while running on a small rod, while in the complex wheel task, mice run on an accelerating wheel with an irregular rung pattern.
Annu Int Conf IEEE Eng Med Biol Soc
August 2016
The quantification of sleep architecture has high clinical value for diagnostic purposes. While the clinical standard to assess sleep architecture is in-lab based polysomnography, higher ecological validity can be obtained with multiple sleep recordings at home. In this paper, we use a dataset composed of fifty sleep EEG recordings at home (10 per study participant for five participants) to analyze the sleep stage transition dynamics using Markov chain based modeling.
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