A global transcriptional atlas of the effect of acute sleep deprivation in the mouse frontal cortex.

Sleep deprivation (SD) has negative effects on brain and body function. Sleep problems are prevalent in a variety of disorders, including neurodevelopmental and psychiatric conditions. Thus, understanding the molecular consequences of SD is of fundamental importance in biology.

A Global Transcriptional Atlas of the Effect of Sleep Deprivation in the Mouse Frontal Cortex.

Sleep deprivation (SD) has negative effects on brain function. Sleep problems are prevalent in neurodevelopmental, neurodegenerative and psychiatric disorders. Thus, understanding the molecular consequences of SD is of fundamental importance in neuroscience.

Activation of Basal Forebrain Astrocytes Induces Wakefulness without Compensatory Changes in Sleep Drive.

Mammalian sleep is regulated by a homeostatic process that increases sleep drive and intensity as a function of prior wake time. Sleep homeostasis has traditionally been thought to be a product of neurons, but recent findings demonstrate that this process is also modulated by glial astrocytes. The precise role of astrocytes in the accumulation and discharge of sleep drive is unknown.

Ontogenesis of the molecular response to sleep loss.

Sleep deprivation (SD) results in profound cellular and molecular changes in the adult mammalian brain. Some of these changes may result in, or aggravate, brain disease. However, little is known about how SD impacts gene expression in developing animals.

Ontogenesis of the molecular response to sleep loss.

Sleep deprivation (SD) results in profound cellular and molecular changes in the adult mammalian brain. Some of these changes may result in, or aggravate, brain disease. However, little is known about how SD impacts gene expression in developing animals.

Noradrenergic Signaling in Astrocytes Influences Mammalian Sleep Homeostasis.

Astrocytes influence sleep expression and regulation, but the cellular signaling pathways involved in these processes are poorly defined. We proposed that astrocytes detect and integrate a neuronal signal that accumulates during wakefulness, thereby leading to increased sleep drive. Noradrenaline (NA) satisfies several criteria for a waking signal integrated by astrocytes.

REM sleep promotes bidirectional plasticity in developing visual cortex .

Sleep is required for the full expression of plasticity during the visual critical period (CP). However, the precise role of rapid-eye-movement (REM) sleep in this process is undetermined. Previous studies in rodents indicate that REM sleep weakens cortical circuits following MD, but this has been explored in only one class of cortical neuron (layer 5 apical dendrites).

Goodnight, astrocyte: waking up to astroglial mechanisms in sleep.

Astrocytes mediate many important aspects of neural homeostasis, but until recently, their role in sleep was largely unknown. The situation has dramatically changed in the last decade. The use of transgenic animals, optogenetics, chemogenetics, brain imaging and sophisticated molecular assays has led to exciting discoveries.

A chemical-genetic investigation of BDNF-NtrkB signaling in mammalian sleep.

Study Objectives: The neurotrophin brain-derived neurotrophic factor (BDNF) is hypothesized to be a molecular mediator of mammalian sleep homeostasis. This hypothesis is supported by correlational findings and results obtained from pharmacology. BDNF binds with high affinity to the membrane-bound receptor Neurotrophin Tyrosine Kinase Receptor B (NtrkB), which triggers several intracellular signaling cascades.

The Ontogenesis of Mammalian Sleep: Form and Function.

Purpose Of Review: To present an up-to-date review and synthesis of findings about perinatal sleep development and function. I discuss landmark events in sleep ontogenesis, evidence that sleep promotes brain development and plasticity, and experimental considerations in this topic.

Recent Findings: Mammalian sleep undergoes dramatic changes in expression and regulation during perinatal development.

Renormalizing synapses in sleep: The clock is ticking.

Sleep has been hypothesized to renormalize synapses potentiated in wakefulness. This is proposed to lead to a net reduction in synaptic strength after sleep in brain areas like the cortex and hippocampus. Biological clocks, however, exert independent effects on these synapses that may explain some of the reported differences after wake and sleep.

Challenging sleep homeostasis.

In this commentary, I play the Devil's advocate and assume the title of High Contrarian. I intend to be provocative to challenge long-standing ideas about sleep. I blame all on Professor Craig Heller, who taught me to think this way as a graduate student in his laboratory.

A Role for Astroglial Calcium in Mammalian Sleep and Sleep Regulation.

Mammalian sleep expression and regulation have historically been thought to reflect the activity of neurons. Changes in other brain cells (glia) across the sleep-wake cycle and their role in sleep regulation are comparatively unexplored. We show that sleep and wakefulness are accompanied by state-dependent changes in astroglial activity.

REM sleep promotes experience-dependent dendritic spine elimination in the mouse cortex.

In many parts of the nervous system, experience-dependent refinement of neuronal circuits predominantly involves synapse elimination. The role of sleep in this process remains unknown. We investigated the role of sleep in experience-dependent dendritic spine elimination of layer 5 pyramidal neurons in the visual (V1) and frontal association cortex (FrA) of 1-month-old mice.

Sleep, brain development, and autism spectrum disorders: Insights from animal models.

Sleep is an evolutionarily conserved and powerful drive, although its complete functions are still unknown. One possible function of sleep is that it promotes brain development. The amount of sleep is greatest during ages when the brain is rapidly developing, and sleep has been shown to influence critical period plasticity.

Sleep pressure regulates mushroom body neural-glial interactions in Drosophila.

Sleep is a behavior that exists broadly across animal phyla, from flies to humans, and is necessary for normal brain function. Recent studies in both vertebrates and invertebrates have suggested a role for glial cells in sleep regulatory processes. Changes in neural-glial interactions have been shown to be critical for synaptic plasticity and circuit function.

The Function(s) of Sleep.

Sleep is a highly conserved phenomenon in endotherms, and therefore it must serve at least one basic function across this wide range of species. What that function is remains one of the biggest mysteries in neurobiology. By using the word neurobiology, we do not mean to exclude possible non-neural functions of sleep, but it is difficult to imagine why the brain must be taken offline if the basic function of sleep did not involve the nervous system.

Shank3 modulates sleep and expression of circadian transcription factors.

Autism Spectrum Disorder (ASD) is the most prevalent neurodevelopmental disorder in the United States and often co-presents with sleep problems. Sleep problems in ASD predict the severity of ASD core diagnostic symptoms and have a considerable impact on the quality of life of caregivers. Little is known, however, about the underlying molecular mechanisms of sleep problems in ASD.

Primed to Sleep: The Dynamics of Synaptic Plasticity Across Brain States.

It is commonly accepted that brain plasticity occurs in wakefulness sleep. However, how these different brain states work in concert to create long-lasting changes in brain circuitry is unclear. Considering that wakefulness and sleep are profoundly different brain states on multiple levels (e.

Cyclic nature of the REM sleep-like state in the cuttlefish .

Sleep is a state of immobility characterized by three key criteria: an increased threshold of arousal, rapid reversal to an alert state and evidence of homeostatic 'rebound sleep' in which there is an increase in the time spent in this quiescent state following sleep deprivation. Common European cuttlefish, , show states of quiescence during which they meet the last two of these three criteria, yet also show spontaneous bursts of arm and eye movements that accompany rapid changes in chromatophore patterns in the skin. Here, we report that this rapid eye movement sleep-like (REMS-like) state is cyclic in nature.

Astrocyte expression of the Drosophila TNF-alpha homologue, Eiger, regulates sleep in flies.

Sleep contributes to cognitive functioning and is sufficient to alter brain morphology and function. However, mechanisms underlying sleep regulation remain poorly understood. In mammals, tumor necrosis factor-alpha (TNFα) is known to regulate sleep, and cytokine expression may represent an evolutionarily ancient mechanism in sleep regulation.

Anatomical correlates of rapid eye movement sleep-dependent plasticity in the developing cortex.

Rapid eye movement (REM) sleep is expressed at its highest levels during early life when the brain is rapidly developing. This suggests that REM sleep may play important roles in brain maturation and developmental plasticity. We investigated this possibility by examining the role of REM sleep in the regulation of plasticity-related proteins known to govern synaptic plasticity in vitro and in vivo.