-
Journal of Pediatric Neurosciences 2021Electrical status epilepticus during slow-wave sleep (ESES) is an epilepsy syndrome with sleep-induced epileptic discharges and acquired impairment of cognition or... (Review)
Review
Electrical status epilepticus during slow-wave sleep (ESES) is an epilepsy syndrome with sleep-induced epileptic discharges and acquired impairment of cognition or behavior. Since the disease's original description in 1971, no clear consensus has emerged on diagnostic criteria or optimal treatment. The treatment of ESES can be challenging, often including numerous antiepileptic drugs, immunomodulatory agents, and even surgical interventions. There is little evidence to guide treatment because only retrospective studies and case reports on the efficacy of treatment of ESES are present in literature. In this paper, we aim to analyze the etiopathogenesis of ESES in the new genetic era and to evaluate the treatment modalities in accordance with the genetic data and electroclinic spectrum of ESES.
PubMed: 35018175
DOI: 10.4103/jpn.JPN_137_20 -
Neuron Apr 2023Although long-term memory consolidation is supported by sleep, it is unclear how it differs from that during wakefulness. Our review, focusing on recent advances in the... (Review)
Review
Although long-term memory consolidation is supported by sleep, it is unclear how it differs from that during wakefulness. Our review, focusing on recent advances in the field, identifies the repeated replay of neuronal firing patterns as a basic mechanism triggering consolidation during sleep and wakefulness. During sleep, memory replay occurs during slow-wave sleep (SWS) in hippocampal assemblies together with ripples, thalamic spindles, neocortical slow oscillations, and noradrenergic activity. Here, hippocampal replay likely favors the transformation of hippocampus-dependent episodic memory into schema-like neocortical memory. REM sleep following SWS might balance local synaptic rescaling accompanying memory transformation with a sleep-dependent homeostatic process of global synaptic renormalization. Sleep-dependent memory transformation is intensified during early development despite the immaturity of the hippocampus. Overall, beyond its greater efficacy, sleep consolidation differs from wake consolidation mainly in that it is supported, rather than impaired, by spontaneous hippocampal replay activity possibly gating memory formation in neocortex.
Topics: Memory Consolidation; Sleep; Memory, Long-Term; Sleep, Slow-Wave; Hippocampus
PubMed: 37023710
DOI: 10.1016/j.neuron.2023.03.005 -
Pharmaceutical Biology Dec 2019γ-Aminobutyric acid (GABA) is the main inhibitory neurotransmitter and it is well established that activation of GABA receptors favours sleep. l-Theanine, a naturally...
CONTEXT
γ-Aminobutyric acid (GABA) is the main inhibitory neurotransmitter and it is well established that activation of GABA receptors favours sleep. l-Theanine, a naturally occurring amino acid first discovered in green tea, is a well-known anti-anxiety supplement with proven relaxation benefits.
OBJECTIVE
This study investigated the potential synergistic sleep enhancement effect of GABA/l-theanine mixture.
MATERIALS AND METHODS
Pentobarbital-induced sleep test was applied to find proper concentration for sleep-promoting effect in ICR mice. Electroencephalogram (EEG) analysis was performed to investigate total sleeping time and sleep quality in normal SD rats and caffeine-induced awareness model. Real-time polymerase chain reaction (RT-PCR) was applied to investigate whether the sleep-promoting mechanism of GABA/l-theanine mixture involved transcriptional processes.
RESULTS
GABA/l-theanine mixture (100/20 mg/kg) showed a decrease in sleep latency (20.7 and 14.9%) and an increase in sleep duration (87.3 and 26.8%) compared to GABA or theanine alone. GABA/l-theanine mixture led to a significant increase in rapid eye movement (REM) (99.6%) and non-REM (NREM) (20.6%) compared to controls. The use of GABA/l-theanine mixture rather than GABA or l-theanine alone restored to normal levels sleep time and quality in the arousal animal model. The administration of GABA/l-theanine led to increased expression of GABA and the glutamate GluN1 receptor subunit.
CONCLUSIONS
GABA/l-theanine mixture has a positive synergistic effect on sleep quality and duration as compared to the GABA or l-theanine alone. The increase in GABA receptor and GluN1 expression is attributed to the potential neuromodulatory properties of GABA/l-theanine combination, which seems to affect sleep behaviour.
Topics: Animals; Drug Synergism; Drug Therapy, Combination; Glutamates; Mice; Mice, Inbred ICR; Random Allocation; Rats; Rats, Sprague-Dawley; Receptors, Glutamate; Sleep Latency; Sleep, Slow-Wave; gamma-Aminobutyric Acid
PubMed: 30707852
DOI: 10.1080/13880209.2018.1557698 -
Scientific Reports May 2022Spontaneous synchronization over large networks is ubiquitous in nature, ranging from inanimate to biological systems. In the human brain, neuronal synchronization and...
Spontaneous synchronization over large networks is ubiquitous in nature, ranging from inanimate to biological systems. In the human brain, neuronal synchronization and de-synchronization occur during sleep, with the greatest degree of neuronal synchronization during slow wave sleep (SWS). The current sleep classification schema is based on electroencephalography and provides common criteria for clinicians and researchers to describe stages of non-rapid eye movement (NREM) sleep as well as rapid eye movement (REM) sleep. These sleep stage classifications have been based on convenient heuristic criteria, with little consideration of the accompanying normal physiological changes across those same sleep stages. To begin to resolve those inconsistencies, first focusing only on NREM sleep, we propose a simple cluster synchronization model to explain the emergence of SWS in healthy people without sleep disorders. We apply the empirical mode decomposition (EMD) analysis to quantify slow wave activity in electroencephalograms, and provide quantitative evidence to support our model. Based on this synchronization model, NREM sleep can be classified as SWS and non-SWS, such that NREM sleep can be considered as an intrinsically bistable process. Finally, we develop an automated algorithm for SWS classification. We show that this new approach can unify brain wave dynamics and their corresponding physiologic changes.
Topics: Electroencephalography; Humans; Sleep; Sleep Stages; Sleep, REM; Sleep, Slow-Wave
PubMed: 35523989
DOI: 10.1038/s41598-022-11513-0 -
Neuron Mar 2018Rapid eye movement (REM) and non-REM (NREM) sleep are controlled by specific neuronal circuits. Here we show that galanin-expressing GABAergic neurons in the dorsomedial...
Rapid eye movement (REM) and non-REM (NREM) sleep are controlled by specific neuronal circuits. Here we show that galanin-expressing GABAergic neurons in the dorsomedial hypothalamus (DMH) comprise separate subpopulations with opposing effects on REM versus NREM sleep. Microendoscopic calcium imaging revealed diverse sleep-wake activity of DMH GABAergic neurons, but the galanin-expressing subset falls into two distinct groups, either selectively activated (REM-on) or suppressed (REM-off) during REM sleep. Retrogradely labeled, preoptic area (POA)-projecting galaninergic neurons are REM-off, whereas the raphe pallidus (RPA)-projecting neurons are primarily REM-on. Bidirectional optogenetic manipulations showed that the POA-projecting neurons promote NREM sleep and suppress REM sleep, while the RPA-projecting neurons have the opposite effects. Thus, REM/NREM switch is regulated antagonistically by DMH galaninergic neurons with intermingled cell bodies but distinct axon projections.
Topics: Animals; Female; Hypothalamus; Male; Mice; Mice, Transgenic; Optogenetics; Random Allocation; Sleep, REM; Sleep, Slow-Wave
PubMed: 29478915
DOI: 10.1016/j.neuron.2018.02.005 -
Nature Neuroscience Mar 2023Poor sleep is associated with the risk of developing chronic pain, but how sleep contributes to pain chronicity remains unclear. Here we show that following peripheral...
Poor sleep is associated with the risk of developing chronic pain, but how sleep contributes to pain chronicity remains unclear. Here we show that following peripheral nerve injury, cholinergic neurons in the anterior nucleus basalis (aNB) of the basal forebrain are increasingly active during nonrapid eye movement (NREM) sleep in a mouse model of neuropathic pain. These neurons directly activate vasoactive intestinal polypeptide-expressing interneurons in the primary somatosensory cortex (S1), causing disinhibition of pyramidal neurons and allodynia. The hyperactivity of aNB neurons is caused by the increased inputs from the parabrachial nucleus (PB) driven by the injured peripheral afferents. Inhibition of this pathway during NREM sleep, but not wakefulness, corrects neuronal hyperactivation and alleviates pain. Our results reveal that the PB-aNB-S1 pathway during sleep is critical for the generation and maintenance of chronic pain. Inhibiting this pathway during the sleep phase could be important for treating neuropathic pain.
Topics: Animals; Mice; Chronic Pain; Sleep; Sleep, Slow-Wave; Neuralgia; Cholinergic Neurons
PubMed: 36690899
DOI: 10.1038/s41593-022-01250-y -
Neuron Jun 2019How general anesthesia (GA) induces loss of consciousness remains unclear, and whether diverse anesthetic drugs and sleep share a common neural pathway is unknown....
How general anesthesia (GA) induces loss of consciousness remains unclear, and whether diverse anesthetic drugs and sleep share a common neural pathway is unknown. Previous studies have revealed that many GA drugs inhibit neural activity through targeting GABA receptors. Here, using Fos staining, ex vivo brain slice recording, and in vivo multi-channel electrophysiology, we discovered a core ensemble of hypothalamic neurons in and near the supraoptic nucleus, consisting primarily of neuroendocrine cells, which are persistently and commonly activated by multiple classes of GA drugs. Remarkably, chemogenetic or brief optogenetic activations of these anesthesia-activated neurons (AANs) strongly promote slow-wave sleep and potentiates GA, whereas conditional ablation or inhibition of AANs led to diminished slow-wave oscillation, significant loss of sleep, and shortened durations of GA. These findings identify a common neural substrate underlying diverse GA drugs and natural sleep and reveal a crucial role of the neuroendocrine system in regulating global brain states. VIDEO ABSTRACT.
Topics: Anesthesia, General; Anesthetics, General; Animals; Dexmedetomidine; Electroencephalography; Electromyography; Electrophysiological Phenomena; Hypnotics and Sedatives; Hypothalamus; Isoflurane; Ketamine; Mice; Neuroendocrine Cells; Neurons; Optogenetics; Patch-Clamp Techniques; Propofol; Proto-Oncogene Proteins c-fos; Sleep; Sleep, Slow-Wave; Supraoptic Nucleus
PubMed: 31006556
DOI: 10.1016/j.neuron.2019.03.033 -
Neurology Mar 2021To test the hypothesis that reduced slow-wave sleep, or N3 sleep, which is thought to underlie the restorative functions of sleep, is associated with MRI markers of...
OBJECTIVE
To test the hypothesis that reduced slow-wave sleep, or N3 sleep, which is thought to underlie the restorative functions of sleep, is associated with MRI markers of brain aging, we evaluated this relationship in the community-based Framingham Heart Study Offspring cohort using polysomnography and brain MRI.
METHODS
We studied 492 participants (age 58.8 ± 8.8 years, 49.4% male) free of neurological diseases who completed a brain MRI scan and in-home overnight polysomnography to assess slow-wave sleep (absolute duration and percentage of total sleep). Volumes of total brain, total cortical, frontal cortical, subcortical gray matter, hippocampus, and white matter hyperintensities were investigated as a percentage of intracranial volume, and the presence of covert brain infarcts was evaluated. Linear and logistic regression models were adjusted for age, age squared, sex, time interval between polysomnography and MRI (3.3 ± 1.0 years), ε4 carrier status, stroke risk factors, sleeping pill use, body mass index, and depression.
RESULTS
Less slow-wave sleep was associated with lower cortical brain volume (absolute duration, β [standard error] = 0.20 [0.08], = 0.015; percentage, 0.16 [0.08], = 0.044), lower subcortical brain volume (percentage, 0.03 [0.02], = 0.034), and higher white matter hyperintensities volume (absolute duration, -0.12 [0.05], = 0.010; percentage, -0.10 [0.04], = 0.033). Slow-wave sleep duration was not associated with hippocampal volume or the presence of covert brain infarcts.
CONCLUSION
Loss of slow-wave sleep might facilitate accelerated brain aging, as evidence by its association with MRI markers suggestive of brain atrophy and injury. Alternatively, subtle injuries and accelerated aging might reduce the ability of the brain to produce slow-wave sleep.
Topics: Aged; Atrophy; Brain; Brain Infarction; Brain Mapping; Cohort Studies; Female; Humans; Longitudinal Studies; Magnetic Resonance Imaging; Male; Middle Aged; Polysomnography; Sleep Wake Disorders; Sleep, Slow-Wave
PubMed: 33361258
DOI: 10.1212/WNL.0000000000011377 -
Cortex; a Journal Devoted To the Study... Nov 2016We investigated whether the benefit of slow wave sleep (SWS) for memory consolidation typically observed in healthy individuals is disrupted in people with accelerated...
We investigated whether the benefit of slow wave sleep (SWS) for memory consolidation typically observed in healthy individuals is disrupted in people with accelerated long-term forgetting (ALF) due to epilepsy. SWS is thought to play an active role in declarative memory in healthy individuals and, furthermore, electrographic epileptiform activity is often more prevalent during SWS than during wakefulness or other sleep stages. We studied the relationship between SWS and the benefit of sleep for memory retention using a word-pair associates task. In both the ALF and the healthy control groups, sleep conferred a memory benefit. However, the relationship between the amount of SWS and sleep-related memory benefits differed significantly between the groups. In healthy participants, the amount of SWS correlated positively with sleep-related memory benefits. In stark contrast, the more SWS, the smaller the sleep-related memory benefit in the ALF group. Therefore, contrary to its role in healthy people, SWS-associated brain activity appears to be deleterious for memory in patients with ALF.
Topics: Adult; Epilepsy; Female; Humans; Male; Memory; Mental Recall; Neuropsychological Tests; Sleep; Wakefulness
PubMed: 27710778
DOI: 10.1016/j.cortex.2016.08.013 -
ISRN Neurology 2014Continuous spike and wave during slow wave sleep (CSWS) is an epileptic encephalopathy that presents with neurocognitive regression and clinical seizures, and that... (Review)
Review
Continuous spike and wave during slow wave sleep (CSWS) is an epileptic encephalopathy that presents with neurocognitive regression and clinical seizures, and that demonstrates an electroencephalogram (EEG) pattern of electrical status epilepticus during sleep, as defined by the Commission on Classification and Terminology of the International League Against Epilepsy 1989. CSWS is an age-related condition, typically presenting in children around 5 years of age, with clinical seizures which progress within 2 years to a severe epileptic encephalopathy. The pathophysiology of CSWS is not completely understood, but the corticothalamic neuronal network involved in sleep patterns is thought to be involved. Genetic predisposition and injury in early development are thought to play etiological roles. Treatment strategies have involved traditional anticonvulsants, hormonal therapies, and other newer techniques. Outcomes are fair, and the thought is that earlier diagnosis and intervention preserve neurocognitive development, as in the case of other epileptic encephalopathies. Further understanding of the mechanisms of CSWS may lead to improved therapeutic options and thus outcomes of children with CSWS.
PubMed: 24634784
DOI: 10.1155/2014/619079