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Slow-wave sleep

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164:. This is sometimes referred to as "sleep-dependent memory processing". Impaired memory consolidation has been seen in individuals with primary insomnia, who thus do not perform as well as those who are healthy in memory tasks following a period of sleep. Furthermore, slow-wave sleep improves declarative memory (which includes semantic and episodic memory). A central model has been hypothesized that the long-term memory storage is facilitated by an interaction between the hippocampal and neocortical networks. In several studies, after the subjects have had training to learn a declarative memory task, the density of human 342:. Neocortical neurons fire spontaneously during slow-wave sleep, thus they seem to play a role during this period of sleep. Also, these neurons appear to have some sort of internal dialogue, which accounts for the mental activity during this state where there is no information from external signals (because of the synaptic inhibition at the thalamic level). The rate of recall of dreams during this state of sleep is relatively high compared to the other levels of the sleep cycle. This indicates that mental activity is closer to real life events. 307:, and is also partially observable in human beings. Indeed, a study reported a unilateral activation of the somatosensorial cortex when a vibrating stimulus was put on the hand of human subjects. The recordings show an important inter-hemispheric change during the first hour of non-REM sleep and consequently the presence of a local and use-dependent aspect of sleep. Another experiment detected a greater number of delta waves in the frontal and central regions of the right hemisphere. 469:. These structural anomalies are linked to disruptions in the sleep-wake cycle, particularly in non-rapid eye movement (NREM), slow wave sleep (SWS). Thus, individuals diagnosed with Alzheimer's often experience disturbances in sleep, resulting in diminished levels of non-rapid eye movement (NREM) sleep and reduced slow wave activity (SWA), that is a prominent brain rhythm during NREM sleep. Similarly, even cognitively healthy individuals with detectable amyloid beta exhibit 486:
with age. Moreover, recent findings indicate that older individuals exhibit a decreased inclination for daytime sleep compared to younger counterparts, and this decline persists even when accounting for variations in habitual sleep duration. This age-related decrease in daytime sleep propensity is evident in middle-aged individuals and coincides with statistically significant reductions in total sleep time, slow-wave sleep (SWS), and slow-wave activity (SWA).
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wake–promoting nodes beyond the wake–promoting PB. ... The intensity of cortical slow–wave–activity (SWA: 0.5–4Hz) during SWS is also widely accepted as a reliable indicator of sleep need ... In conclusion, in the present study we demonstrated that all polygraphic and neurobehavioral manifestation of SWS, including SWA, can be initiated in behaving animals by the selective activation of a delimited node of GABAergic medullary neurons.
425:. The activity falls to about 75 percent of the normal wakefulness level. The regions of the brain that are most active when awake have the highest level of delta waves during slow-wave sleep. This indicates that rest is geographical. The "shutting down" of the brain accounts for the grogginess and confusion if someone is awakened during deep sleep, since it takes the cerebral cortex time to resume its normal functions. 581:. The notable increase in SWA following sleep deprivation in the frontal areas, coupled with the prevailing presence of SWA in the frontal regions even during baseline sleep, has been construed as evidence supporting the involvement of slow-wave sleep (SWS) in functions typically linked to the frontal cortices. Thus, the prevalence of slow-wave sleep (SWS) in the frontal regions, particularly those linked to advanced 234: 527: 367:; SWS is associated with the regulation of synapses thus potentiated. SWS has been found to be involved in the downscaling of synapses, in which strongly stimulated or potentiated synapses are kept while weakly potentiated synapses either diminish or are removed. This may be helpful for recalibrating synapses for the next potentiation during wakefulness and for maintaining 46: 490:
regular and recuperative sleep, along with higher occurrences of stage 3 and 4 which are considered as NREM sleep. There have also been studies that have shown differences between races. The results showed that there was a lower percentage of SWS in African Americans compared to Caucasians, but since there are many influencing factors (e.g.,
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thereby promoting NREM sleep at the expense of wakefulness and REM sleep. ... Sleep is regulated by GABAergic populations in both the preoptic area and the brainstem; increasing evidence suggests a role for the melanin-concentrating hormone cells of the lateral hypothalamus and the parafacial zone of the brainstem
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Neurons containing the neuropeptide melanin-concentrating hormone (MCH) are mainly located in the lateral hypothalamus and the incerto-hypothalamic area, and have widespread projections throughout the brain. ... Intraventricular microinjection of MCH increases both slow wave sleep (SWS) and REM
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in the brain. Free radicals are oxidizing agents that have one unpaired electron, making them highly reactive. These free radicals interact with electrons of biomolecules and damage cells. In slow-wave sleep, the decreased rate of metabolism reduces the creation of oxygen byproducts, thereby allowing
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are all common behaviors that can occur during stage three of sleep. These occur most frequently amongst children, who then generally outgrow them. Another problem that may arise is sleep-related eating disorder. An individual will sleep-walk leaving his or her bed in the middle of the night seeking
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Furthermore, a faster behavioral reactivity is detected in the left hemisphere during SWS of the first night. The rapid awakening is correlated to the regional asymmetry in the activities of SWS. These findings show that the hemispheric asymmetry in SWS plays a role as a protective mechanism. SWS is
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The nucleus accumbens comprises a contingent of neurons specifically expressing the post-synaptic A2A-receptor (A2AR) subtype making them excitable by adenosine, its natural agonist endowed with powerful sleep-promoting properties. ... In both cases, large activation of A2AR-expressing neurons
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More recently, the medullary parafacial zone (PZ) adjacent to the facial nerve was identified as a sleep-promoting center on the basis of anatomical, electrophysiological and chemo- and optogenetic studies. GABAergic PZ neurons inhibit glutamatergic parabrachial (PB) neurons that project to the BF,
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Slow-wave sleep is the constructive phase of sleep for recuperation of the mind-body system in which it rebuilds itself after each day. Substances that have been ingested into the body while an organism is awake are synthesized into complex proteins of living tissue. Growth hormone is also secreted
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The left hemisphere is shown to be more sensitive to deviant stimuli during the first night—compared to the following nights of an experiment. This asymmetry explains further the reduced sleep of half the brain during SWS. Indeed, in comparison to the right one, the left hemisphere plays a vigilant
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The slow-wave seen in the cortical EEG is generated through recurrent connections within the cerebral cortex, where cortical pyramidal cells excite one another in a positive feedback loop. This recurrent excitation is balanced by inhibition, resulting in the active state of the slow oscillation of
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lasting at least 0.5 seconds, consisting of a distinct negative sharp wave followed by a positive component, and slow waves or delta waves characterized by slow frequency (< 2 Hz) and high amplitude (> 75 μV) are key indicators. The presence and distribution of sleep spindle activity and
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When sleep-deprived humans sleep normally again, the recovery percentage for each stage of sleep is not the same. Only seven percent of stages one and two are regained, but 68 percent of stage-four slow-wave sleep and 53 percent of REM sleep are regained. This suggests that stage-four sleep (known
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performance, such as route retrieval, on the following day. Additionally, studies have found that when odour cues are given to subjects during sleep, this stage of sleep excluslvely allows contextual cues to be reactivated after sleep, favoring their consolidation. A separate study found that when
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Here, we show that chemogenetic or optogenetic activation of excitatory adenosine A2A receptor-expressing indirect pathway neurons in the core region of the NAc strongly induces slow-wave sleep. Chemogenetic inhibition of the NAc indirect pathway neurons prevents the sleep induction, but does not
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Slow-wave sleep (SWS) and slow-wave activity (SWA) undergo significant transformations throughout one's lifespan, with aging serving as a particularly influential factor in predicting individual variations. Aging is inversely proportional to the amount of SWS beginning by midlife, so SWS declines
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Results from a number of research have shown how sleep affects Aβ dynamics. A good candidate for slow wave activity (SWA), which occurs during deep non-REM sleep, is amyloid-b modulation. The researchers also highlighted a strong relationship between amyloid-b and SWA, pointing out that increased
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J. A. Horne (1978) reviewed several experiments with humans and concluded that sleep deprivation has no effects on people's physiological stress response or ability to perform physical exercise. It did, however, have an effect on cognitive functions. Some people reported distorted perceptions or
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Sex differences have also been found, such that females tend to have higher levels of SWS compared to males, at least up until menopause. Older individuals exhibit gender-based variations in non-rapid eye movement (NREM) sleep, where women demonstrate increased slow-wave sleep (SWS) during both
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show a lower amplitude of slow-wave activity (SWA) compared to healthy participants. Sex differences also persist in the former group: depressed men present significantly lower SWA amplitude. This sex divergence is twice as large as the one observed in healthy subjects. However, no age-related
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In the present study we show, for the first time, that activation of a delimited node of GABAergic neurons located in the medullary PZ can potently initiate SWS and cortical SWA in behaving animals. ... For now however it remains unclear if the PZ is interconnected with other sleep– and
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MCHergic neurons are silent during wakefulness (W), increase their firing during slow wave sleep (SWS) and still more during REM sleep (REMS). Studies in knockout mice for MCH (MCH(-/-)) have shown a reduction in SWS and an increase of W during the light and the dark phase of the light-dark
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are silent. This is the period when the neocortical neurons are able to rest. The second section of the wave signifies an "up state", an excitation or depolarizing phase in which the neurons fire briefly at a high rate. The principal characteristics during slow-wave sleep that contrast with
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Varga, Andrew W.; Wohlleber, Margaret E.; Giménez, Sandra; Romero, Sergio; Alonso, Joan F.; Ducca, Emma L.; Kam, Korey; Lewis, Clifton; Tanzi, Emily B.; Tweardy, Samuel; Kishi, Akifumi; Parekh, Ankit; Fischer, Esther; Gumb, Tyler; Alcolea, Daniel; Fortea, Juan; Lleó, Alberto; Blennow, Kaj;
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Affective representations are generally better remembered during sleep compared to neutral ones. Emotions with negative salience presented as a cue during SWS show better reactivation, and therefore an enhanced consolidation in comparison to neutral memories. The former was predicted by
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Though SWS is fairly consistent within the individual, it can vary across individuals. To some degree, individual variations seem to be influenced by demographic factors such as gender and age. Age and sex have been noted as two of the biggest factors that affect this period of sleep.
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The sleep-promoting action of GABAergic neurons located in the preoptic hypothalamus (6–8) is now well-known and accepted (9). More recently, other groups of sleep-promoting GABAergic neurons in the lateral hypothalamus (melanin-concentrating hormone neurons) and brainstem have been
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in NAc promotes slow wave sleep (SWS) by increasing the number and duration of episodes. ... After optogenetic activation of the core, a similar promotion of SWS was observed, whereas no significant effects were induced when activating A2AR-expressing neurons within the shell.
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present was significantly higher than the signals observed during the control tasks, which involved similar visual stimulation and cognitively-demanding tasks but did not require learning. This associated with the spontaneously occurring wave oscillations that account for the
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slow waves vary across NREM sleep, leading to its subdivision into stages 1–4. While slow waves and sleep spindles are present in stages 2, 3, and 4, stage 2 sleep is characterized by a higher prevalence of spindles, while slow waves dominate the EEG during stages 3 and 4.
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Longer periods of SWS occur in the first part of the night, primarily in the first two sleep cycles (roughly three hours). Children and young adults will have more total SWS in a night than older adults. The elderly may not go into SWS at all during many nights of sleep.
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Isotalus, Hanna K.; Carr, Will J.; Blackman, Jonathan; Averill, George G.; Radtke, Oliver; Selwood, James; Williams, Rachel; Ford, Elizabeth; McCullagh, Liz; McErlane, James; O'Donnell, Cian; Durant, Claire; Bartsch, Ullrich; Jones, Matt W.; Muñoz-Neira, Carlos (2023).
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slow wave sleep. Failure of this mechanism results in a silencing of activity for a brief period of time. The recurrence of active and silent periods occurs at a rate of 0.5–4 Hz, giving rise to the slow waves of the EEG seen during slow wave sleep.
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Slow-wave sleep usually lasts between 70 and 90 minutes, taking place during the first hours of the night. SWS is characterised by moderate muscle tone, slow or absent eye movement, and lack of genital activity. Slow-wave sleep is considered important for
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Iber, C; Ancoli-Israel, S; Chesson, A; Quan, SF. for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. Westchester: American Academy of Sleep Medicine;
48: 47: 152:(AASM) divided slow-wave sleep into stages 3 and 4. The two stages are now combined as Stage three or N3. An epoch (30 seconds of sleep) which consists of 20% or more slow-wave (delta) sleep is now considered to be in slow-wave sleep. 50: 201:
plays an essential role in hippocampus-dependent memory consolidation. An increased level of cholinergic activity during SWS is known to be disruptive for memory processing. Considering that acetylcholine is a
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Some drugs influence sleep architecture by encroaching upon or prolonging deep sleep. Many drugs known to increase deep sleep in humans are of the GABAergic, dopaminergic, and anti-serotonergic classes.
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Ju, Yo-El; Ooms, Sharon J.; Sutphen, Courtney; Macauley, Shannon L.; Zangrilli, Margaret A.; Jerome, Gina; Fagan, Anne M.; Mignot, Emmanuel; Zempel, John M.; Claassen, Jurgen A.; Holtzman, David (2017).
673:(CNS) from gamma-aminobutyric acid (GABA). Oral administration of GHB has been shown to enhance SWS without suppressing REM sleep. In the United States, GHB is a prescription drug under the brand name 189:
subjects hear sounds associated with previously shown pictures of locations, the reactivation of individual memory representations was significantly higher during SWS as compared to other sleep stages.
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that modulates the direction of information flow between the hippocampus and neocortex during sleep, its suppression is necessary during SWS in order to consolidate sleep-related declarative memory.
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and a relatively high amplitude power with peak-to-peak amplitude greater than 75 μV. The first section of the wave signifies a "down state", an inhibition or hyperpolarizing phase in which the
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out food, and will eat not having any memory of the event in the morning. Over half of individuals with this disorder become overweight. Sleep-related eating disorder can usually be treated with
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and birds, have the ability to sleep with only one hemisphere of the brain, leaving the other hemisphere awake to carry out normal functions and to remain alert. This kind of sleep is called
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Considering that SWS is the only sleep stage that reports human deep sleep as well as being used in studies with mammals and birds, it is also adopted in experiments revealing the role of
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sleep; however, the increment in REM sleep is more pronounced. ... Although both SWS and REM sleep are facilitated by MCH, REM sleep seems to be more sensitive to MCH modulation.
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Zetterberg, Henrik; Mosconi, Lisa; Glodzik, Lidia; Pirraglia, Elizabeth; Burschtin, Omar; Leon, Mony J.; Rapoport, David M.; Lu, Shou-en Lu; Ayappa, Indu; Osorio, Ricardo S. (2016).
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during this stage, which leads some scientists to hypothesize that a function of slow wave sleep is to facilitate the healing of muscles as well as repair damage to tissues. Lastly,
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Peigneux P, Laureys S, Fuchs S, Collette F, Perrin F, Reggers J, et al. (October 2004). "Are spatial memories strengthened in the human hippocampus during slow wave sleep?".
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during SWS is detected after the spatial learning task. In addition, a correlation can be observed between the amplitude of hippocampal activity during SWS and the improvement in
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Prior to 2007, the term SWS referred to both the third and fourth stages of NREM. However, after both stages were combined into stage three, SWS refers only to the third stage.
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Oishi Y, Xu Q, Wang L, Zhang BJ, Takahashi K, Takata Y, Luo YJ, Cherasse Y, Schiffmann SN, de Kerchove d'Exaerde A, Urade Y, Qu WM, Huang ZL, Lazarus M (September 2017).
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during sleep. A predominance of the left hemisphere in the neural activity can be observed in the default-mode network during SWS. This asymmetry is correlated with the
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disruption in SWA is correlated with elevated levels of amyloid-b. Hence, Slow waves of non-rapid eye movement sleep, or NREM sleep, are disrupted or decrease when
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Sleep deprivation studies with humans suggest that the primary function of slow-wave sleep may be to allow the brain to recover from its daily activities.
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Sekimoto M, Kato M, Kajimura N, Watanabe T, Takahashi K, Okuma T (May 2000). "Asymmetric interhemispheric delta waves during all-night sleep in humans".
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hallucinations and lack of concentration on mental tasks. Thus, the major role of sleep does not appear to be rest for the body, but rest for the brain.
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Although the sequence of non-REM (NREM) sleep stages one to four (R&K classification) or N1 to N3 (AASM classification) fulfills the criteria...
3480:"Tiagabine increases slow-wave sleep in a dose-dependent fashion without affecting traditional efficacy measures in adults with primary insomnia" 3708:
Massimini M, Ferrarelli F, Huber R, Esser SK, Singh H, Tononi G (September 2005). "Breakdown of cortical effective connectivity during sleep".
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in the brain increases as a result of tasks that demand mental activity. Another function affected by slow-wave sleep is the secretion of
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Sharpley, AL; Elliott, JM; Attenburrow, MJ; Cowen, PJ (March 1994). "Slow wave sleep in humans: role of 5-HT2A and 5-HT2C receptors".
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Yuan XS, Wang L, Dong H, Qu WM, Yang SR, Cherasse Y, Lazarus M, Schiffmann SN, d'Exaerde AK, Li RX, Huang ZL (October 2017).
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Rasch B, Büchel C, Gais S, Born J (March 2007). "Odor cues during slow-wave sleep prompt declarative memory consolidation".
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Sanchez-Vives, MV; McCormick, DA (2000). "Cellular and network mechanisms of rhythmic recurrent activity in neocortex".
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medication. This nocturnal eating throughout a family suggests that heredity may be a potential cause of this disorder.
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over SWS, which discriminates the memory processes during sleep as well as facilitating emotional memory consolidation.
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therefore sensitive to danger and non-familiar environment, creating a need for vigilance and reactivity during sleep.
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Dijk, DJ (June 2010). "Slow-wave sleep deficiency and enhancement: implications for insomnia and its management".
3579:"Effects of trazodone and imipramine on the biological rhythm: an analysis of sleep EEG and body core temperature" 4545: 4326: 4135: 4083: 1302: 262:
NREM sleep, as observed on the electroencephalogram (EEG), is distinguished by certain characteristic features.
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Lesku JA, Meyer LC, Fuller A, Maloney SK, Dell'Omo G, Vyssotski AL, Rattenborg NC (2011). Balaban E (ed.).
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Mental disorders play a role in individual differences in the quality and quantity of SWS: subjects with
4341: 4073: 3520:"L-DOPA increases slow-wave sleep duration and selectively modulates memory persistence in older adults" 3478:
Walsh, James K.; Perlis, Michael; Rosenthal, Murray; Krystal, Andrew; Jiang, John; Roth, Thomas (2006).
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Monti JM, Torterolo P, Lagos P (2013). "Melanin-concentrating hormone control of sleep-wake behavior".
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or cognitive regions highly active during wakefulness, underscores the considerable importance of SWS.
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A Manual of Standardized Terminology, Techniques and Scoring System for Sleep Stages of Human Subjects
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Lee, Lee Fun; Gerashchenko, Dmitry; Timofeev, Igor; Bacskai, Brian J.; Kastanenka, Ksenia V. (2020).
2025: 1673: 1587: 1427: 862: 643: 451: 371:. Notably, new evidence is showing that reactivation and rescaling may be co-occurring during sleep. 248: 217:, which is always greatest during this stage. It is also thought to be responsible for a decrease in 161: 93: 2860:"Turning a Negative into a Positive: Ascending GABAergic Control of Cortical Activation and Arousal" 2112: 334:
Several neurotransmitters are involved in sleep and waking patterns: acetylcholine, norepinephrine,
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During sleep, the distribution of slow-wave activity (SWA) typically exhibits a prevalence in the
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The 1968 categorization of the combined Sleep Stages 3 – 4 was reclassified in 2007 as Stage N3.
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Vogel G, Foulkes D, Trosman H (March 1966). "Ego functions and dreaming during sleep onset".
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Cicogna P, Natale V, Occhionero M, Bosinelli M (2000). "Slow wave and REM sleep mentation".
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activity is synchronized, and characterised by slow waves with a frequency range of 0.5–4.5
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Walsh, James K.; Zammit, Gary; Schweitzer, Paula K.; Ondrasik., John; Roth, Thomas (2005).
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in any given 30-second epoch of the EEG during sleep, by the current 2007 AASM guidelines.
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enhances both deep sleep while also positively impacting various indicators of insomnia.
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the existing radical species to clear. This is a means of preventing damage to the brain.
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today as the deepest part of stage-three sleep) is more important than the other stages.
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Anaclet C, Ferrari L, Arrigoni E, Bass CE, Saper CB, Lu J, Fuller PM (September 2014).
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receptor may contribute to this effect. A variety of drugs that antagonise the on 5-HT
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and to significantly increase SWS in healthy elderly subjects and adult patients with
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During slow-wave sleep, there is a significant decline in cerebral metabolic rate and
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Moran, Maria; Lynch, C. A.; Walsh, C.; Coen, R.; Coakley, D.; Lawlor, B. A. (2005).
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Slow-wave sleep is an active phenomenon probably brought about by the activation of
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Some of the brain regions implicated in the induction of slow-wave sleep include:
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Mander BA, Marks SM, Vogel JW, Rao V, Lu B, Saletin JM, et al. (July 2015).
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Tononi G, Cirelli C (February 2006). "Sleep function and synaptic homeostasis".
352: 267: 233: 181: 138: 3536: 3382: 3245: 3140: 2991: 2727:"The GABAergic parafacial zone is a medullary slow wave sleep-promoting center" 2173: 1685: 1580:
Proceedings of the National Academy of Sciences of the United States of America
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exhibits the most significant rise in slow-wave activity (SWA) compared to the
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According to J. Siegel (2005), sleep deprivation results in the build-up of
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within the brain are restored with sugars to provide energy for the brain.
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Learning and memory formation occurs during wakefulness by the process of
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Dijk, Derk-Jan; Groeger, John A.; Stanley, Neil; Deacon, Stephen (2010).
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of the brain. In the subsequent recovery sleep after experiencing
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difference concerning SWS can be observed in the depressed group.
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Slow-wave sleep is necessary for survival. Some animals, such as
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This period of sleep is called slow-wave sleep because the
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attacks and excessive daytime sleepiness in patients with
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1321:"Learning-dependent increases in sleep spindle density" 538: 100:, and the recovery of the brain from daily activities. 1264:"Grouping of brain rhythms in corticothalamic systems" 1111:"Aging in Brain Found to Hurt Sleep Needed for Memory" 1094: 1092: 3326:
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have been shown to increase SWS by 10.6% in elderly.
3168:"Melanin-concentrating hormone: a new sleep factor?" 2678:
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Tamaki M, Bang JW, Watanabe T, Sasaki Y (May 2016).
4354: 4314: 4262: 4192: 4144: 4092: 4034: 3974: 3965: 3902: 3873: 2070:"What Happens When You Sleep: The Science of Sleep" 1368: 1366: 773:receptors exhibit SWS-enhancing effects in humans. 1631: 1629: 1215:"The role of slow wave sleep in memory processing" 1179:"The Role of Slow Wave Sleep in Memory Processing" 251:(EEG). Stage N3 is defined by the presence of 20% 1915:Kattler H, Dijk DJ, Borbély AA (September 1994). 610:; specifically, the subset of these neurons that 1781:Dijk, D. J.; Hayes, B.; Czeisler, C. A. (1993). 1319:Gais S, Mölle M, Helms K, Born J (August 2002). 3415:"Xyrem - European Drugs Reference Encyclopedia" 3328:"The effects of gamma-hydroxybutyrate on sleep" 929:Anales de la Real Academia Nacional de Medicina 925:"[The neurobiology of slow-wave sleep]" 2139:"The importance of sleep & why we need it" 972: 970: 968: 966: 964: 962: 960: 958: 3847: 1172: 1170: 176:Specifically, SWS presents a role in spatial 8: 2104:INSOM: INSomnia and Its Optimized Management 237:Polysomnogram demonstrating SWS, stage four. 160:Slow-wave sleep is considered important for 2913:Valencia Garcia S, Fort P (December 2017). 2802:"The Neurobiology of Sleep and Wakefulness" 27:Period of sleep in humans and other animals 4169:Rapid eye movement sleep behavior disorder 3971: 3854: 3840: 3832: 3663:The World Journal of Biological Psychiatry 2100:"Review article: Does delta sleep matter?" 1001:: CS1 maint: location missing publisher ( 295:Hemispheric asymmetries in the human sleep 3594: 3553: 3535: 3390: 3302: 3253: 3193: 3183: 3103: 3054: 3044: 2999: 2938: 2885: 2875: 2825: 2800:Schwartz MD, Kilduff TS (December 2015). 2753: 2601: 2552: 2451: 2441: 2400: 2351: 2298: 2228: 2111: 2045: 1932: 1848: 1757: 1693: 1609: 1599: 1550: 1490: 1346: 1336: 1238: 1041: 884: 874: 239:High amplitude EEG is highlighted in red. 2806:The Psychiatric Clinics of North America 724:availability. Nocturnal single doses of 650:-releasing neurons), located within the 636:(GABAergic neurons), located within the 596:(GABAergic neurons), located within the 375:Problems associated with slow-wave sleep 44: 3166:Torterolo P, Lagos P, Monti JM (2011). 2007: 2005: 2003: 1520: 1518: 841: 229:Electroencephalographic characteristics 3812:Warren, Jeff (2007). "The Slow Wave". 3228:Roehrs, Timothy; Roth, Thomas (2011). 3015:affect the homoeostatic sleep rebound. 1413: 1411: 994: 243:Large 75-microvolt (0.5–2.0 Hz) 34:. For the therapeutic treatment, see 7: 3788:10.1001/archpsyc.1966.01730090014003 3524:Frontiers in Behavioral Neuroscience 1188:. Supplement to Vol.5, No. 2, 2009. 720:which acts to increases the brain's 173:from thalamic and cortical neurons. 2149:from the original on July 11, 2019. 1639:. Wolters Kluwer Pharma Solutions. 3365:Roehrs T, Roth T (December 2010). 2858:Brown RE, McKenna JT (June 2015). 1934:10.1111/j.1365-2869.1994.tb00123.x 1338:10.1523/JNEUROSCI.22-15-06830.2002 1283:10.1016/j.neuroscience.2005.10.029 1219:Journal of Clinical Sleep Medicine 1186:Journal of Clinical Sleep Medicine 1022:Journal of Clinical Sleep Medicine 935:(1): 209–224, discussion 224–226. 395:, or topiramate, which is an anti- 150:American Academy of Sleep Medicine 84:activity is characterised by slow 25: 2098:Payne JD, Walker WP (June 2008). 908:Rechtschaffen A, Kales A (1968). 851:"Ostriches sleep like platypuses" 716:is a drug commonly used to treat 359:Learning and synaptic homeostasis 330:Neural control of slow-wave sleep 38:. For the underground hotel, see 4009:Obesity hypoventilation syndrome 4004:Central hypoventilation syndrome 3583:Journal of Nippon Medical School 2696:10.1046/j.0953-816x.2001.01597.x 2545:10.1111/j.1365-2869.2011.00959.x 2523:Mokhlesi B, Pannain S, Ghods F, 1637:Slow-Wave Sleep: Beyond Insomnia 1574:Gais S, Born J (February 2004). 525: 145:, and lack of genital activity. 4164:Periodic limb movement disorder 4131:Non-24-hour sleep–wake disorder 3421:from the original on 2013-08-21 2773:from the original on 2018-11-04 2120:from the original on 2021-06-25 2080:from the original on 2021-06-21 1195:from the original on 2013-05-09 1121:from the original on 2017-03-17 1075:from the original on 2018-10-04 3776:Archives of General Psychiatry 3096:10.1523/JNEUROSCI.0609-15.2015 1379:Archives Italienne de Biologie 1109:Carey, Benedict (2013-01-27). 830:Unihemispheric slow-wave sleep 688:The administration of the GABA 677:. It has been shown to reduce 494:, sleep-disordered breathing, 305:unihemispheric slow-wave sleep 1: 4436:Biphasic and polyphasic sleep 4244:Nocturnal clitoral tumescence 4106:Advanced sleep phase disorder 2646:10.1016/S0165-1781(00)00178-5 1978:10.1016/S1388-2457(00)00258-3 1262:Steriade M (1 January 2006). 981:(Eleventh ed.). Boston. 648:melanin-concentrating hormone 4116:Delayed sleep phase disorder 4044:Excessive daytime sleepiness 3632:10.1016/0028-3908(94)90077-9 1799:10.1016/0006-8993(93)90579-c 1483:10.1016/j.neuron.2004.10.007 1141:Harvard Review of Psychiatry 1071:. Harvard University. 2008. 876:10.1371/journal.pone.0023203 799:Non-rapid eye movement sleep 784:Delta sleep-inducing peptide 669:(GHB) is synthesized in the 403:Effects of sleep deprivation 78:non-rapid eye movement sleep 4556:Biology of bipolar disorder 4249:Nocturnal penile tumescence 4121:Irregular sleep–wake rhythm 3457:10.1016/j.sleep.2005.05.004 3084:The Journal of Neuroscience 2493:10.1016/j.sleep.2004.12.005 1325:The Journal of Neuroscience 1018:"Rethinking sleep analysis" 923:Reinoso Suárez, F. (1999). 810:Sharp wave–ripple complexes 634:ventrolateral preoptic area 346:Physical healing and growth 4572: 4111:Cyclic alternating pattern 3537:10.3389/fnbeh.2023.1096720 3383:10.1016/j.jsmc.2010.08.002 3246:10.1016/j.jsmc.2010.08.002 3141:10.1016/j.smrv.2012.10.002 2992:10.1038/s41467-017-00781-4 2919:Acta Pharmacologica Sinica 2174:10.1016/j.smrv.2005.05.002 1686:10.1038/s41598-020-63933-5 616:D2-type dopamine receptors 406: 61:and slow-wave sleep phases 29: 4327:Behavioral sleep medicine 4136:Shift work sleep disorder 4084:Sleep state misperception 3675:10.3109/15622971003637645 2818:10.1016/j.psc.2015.07.002 2533:Journal of Sleep Research 2038:10.1016/j.cub.2016.02.063 1921:Journal of Sleep Research 1153:10.1080/10673220802432517 3884:Rapid eye movement (REM) 3277:Walsh, James K. (2009). 3185:10.3389/fneur.2011.00014 2877:10.3389/fneur.2015.00135 2443:10.3389/fnins.2020.00705 1966:Clinical Neurophysiology 1213:Walker MP (April 2009). 794:Large irregular activity 171:intracellular recordings 76:, is the third stage of 72:), often referred to as 4205:Exploding head syndrome 4014:Obstructive sleep apnea 3730:10.1126/science.1117256 1837:Frontiers in Bioscience 1732:Dijk, Derk-Jan (2009). 1601:10.1073/pnas.0305404101 1440:10.1126/science.1138581 1016:Schulz H (April 2008). 759:atypical antidepressant 731:Antagonists of certain 467:neurofibrillary tangles 457:Moreover, the onset of 409:Fatal familial insomnia 312:hemispheric asymmetries 4551:Electroencephalography 4520:Sleeping while on duty 4069:Idiopathic hypersomnia 3371:Sleep Medicine Clinics 3172:Frontiers in Neurology 3129:Sleep Medicine Reviews 2594:10.1093/sleep/33.2.211 2162:Sleep Medicine Reviews 2143:Human Givens Institute 2127:– via CiteSeerX. 979:Physiology of behavior 733:serotonergic receptors 671:central nervous system 626:), located within the 604:nucleus accumbens core 477:Individual differences 441:Amyloid beta pathology 365:long-term potentiation 240: 180:. Reactivation of the 82:electroencephalography 62: 4342:Neuroscience of sleep 4074:Night eating syndrome 4059:Kleine–Levin syndrome 3755:Sleep Research Online 3332:Biological Psychiatry 3295:10.5664/jcsm.5.2S.S27 2972:Nature Communications 1373:Steriade, M. (2004). 1231:10.5664/jcsm.5.2S.S20 667:Gamma-hydroxybutyrate 393:dopaminergic agonists 236: 53: 4496:Sleep and creativity 2931:10.1038/aps.2017.168 2344:10.1093/brain/awx148 1750:10.5664/jcsm.5.2S.S6 644:lateral hypothalamus 608:medium spiny neurons 539:adding missing items 452:memory consolidation 249:electroencephalogram 162:memory consolidation 94:memory consolidation 4491:Sleep and breathing 3947:Sensorimotor rhythm 3722:2005Sci...309.2228M 3596:10.1272/jnms.69.333 3046:10.7554/eLife.29055 2984:2017NatCo...8..734O 2634:Psychiatry Research 2381:Nature Neuroscience 2209:Nature Neuroscience 2030:2016CBio...26.1190T 1678:2020NatSR..10.6976B 1592:2004PNAS..101.2140G 1432:2007Sci...315.1426R 1177:Walker, Matthew P. 977:Carlson NR (2013). 867:2011PLoSO...623203L 718:Parkinson's disease 583:cognitive functions 459:Alzheimer's disease 423:cerebral blood flow 369:synaptic plasticity 316:sleep onset latency 148:Prior to 2007, the 137:sleep are moderate 4501:Sleep and learning 4254:Nocturnal emission 4154:Nightmare disorder 4019:Periodic breathing 3496:10.5664/jcsm.26433 3289:(2 Suppl): 27–32. 2291:10.5665/sleep.6240 1666:Scientific Reports 1543:10.5665/sleep.3572 1537:(4): 701–7, 707A. 1225:(2 Suppl): S20-6. 1115:The New York Times 1034:10.5664/jcsm.27124 815:Sleep and learning 537:; you can help by 471:sleep disturbances 241: 211:Glucose metabolism 178:declarative memory 98:declarative memory 63: 40:Deep Sleep (hotel) 36:Deep sleep therapy 4533: 4532: 4511:Sleep deprivation 4350: 4349: 3823:978-0-679-31408-0 3805:The Mind at Night 3716:(5744): 2228–32. 3669:(Suppl 1): 22–8. 3620:Neuropharmacology 2285:(11): 2041–2048. 1880:(10): 1027–1034. 1833:"Arousal systems" 1744:(2 Suppl): 6–15. 1646:978-0-9561387-1-2 1308:on 18 April 2017. 988:978-0-205-23939-9 704:sleep maintenance 598:medulla oblongata 563:sleep deprivation 555: 554: 338:, histamine, and 322:role during SWS. 225:neural activity. 141:, slow or absent 51: 16:(Redirected from 4563: 4546:Sleep physiology 4506:Sleep and memory 4446:Circadian rhythm 4193:Benign phenomena 4095:Circadian rhythm 3972: 3856: 3849: 3842: 3833: 3827: 3816:. Random House. 3808: 3799: 3770: 3749: 3695: 3694: 3658: 3652: 3651: 3615: 3609: 3608: 3598: 3574: 3568: 3567: 3557: 3539: 3514: 3508: 3507: 3484:J Clin Sleep Med 3475: 3469: 3468: 3436: 3430: 3429: 3427: 3426: 3411: 3405: 3404: 3394: 3362: 3356: 3355: 3323: 3317: 3316: 3306: 3283:J Clin Sleep Med 3274: 3268: 3267: 3257: 3225: 3212: 3211: 3197: 3187: 3163: 3157: 3156: 3124: 3118: 3117: 3107: 3075: 3069: 3068: 3058: 3048: 3024: 3018: 3017: 3003: 2963: 2957: 2956: 2942: 2910: 2904: 2903: 2889: 2879: 2855: 2844: 2843: 2829: 2797: 2786: 2785: 2779: 2778: 2772: 2757: 2740:(9): 1217–1224. 2731: 2722: 2716: 2715: 2675: 2666: 2665: 2631: 2622: 2616: 2615: 2605: 2573: 2567: 2566: 2556: 2520: 2505: 2504: 2472: 2466: 2465: 2455: 2445: 2421: 2415: 2414: 2404: 2372: 2366: 2365: 2355: 2338:(8): 2104–2111. 2322: 2313: 2312: 2302: 2269: 2260: 2249: 2243: 2242: 2232: 2215:(9): 1277–1284. 2200: 2194: 2193: 2157: 2151: 2150: 2135: 2129: 2128: 2126: 2125: 2115: 2095: 2089: 2088: 2086: 2085: 2074:Sleep Foundation 2066: 2060: 2059: 2049: 2009: 1998: 1997: 1961: 1955: 1954: 1936: 1912: 1906: 1905: 1874:Nat Neuroscience 1869: 1863: 1862: 1852: 1825: 1819: 1818: 1778: 1772: 1771: 1761: 1738:J Clin Sleep Med 1729: 1708: 1707: 1697: 1657: 1651: 1650: 1633: 1624: 1623: 1613: 1603: 1571: 1565: 1564: 1554: 1522: 1513: 1512: 1494: 1466: 1460: 1459: 1426:(5817): 1426–9. 1415: 1406: 1405: 1403: 1402: 1393:. 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Neurosci 2423: 2422: 2418: 2393:10.1038/nn.4035 2374: 2373: 2369: 2324: 2323: 2316: 2271: 2270: 2263: 2250: 2246: 2221:10.1038/nn.4601 2202: 2201: 2197: 2159: 2158: 2154: 2137: 2136: 2132: 2123: 2121: 2113:10.1.1.723.1235 2097: 2096: 2092: 2083: 2081: 2068: 2067: 2063: 2018:Current Biology 2011: 2010: 2001: 1963: 1962: 1958: 1914: 1913: 1909: 1871: 1870: 1866: 1827: 1826: 1822: 1780: 1779: 1775: 1731: 1730: 1711: 1659: 1658: 1654: 1647: 1635: 1634: 1627: 1573: 1572: 1568: 1524: 1523: 1516: 1468: 1467: 1463: 1417: 1416: 1409: 1400: 1398: 1372: 1371: 1364: 1318: 1317: 1313: 1305: 1277:(4): 1087–106. 1266: 1261: 1260: 1256: 1212: 1211: 1207: 1198: 1196: 1192: 1181: 1176: 1175: 1168: 1138: 1137: 1133: 1124: 1122: 1108: 1107: 1103: 1097: 1090: 1078: 1076: 1067: 1066: 1062: 1015: 1014: 1010: 993: 989: 976: 975: 956: 922: 921: 917: 907: 906: 902: 848: 847: 843: 839: 834: 779: 772: 768: 764: 747: 740: 691: 660: 623: 594:parafacial zone 575:parietal region 551: 545: 542: 526: 520: 492:body mass index 479: 443: 411: 405: 377: 361: 348: 332: 297: 292: 278:neurons of the 238: 231: 223:parasympathetic 158: 114: 109: 66:Slow-wave sleep 57:sleeping, with 45: 43: 28: 23: 22: 15: 12: 11: 5: 4569: 4567: 4559: 4558: 4553: 4548: 4538: 4537: 4531: 4530: 4528: 4527: 4522: 4517: 4508: 4503: 4498: 4493: 4488: 4483: 4478: 4473: 4468: 4463: 4458: 4453: 4451:Comfort object 4448: 4443: 4438: 4433: 4432: 4431: 4426: 4416: 4411: 4406: 4401: 4400: 4399: 4394: 4389: 4384: 4379: 4374: 4369: 4358: 4356: 4352: 4351: 4348: 4347: 4345: 4344: 4339: 4334: 4329: 4324: 4322:Sleep medicine 4318: 4316: 4312: 4311: 4309: 4308: 4307: 4306: 4296: 4295: 4294: 4289: 4279: 4274: 4268: 4266: 4260: 4259: 4257: 4256: 4251: 4246: 4241: 4236: 4231: 4226: 4221: 4212: 4207: 4202: 4196: 4194: 4190: 4189: 4187: 4186: 4181: 4176: 4171: 4166: 4161: 4156: 4150: 4148: 4142: 4141: 4139: 4138: 4133: 4128: 4123: 4118: 4113: 4108: 4102: 4100: 4093: 4090: 4089: 4087: 4086: 4081: 4076: 4071: 4066: 4061: 4056: 4051: 4046: 4040: 4038: 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Index

Deep sleep
Deep Sleep
Deep sleep therapy
Deep Sleep (hotel)
Ostriches
REM
non-rapid eye movement sleep
electroencephalography
delta waves
memory consolidation
declarative memory
EEG
Hz
neurons
neocortex
REM
muscle tone
eye movement
American Academy of Sleep Medicine
memory consolidation
sleep spindles
intracellular recordings
declarative memory
hippocampus
spatial memory
sleep spindles
Acetylcholine
neurotransmitter
Glucose metabolism
growth hormone

Text is available under the Creative Commons Attribution-ShareAlike License. Additional terms may apply.