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Slow-wave sleep

slow-wave sleep, slow-wave sleep promotes
Slow-wave sleep SWS, often referred to as deep sleep, consists of Stage three combined stages 3 and 4 of non-rapid eye movement sleep2 Initially, SWS consisted of both Stage 3 N3, which has 20-50 percent delta wave activity, and Stage four N4, which has more than 50 percent delta wave activity3 However, as of 2008, the American Academy of Sleep Medicine AASM has discontinued the use of Stage four as a separate stage456 Thus, the two stages are now combined as "Stage three" An epoch 30 seconds of sleep which consists of 20% or more slow-wave delta sleep is now considered to be stage three

This period of sleep is called slow-wave sleep because the EEG activity is synchronized, producing slow waves with a frequency of less than 1 Hz and a relatively high amplitude The first section of the wave signifies a "down state," which is an inhibition or hyperpolarizing phase in which the neurons in the neocortex are silent This is the period when the neocortical neurons are able to rest The second section of the wave signifies an "up state," which is 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 REM sleep are moderate muscle tone, slow or absent eye movement, and lack of genital activity7

Slow-wave sleep is considered important for memory consolidation8 This is sometimes referred to as "sleep-dependent memory processing"9 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 sleep1011 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 networks10 In several studies, after the subjects have had training to learn a declarative memory task, the density of human sleep spindles present was significantly higher than the signals observed during the control tasks that involved similar visual stimulation and cognitively-demanding tasks but did not require learning1213This associated with the spontaneously occurring wave oscillations that account for the intracellular recordings from thalamic and cortical neurons14

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 Glucose metabolism in the brain increases as a result of tasks that demand mental activity15 Another function affected by slow-wave sleep is the secretion of growth hormone, which is always greatest during this stage16 It is also thought to be responsible for a decrease in sympathetic and increase in parasympathetic neural activity16

Contents

  • 1 Electroencephalographic characteristics
  • 2 Functions of slow-wave sleep
    • 21 Neural control of slow-wave sleep
    • 22 Physical healing and growth
    • 23 Learning and synaptic homeostasis
  • 3 Problems associated with slow-wave sleep
    • 31 Effects of sleep deprivation
    • 32 Amyloid-beta pathology
  • 4 Individual differences in slow-wave sleep
  • 5 Drugs
  • 6 See also
  • 7 References

Electroencephalographic characteristicsedit

Polysomnogram demonstrating SWS, stage four
High amplitude EEG is highlighted in red

Large 75-microvolt 05–3 Hz delta waves predominate the electroencephalogram EEG Stage N3 is defined by the presence of 20% delta waves in any given 30-second epoch of the EEG during sleep, by the current 2007 AASM guidelines6

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

Slow-wave sleep is an active phenomenon probably brought about by the activation of serotonergic neurons of the raphe system17

The slow wave seen in the cortical EEG is generated through thalamocortical communication through the thalamocortical neurons18 In the TC neurons this is generated by the "slow oscillation" and is dependent on membrane potential bistability, a property of these neurons due to an electrophysiological component known as "I t window" "I t window" is due to the overlap underneath activation and inactivation curves if plotted for T-type calcium channels inward current If these two curves are multiplied, and another line superimposed on the graph to show a small Ik leak current outward, then the interplay between these inward I t window and outward small Ik leak, three equilibrium points are seen at −90, −70 and −60 mv, −90 and −60 being stable and −70 unstable This property allows the generation of slow waves due to an oscillation between two stable points It is important to note that in in vitro, mGluR must be activated on these neurons to allow a small Ik leak, as seen in in vivo situations

Functions of slow-wave sleepedit

Slow-wave sleep is necessary for survival Some animals, such as dolphins 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

Neural control of slow-wave sleepedit

Several neurotransmitters are involved in sleep and waking patterns: acetylcholine, norepinephrine, serotonin, histamine, and orexin19 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 the mental activity is closer to real life events14

Physical healing and growthedit

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 hormones are also secreted to facilitate the healing of muscles as well as repairing damage to any tissues Lastly, glial cells within the brain are restored with sugars to provide energy for the brain20

Learning and synaptic homeostasisedit

Learning and memory formation occurs during wakefulness by the process of long-term potentiation; 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 removed21 This may be helpful for recalibrating synapses for the next potentiation during wakefulness and for maintaining synaptic plasticity

Problems associated with slow-wave sleepedit

Bedwetting, night terrors, and sleepwalking are all common behaviors that can occur during stage three of sleep These occur most frequently amongst children, who then generally outgrow them15 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 out food, and will eat not having any memory of the event in the morning15 Over half of individuals with this disorder become overweight22 Sleep-related eating disorder can usually be treated with dopaminergic agonists, or topiramate, which is an anti-seizure medication This nocturnal eating throughout a family suggests that heredity may be a potential cause of this disorder15

Effects of sleep deprivationedit

See also: Fatal familial insomnia

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 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

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 today as the deepest part of stage-three sleep is more important than the other stages

During slow-wave sleep, there is a significant decline in cerebral metabolic rate and cerebral blood flow 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 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

According to J Siegel 2005, sleep deprivation results in the build-up of free radicals and superoxides 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 the existing radical species to clear This is a means of preventing damage to the brain23

Amyloid-beta pathologyedit

The accumulation of Amyloid beta Aβ in the prefrontal cortex is associated with the disruption or reduction of slow waves of NREM sleep Therefore, this may reduce the ability for memory consolidation in older adults24

Individual differences in slow-wave sleepedit

Though SWS is fairly consistent within the individual, it can vary across individuals Age and gender have been noted as two of the biggest factors that affect this period of sleep Aging is inversely proportional to the amount of SWS beginning by midlife and therefore, SWS declines with age Sex differences have also been found, such that females tend to have higher levels of SWS compared to males, at least up until menopause 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 eg body mass index, sleep-disordered breathing, obesity, diabetes, and hypertension this potential difference must be investigated further25

Drugsedit

The chemical gamma-hydroxybutyric acid GHB has been studied to increase SWS2627 In the United States, the Food and Drug Administration FDA permits the use of GHB under the trade name Xyrem to reduce cataplexy attacks and excessive daytime sleepiness in patients with narcolepsy

See alsoedit

Referencesedit

Notes

  1. ^ Lesku, J A; Meyer, L C R; Fuller, A; Maloney, S K; Dell'Omo, G; Vyssotski, A L; Rattenborg, N C 2011 Balaban, Evan, ed "Ostriches Sleep like Platypuses" PLoS ONE 6 8: e23203 doi:101371/journalpone0023203 PMC 3160860 PMID 21887239 
  2. ^ Rechtschaffen, A; Kales, A 1968 A Manual of Standardized Terminology, Techniques and Scoring System For Sleep Stages of Human Subjects US Dept of Health, Education, and Welfare; National Institutes of Health 
  3. ^ Carlson, Neil R 2012 Physiology of Behavior Pearson p 291 ISBN 0205239390
  4. ^ Schulz, Hartmut 2008 "Rethinking sleep analysis Comment on the AASM Manual for the Scoring of Sleep and Associated Events" J Clin Sleep Med American Academy of Sleep Medicine 4 2: 99–103 PMC 2335403 PMID 18468306 Although the sequence of non-REM NREM sleep stages one to four R&K classification or N1 to N3 AASM classification fulfills the criteria 
  5. ^ "Glossary A resource from the Division of Sleep Medicine at Harvard Medical School, Produced in partnership with WGBH Educational Foundation" Harvard University 2008 Retrieved 2009-03-11 The 1968 categorization of the combined Sleep Stages 3 - 4 was reclassified in 2007 as Stage N3 
  6. ^ a b 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; 2007
  7. ^ Carlson, Neil R 2012 Physiology of Behavior Pearson p 291,293 ISBN 0205239390
  8. ^ https://wwwnytimescom/2013/01/28/health/brain-aging-linked-to-sleep-related-memory-declinehtml
  9. ^ Walker, Matthew P 1 January 2008 "Sleep-Dependent Memory Processing" PDF Harvard Review of Psychiatry 16 5: 287–298 doi:101080/10673220802432517 ISSN 1067-3229 
  10. ^ a b http://walkerlabberkeleyedu/reprints/Walker_JCSM_2009pdf
  11. ^ Walker, Matthew P 15 April 2009 "The Role of Slow Wave Sleep in Memory Processing" Journal of Clinical Sleep Medicine : JCSM : Official Publication of the American Academy of Sleep Medicine 5 2 Suppl: S20–S26 ISSN 1550-9389 PMC 2824214 
  12. ^ Steriade, M 1 January 2006 "Grouping of brain rhythms in corticothalamic systems" PDF Neuroscience 137 4: 1087–f1106 doi:101016/jneuroscience200510029 
  13. ^ Gais, Steffen; Mölle, Matthias; Helms, Kay; Born, Jan 1 August 2002 "Learning-Dependent Increases in Sleep Spindle Density" Journal of Neuroscience 22 15: 6830–6834 ISSN 0270-6474 
  14. ^ a b http://wwwarchitalbiolorg/aib/article/viewFile/411/370
  15. ^ a b c d Carlson, Neil R 2012 Physiology of Behavior Pearson pp 297–298 ISBN 0205239390 
  16. ^ a b Slow-Wave Sleep: Beyond Insomnia Wolters Kluwer Pharma Solutions ISBN 978-0-9561387-1-2 
  17. ^ Jones, BE 1 May 2003 "Arousal systems" Frontiers in bioscience : a journal and virtual library 8: s438–51 ISSN 1093-9946 PMID 12700104 
  18. ^ Williams SR, Tóth TI, Turner JP, Hughes SW, Crunelli W 1997 The window component of the low threshold Ca2+ current produces input signal amplification and bistability in cat and rat thalamocortical neurons J Physiol 505:689–705
  19. ^ Carlson, Neil R 2012 Physiology of Behavior Pearson p 305-307 ISBN 0205239390
  20. ^ http://wwwhgiorguk/archive/sleepanddream1htm#U2kpm8fhjys
  21. ^ Tononi, Giulio; Cirelli, Chiara February 2006 "Sleep function and synaptic homeostasis" Sleep Medicine Reviews 10 1: 49–62 doi:101016/jsmrv200505002 PMID 16376591 
  22. ^ Carlson, Neil R 2012 Physiology of Behavior Pearson p 298 ISBN 0205239390
  23. ^ Carlson, Neil R 2012 Physiology of Behavior Pearson p 299-300 ISBN 0205239390
  24. ^ Mander, Bryce A; Marks, Shawn M; Vogel, Jacob W; Rao, Vikram; Lu, Brandon; Saletin, Jared M; Ancoli-Israel, Sonia; Jagust, William J; Walker, Matthew P 1 June 2015 "β-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation" Nature Neuroscience 18 7: 1051–1057 doi:101038/nn4035 
  25. ^ http://onlinelibrarywileycom/enhanced/doi/101111/j1365-2869201100959x/
  26. ^ Roehrs, Timothy; Roth, Thomas December 2010 "Drug-Related Sleep Stage Changes: Functional Significance and Clinical Relevance" Sleep Medicine Clinics 5 4: 559–570 doi:101016/jjsmc201008002 PMC 3041980 
  27. ^ http://wwwtheodoracom/drugs/eu/xyremhtml

Further reading

  • M Massimini, G Tononi, et al, "Breakdown of Cortical Effective Connectivity During Sleep," Science, vol 309, 2005, pp 2228–32
  • P Cicogna, V Natale, M Occhionero, and M Bosinelli, "Slow Wave and REM Sleep Mentation," Sleep Research Online, vol 3, no 2, 2000, pp 67–72
  • D Foulkes et al, "Ego Functions and Dreaming During Sleep Onset," in Charles Tart, ed, Altered States of Consciousness, p 75
  • Rock, Andrea 2004 The Mind at Night 
  • Warren, Jeff 2007 "The Slow Wave" The Head Trip: Adventures on the Wheel of Consciousness ISBN 978-0-679-31408-0 

slow-wave sleep, slow-wave sleep (sws), slow-wave sleep induction, slow-wave sleep is comprised of, slow-wave sleep occurs during, slow-wave sleep promotes


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