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Slow-wave sleep (SWS), often referred to as deep sleep, consists of stage three of non-rapid eye movement sleep, according to the Rechtschaffen & Kales (R & K) standard of 1968. There is not a clear distinction between stages three and four. Stage three has 20-50 percent delta activity, whereas stage four has more than 50 percent.〔Carlson, Neil R. (2012). Physiology of Behavior. Pearson. p. 291. ISBN 0205239390.〕 As of 2008, the American Academy of Sleep Medicine (AASM) has discontinued the use of stage four,〔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.〕 such that the previous stages three and four now are combined as stage three. An epoch (30 seconds of sleep) which consists of 20% or more slow-wave (delta) sleep, now is 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 period 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 period in which the neurons fire briefly at a high rate. The former state is a hyperpolarizing phase and the latter is a depolarizing phase. 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 activity.〔Carlson, Neil R. (2012). Physiology of Behavior. Pearson. p. 291,293. ISBN 0205239390.〕 Slow-wave sleep is considered important to consolidate new memories.〔http://www.nytimes.com/2013/01/28/health/brain-aging-linked-to-sleep-related-memory-decline.html〕 This is sometimes referred to as "sleep-dependent memory processing". Impaired memory consolidation has been effected in individuals with primary insomnia who thus do not perform as well as normal patients in memory tasks following a period of sleep. Furthermore, slow-wave sleep improves declarative memory, which is the fact-based, or 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.〔http://walkerlab.berkeley.edu/reprints/Walker_JCSM_2009.pdf〕 In several studies, after the subjects have had training to learn a declarative memory task, the density of human sleep spindles was significantly higher compared to the non-learning control task. This is the result of the spontaneously occurring wave oscillations that account for the intracellular recordings from thalamic and cortical neurons.〔http://www.architalbiol.org/aib/article/viewFile/411/370〕 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 activity.〔 Another function affected by slow-wave sleep is the secretion of growth hormone, which is always greatest during this stage. It is also thought to be responsible for a decrease in sympathetic and increase in parasympathetic neural activity.〔 ==Discussion== The highest arousal thresholds (i.e. difficulty of awakening, such as by a sound of a particular volume) are observed in deep sleep. A person will typically feel more groggy when awoken from slow-wave sleep, and indeed, cognitive tests administered after awakening then indicate that mental performance is somewhat impaired for periods of up to 30 minutes, relative to awakenings from other stages. This phenomenon has been called "sleep inertia". After sleep deprivation there is a sharp rebound of SWS, that is, the following bout of sleep will include more and deeper SWS than normal.The duration of slow-wave sleep is determined by the previous duration of this stage as well as the duration of prior wakefulness.〔 The major factor determining how much slow-wave sleep is observed in a given sleep period is the duration of preceding wakefulness, likely related to accumulation of sleep-promoting substances in the brain. Some of the factors known to increase slow-wave sleep in the sleep period that follows them include body heating (as by immersion in a hot tub), high carbohydrate ingestion , and intense prolonged exercise. Studies have shown, slow-wave sleep is enabled when brain temperature surpasses a certain threshold. It is hypothesized that the threshold is regulated by circadian and homeostatic processes. In healthy sleepers, a very low carbohydrate diet over the short-term promotes increases in the percentage of SWS (deep sleep stage four) and a reduction in the percentage of REM sleep (dreaming sleep) compared to the control with a mixed diet - the sleep changes may be linked to the metabolism of the fat content of the very low carbohydrate diet. In addition to these factors, the duration of SWS periods can be increased by the ingestion of certain SSRI, and other antidepressants, whereas the effects of THC on SWS remain controversial. In instances such as these, total sleep time (TST) is often unaffected due to circadian rhythms, a person's alarm clock, or early morning obligations. This increase of SWS can lead to increased REM latency and a decrease in REM period duration. If the total time spent in REM sleep is decreased long enough and repeatedly over a substantial number of nights a "REM rebound" will occur in response to the removal of its inhibitor. An increase in REM sleep is believed to produce symptoms of depression and bipolar disorder in many patients for an amount of time relative to the severity of the previous REM suppression. It is debatable whether this explains the return in symptoms of depression disorder after removal of SSRI medications. Certain substances, such as benzodiazepines (e.g. Ativan, Valium, Klonopin), seem to have the reverse effect on the time spent in SWS. Instead of lengthening SWS (as do the substances mentioned above), they are known to shorten the time. While these sedatives can increase sleep duration or shorten the time it takes before sleep-onset occurs, they tend to deprive patients of deep sleep. The chemical gamma-hydroxybutyric acid (GHB) is known to promote SWS.〔http://www.theodora.com/drugs/eu/xyrem.html〕 In the United States, the Food and Drug Administration permits the use of GHB under the trade name Xyrem to reduce cataplexy attacks and excessive daytime sleepiness in patients with narcolepsy. Reduced slow-wave sleep (SWS) may predict high blood pressure in older men.〔http://www.brighamandwomens.org/about_bwh/publicaffairs/news/pressreleases/PressRelease.aspx?sub=0&PageID=942〕 A study from the Department of Endocrinology at Boston Children's Hospital, an affiliate of Harvard Medical School, indicated that regular deep sleep in children is helpful in triggering the steady release of the hormones that cause puberty.〔http://www.massgeneral.org/about/pressrelease.aspx?id=1502〕 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Slow-wave sleep」の詳細全文を読む スポンサード リンク
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