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1.3.7 睡眠&大脑神经是否兴奋
分泌excrete
大逻辑:
---开始就是一个问题,问人们为什么要睡觉,也就是睡觉的作用。后边就开始进行解释。人在醒的时候特别在learning时大脑中某种s东东会很active, 然后就消耗很多能量。为了recover这些能量就睡觉了。
---发现在慢波睡眠slow-wave sleep时这些wave会减慢s东东的active level,然后s 东东歇了,能量就recovered了。从而使人们在醒了以后更有效的进行记忆。
---研究还发现慢波的wave越强的地方就是在白天s东东最活跃的地方。
考题:
1.人为什么要睡觉:
我选得为了recover 能量。
2.还有为什么slow-wave 开始强慢慢变弱?
我说因为slow-wave开始要减弱s东东,但是等s东东被减弱了也就不需要那么强的slow-wave了。
Q: 怎样让大脑恢复:
选 SLEEP,就一个单词,
干扰选项:slow wave.
Q: 一个说为什么睡眠中short wave越来越弱
选因为它要抑制的什么connetion越来越弱 这个确定
Sleep timing
Sleep timing is controlled by the circadian clock, by homeostasis and, in humans, by willed behavior. The circadian clock, an inner time-keeping, temperature-fluctuating, enzyme-controlling device, works in tandem with adenosine, a neurotransmitter which inhibits many of the bodily processes that are associated with wakefulness. Adenosine is created over the course of the day; high levels of adenosine lead to sleepiness. In diurnal animals, sleepiness occurs as the circadian element causes the release of the hormone melatonin and a gradual decrease in core body temperature. The timing is affected by one's chronotype. It is the circadian rhythm which determines the ideal timing of a correctly structured and restorative sleep episode.[5]
Homeostatic sleep propensity, the need for sleep as a function of the amount of time elapsed since the last adequate sleep episode, is also important and must be balanced against the circadian element for satisfactory sleep. Along with corresponding messages from the circadian clock, this tells the body it needs to sleep.[6] Sleep offset, awakening, is primarily determined by circadian rhythm. A normal person who regularly awakens at an early hour will generally not be able to sleep much later than the person's normal waking time, even if moderately sleep deprived.
The chemical adenosine is released by brain cells when those cells are active. Adenosine then binds to more and more sites on cells in certain areas of the brain, as the total amount released gradually increases during wakefulness. During sleep, the number of sites to which adenosine is bound decreases. Some researchers have hypothesized that it is the cumulative binding of adenosine to a large number of sites that causes the onset of sleep. Some scientists believe that adenosine promotes sleepiness by targeting arousal networks in the brain such as the cholinergic system (see arrows). Research shows that increasing levels of adenosine in two parts of the system, the cholinergic basal forebrain and the mesopontine cholinergic nuclei, spurs slumber.
http://www.sfn.org/index.cfm?pag ... s_adenosineAndSleep
Slow-wave sleep (SWS) is stage three and four of non-rapids eye movement sleep. These two stages are often referred to as deep sleep.
The highest arousal thresholds (e.g. difficulty of awakening, such as by a sound of a particular volume) are observed in stages four and three, respectively. A person will typically feel groggier (tired, weak) when awoken from these stages, and indeed, cognitive tests administered after awakening from stages 3-4 indicate that mental performance is somewhat impaired for periods up to 30 minutes or so, relative to awakenings from other stages. This phenomenon has been called "sleep inertia."
As of 2008, the American Academy of Sleep Medicine (AASM) has discontinued the use of stage 4. [Citation needed] If an epoch (or 30 seconds of sleep) has anywhere from 20% to 100% of it as slow wave/delta sleep, then it is considered stage 3.
After sleep deprivation there is a sharp rebound of SWS, suggesting there is a "need" for this stage. 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 few 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. The latter probably exerts its influence by increasing body temperature. [Citation needed]
In addition to these factors, the duration of SWS periods can be increased by ingestion of alcohol, THC, SSRIs, and other drugs. In instances such as these, TST (Total Sleep Time) is often unaffected due to circadian rhythms and/or a person's alarm clock and early morning obligations. This increase of SWS can lead to increased REM latency and a decrease in REM period durations. If the total time spent in REM is decreased long enough and repeatedly over a substantial number of nights a "REM rebound" will occur in response to removal of its inhibitor. An increase in REM 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 or not this could explain the return in symptoms of depression disorder after removal of SSRI medications.
Certain substances, such as benzodiazepines (e.g. Ativan, Valium, and 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. |
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