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 [[File:Normal EEG of mouse.png|thumb|300px|EEG of a mouse. REM sleep is characterized by prominent theta-rhythm]]
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-'''Rapid eye movement sleep''' ('''REM sleep''', '''REMS''') is a unique phase of mammalian [[sleep]] characterized by random movement of the [[eye]]s, low [[muscle tone]] throughout the body, and the propensity of the sleeper to [[dream]] vividly. This phase is also known as '''paradoxical sleep''' ('''PS''') and sometimes '''desynchronized sleep''' because of physiological similarities to waking states, including rapid, low-voltage desynchronized [[neural oscillations|brain waves]]. Electrical and chemical activity regulating this phase seems to originate in the [[brain stem]] and is characterized most notably by an abundance of the [[neurotransmitter]] [[acetylcholine]], combined with a nearly complete absence of [[monoamine]] neurotransmitters histamine, serotonin, and norepinephrine.<ref name=Horne2013>Jim Horne (2013), “Why REM sleep? Clues beyond the laboratory in a more challenging world”, ''Biological Psychology'' 92.</ref> The cortical and thalamic neurons of the waking or paradoxically sleeping brain are more depolarized—i.e., can "fire" more readily—than in the deeply sleeping brain.<ref>Steriade & McCarley (1990), ''Brainstem Control of Wakefulness and Sleep", §8.1 (pp. 232–243).</ref> The right and left hemispheres of the brain are more [[Brain connectivity estimators|coherent]] in REM sleep, especially during [[lucid dream]]s.<ref>Jayne Gackenbach, “Interhemispheric EEG Coherence in REM Sleep and Meditation: The Lucid Dreaming Connection” in Antrobus & Bertini (eds.), ''The Neuropsychology of Sleep and Dreaming''.</ref>
-REM sleep is punctuated and immediately preceded by [[PGO waves|PGO (ponto-geniculo-occipital) waves]], bursts of electrical activity originating in the brain stem.<ref>Steriade & McCarley (1990), ''Brainstem Control of Wakefulness and Sleep", §9.1–2 (pp. 263–282).</ref> These waves occur in clusters about every 6 seconds for 1–2 minutes during the transition from deep to paradoxical sleep.<ref name=SteriadeMcCarley1.3>Steriade & McCarley (1990), ''Brainstem Control of Wakefulness and Sleep", §1.2 (pp. 7–23).</ref> They exhibit their highest amplitude upon moving into the [[visual cortex]] and are a cause of the "rapid eye movements" in paradoxical sleep.<ref name=Datta>Subimal Datta (1999), "PGO Wave Generation: Mechanism and functional significance", in ''Rapid Eye Movement Sleep'' ed. Mallick & Inoué.</ref><ref name=ErmisEtAl />
-Brain energy use in REM sleep, as measured by oxygen and glucose metabolism, equals or exceeds energy use in waking. The rate in non-REM sleep is 11–40% lower.<ref name=HobsonEtAl2000 />
-== Chemicals in brain ==
-Compared to slow-wave sleep, both waking and paradoxical sleep involve higher use of the neurotransmitter [[acetylcholine]], which may cause the faster brainwaves. The  [[monoamine]] neurotransmitters [[norepinephrine]], [[serotonin]] and [[histamine]] are completely unavailable. Injections of [[acetylcholinesterase inhibitor]], which effectively increases available acetylcholine, have been found to induce paradoxical sleep in humans and other animals already in slow-wave sleep. [[Carbachol]], which mimics the effect of acetylcholine on neurons, has a similar influence. In waking humans, the same injections produce paradoxical sleep only if the monamine neurotransmitters have already been depleted.<ref name=BrownMcCarley>Ritchie E. Brown & Robert W. McCarley (2008), "Neuroanatomical and neurochemical basis of wakefulness and REM sleep systems", in ''Neurochemistry of Sleep and Wakefulness'' ed. Monti et al.</ref><ref name=MallickEtAl>Birendra N. Mallick, Vibha Madan, & Sushil K. Jha (2008), "Rapid eye movement sleep regulation by modulation of the noradrenergic system", in ''Neurochemistry of Sleep and Wakefulness'' ed. Monti et al.</ref><ref name=Hobson2009>{{cite journal | author = Hobson JA | title = REM sleep and dreaming: towards a theory of protoconsciousness | journal = Nature Reviews | volume = 10 | issue = 11 | pages = 803–813 | year = 2009 | pmid = 19794431 | doi = 10.1038/nrn2716 }}</ref><ref name=AstonJonesEtAl>Aston-Jones G., Gonzalez M., & Doran S. (2007). "Role of the locus coeruleus-norepinephrine system in arousal and circadian regulation of the sleep-wake cycle." Ch. 6 in ''Brain Norepinephrine: Neurobiology and Therapeutics''. G.A. Ordway, M.A. Schwartz, & A. Frazer, eds. Cambridge UP. 157–195. Accessed 21 Jul. 2010. [http://academicdepartments.musc.edu/neuromodulation/epapers/Aston-JonesetalLCsleepOrdway07.pdf Academicdepartments.musc.edu]</ref><ref>Siegel J.M. (2005). "REM Sleep." Ch. 10 in ''Principles and Practice of Sleep Medicine''. 4th ed. M.H. Kryger, T. Roth, & W.C. Dement, eds. Elsevier. 120–135.</ref>
-Two other neurotransmitters, [[orexin]] and [[gamma-Aminobutyric acid]] (GABA), seem to promote wakefulness, diminish during deep sleep, and inhibit paradoxical sleep.<ref name=BrownMcCarley /><ref name=LuppiEtAl>Pierre-Hervé Luppi et al. (2008), "Gamma-aminobutyric acid and the regulation of paradoxical, or rapid eye movement, sleep", in ''Neurochemistry of Sleep and Wakefulness'' ed. Monti et al.</ref>
-Unlike the abrupt transitions in electrical patterns, the chemical changes in the brain show continuous periodic oscillation.<ref name=McCarley2007>Robert W. McCarley (2007), “Neurobiology of REM and NREM sleep”, ''Sleep Medicine'' 8.</ref>
-== Role of brain stem ==
-Neural activity during REM sleep seems to originate in the [[brain stem]], especially the [[pontine tegmentum]] and [[locus coeruleus]]. According to the [[activation-synthesis hypothesis]] proposed by [[Robert McCarley]] and [[Allan Hobson]] in 1975–1977, control over REM sleep involves pathways of "REM-on" and "REM-off" neurons in the brain stem. REM-on neurons are primarily cholinergic (i.e., involve acetylcholine); REM-off neurons activate serotonin and noradrenaline, which among other functions suppress the REM-on neurons. McCarley and Hobson suggested that the REM-on neurons actually stimulate REM-off neurons, thereby serving as the mechanism for the cycling between REM and non-REM sleep.<ref name=BrownMcCarley /><ref name=MallickEtAl /><ref name=AstonJonesEtAl /><ref name=HobsonMcCarley1977>J. Alan Hobson & Robert W. McCarley, “The Brain as a Dream-State Generator: An Activation-Synthesis Hypothesis of the Dream Process”, ''American Journal of Psychiatry'' 134.12, December 1977.</ref> They used [[Lotka–Volterra equation]]s to describe this cyclical inverse relationship.<ref>Steriade & McCarley (1990), ''Brainstem Control of Wakefulness and Sleep", §12.2 (pp. 369–373).</ref>  Kayuza Sakai and Michel Jouvet advanced a similar model in 1981.<ref name=LuppiEtAl /> Whereas acetylcholine manifests in the cortex equally during wakefulness and REM, it appears in higher concentrations in the brain stem during REM.<ref>Ralph Lydic & Helen A. Baghdoyan, "Acetylcholine modulates sleep and wakefulness: a synaptic perspective", in ''Neurochemistry of Sleep and Wakefulness'' ed. Monti et al.</ref> The withdrawal of orexin and GABA  may cause the absence of the other excitatory neurotransmitters.<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', p. 16.</ref>
-Research in the 1990s using [[positron emission tomography]] confirmed the role of the brain stem. It also suggested that, within the [[forebrain]], the [[limbic]] and [[paralimbic cortex|paralimbic]] systems, generally connected with [[emotion]] showed more activation than other areas. The areas activated during REM sleep are approximately inverse to those activated during non-REM sleep.<ref name=HobsonEtAl2000 />
-== Eye movements ==
-Most of the [[eye movements]] in “rapid eye movement” sleep are in fact more rapid than those normally exhibited by waking humans. They are also longer in duration and more likely to loop back to their starting point. About six of such loops take place over one minute of REM sleep. Whereas in slow-wave sleep the eyes can drift apart, the eyes of the paradoxical sleeper move in tandem.<ref>Steriade & McCarley (1990), ''Brainstem Control of Wakefulness and Sleep", §10.7.2 (pp. 307–309).</ref> These eye movements follow the ponto-geniculo-occipital waves originating in the brain stem.<ref name=Datta /><ref name=ErmisEtAl /> The eye movements themselves may relate to the sense of vision experienced in the dream,<ref>{{cite journal |last=Andrillon |first=Thomas |last2=Nir |first2=Yuval |last3=Cirelli |first3=Chiara |last4=Tononi |first4=Giulio |last5=Fried |first5=Itzhak |display-authors=1 |date=2015 |title=Single neuron activity and eye movements during human REM sleep and awake vision |url=http://www.nature.com/articles/ncomms8884 |journal=Nature Communications |volume=6 |issue=1038 |pages= 7884|doi=10.1038/ncomms8884 |access-date=2 September 2016 |pmid=26262924 |pmc=4866865}}</ref> but a direct relationship remains to be clearly established. Congenitally blind people, who do not typically have visual imagery in their dreams,  still move their eyes in REM sleep.<ref name=HobsonEtAl2000 /> An alternative explanation of the rapid eye movement is proposed by Jie Zhang. He suggests that the functional purpose of REM sleep is for procedural memory processing, and the rapid eye movement is only an external manifestation of the brain processing the eye-related procedural memory.<ref>{{cite book |last=Zhang |first=Jie |year=2005 |title=Continual-activation theory of dreaming, Dynamical Psychology |url=http://www.goertzel.org/dynapsyc/2005/ZhangDreams.htm}}</ref><ref>{{cite book |last=Zhang |first=Jie |year=2016 |title=Towards a comprehensive model of human memory, DOI: 10.13140/RG.2.1.2103.9606 |url=https://www.researchgate.net/publication/304604880_Towards_a_comprehensive_model_of_human_memory}}</ref>
-== Circulation, respiration, and thermoregulation ==
-Generally speaking, the body suspends [[homeostasis]] during paradoxical sleep. [[Heart rate]], cardiac pressure, cardiac output, arterial pressure, and [[respiratory rate|breathing rate]] quickly become irregular when the body moves into REM sleep.<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', p. 12–15.</ref> In general, respiratory reflexes such as response to hypoxia diminish. Overall, the brain exerts less control over breathing; electrical stimulation of respiration-linked brain areas does not influence the lungs, as it does during non-REM sleep and in waking.<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', p. 22–27.</ref> The fluctuations of heart rate and arterial pressure tend to coincide with PGO waves and rapid eye movements, twitches, or sudden changes in breathing.<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', p. 35–37</ref>
-[[Erection]]s of the [[penis]] ([[nocturnal penile tumescence]] or NPT) normally accompany REM sleep in rats and humans.<ref>Jouvet (1999), ''The Paradox of Sleep'', pp. 169–173.</ref> If a male has erectile dysfunction (ED) while awake, but has NPT episodes during REM, it would suggest that the ED is from a psychological rather than a physiological cause. In females, erection of the [[clitoris]] ([[nocturnal clitoral tumescence]] or NCT) causes enlargement, with accompanying vaginal blood flow and transudation (i.e. lubrication). During a normal night of sleep the penis and clitoris may be erect for a total time of from one hour to as long as three and a half hours during REM.<ref>Brown ''et al.'' (2012), “Control of Sleep and Wakefulness”, p. 1127.</ref>
-Body temperature is not well regulated during REM sleep, and thus organisms become more sensitive to temperatures outside their [[thermoneutral zone]]. Cats and other small furry mammals will [[shiver]] and [[tachypnea|breathe faster]] to regulate temperature during NREMS but not during REMS.<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', p. 12–13.</ref> With the loss of muscle tone, animals lose the ability to regulate temperature through body movement. (However, even cats with pontine lesions preventing muscle atonia during REM did not regulate their temperature by shivering.)<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', pp. 46–47.</ref> Neurons which typically activate in response to cold temperatures—triggers for neural thermoregulation—simply do not fire during REM sleep, as they do in NREM sleep and waking.<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', pp. 51–52.</ref>
-Consequently, hot or cold environmental temperatures can reduce the proportion of REM sleep, as well as amount of total sleep.<ref>Ronald Szymusiak, Md. Noor Alam, & Dennis McGinty (1999), "Thermoregulatory Control of the NonREM-REM Sleep Cycle", in ''Rapid Eye Movement Sleep'' ed. Mallick & Inoué.</ref><ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', pp. 57–59.</ref> In other words, if at the end of a phase of deep sleep, the organism's thermal indicators fall outside of a certain range, it will not enter paradoxical sleep lest deregulation allow temperature to drift further from the desirable value.<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', p. 45. “Therefore, it appears that the onset of REM sleep requires the inactivation of the central thermostat in late NREM sleep. However, only a restricted range of preoptic-hypothalamic temperatures at the end of NREM sleep is compatible with REM sleep onset. This range may be considered a sort of temperature gate for REM sleep, that is constrained in width more at low than at neutral ambient temperature.”</ref> This mechanism can be 'fooled' by artificially warming the brain.<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', p. 61. “On the other hand, a balance between opposing ambient and preoptic-anterior hypothalamic thermal loads influencing peripheral and central thermoreceptors, respectively, may be experimentally achieved so as to promote sleep. In particular, warming of the preoptic-anterior hypothalamic region in a cold environment hastens REM sleep onset and increases its duration (Parmeggiana ''et al''., 1974, 1980; Sakaguchi ''et al''., 1979).”</ref>
-== Muscle ==
-'''REM atonia''', an almost complete paralysis of the body, is accomplished through the inhibition of [[motor neuron]]s. When the body shifts into REM sleep, motor neurons throughout the body undergo a process called [[hyperpolarization (biology)|hyperpolarization]]: their already-negative [[membrane potential]] decreases by another 2–10 millivolts, thereby raising the threshold which a stimulus must overcome to excite them. Muscle inhibition may result from unavailability of monoamine neurotransmitters (restraining the abundance of acetylcholine in the brainstem) and perhaps from mechanisms used in waking muscle inhibition.<ref>Steriade & McCarley (1990), ''Brainstem Control of Wakefulness and Sleep", §10.8–9 (pp. 309–324).</ref> The [[medulla oblongata]], located between pons and spine, seems to have the capacity for organism-wide muscle inhibition.<ref name=LaiSiegel>Yuan-Yang Lai & Jerome M. Siegel (1999), "Muscle Atonia in REM Sleep", in ''Rapid Eye Movement Sleep'' ed. Mallick & Inoué.</ref> Some localized twitching and reflexes can still occur.<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', p. 17. “In other words, the functional controls requiring high hierarchical levels of integration are the most affected during REM sleep, whereas reflex activity is only altered but not obliterated.”</ref>
-Lack of REM [[atonia]] causes [[REM behavior disorder]], sufferers of which physically act out their dreams.<ref name="pmid1620348">{{cite journal |vauthors=Lapierre O, Montplaisir J | title = Polysomnographic features of REM sleep behavior disorder: development of a scoring method | journal = Neurology | volume = 42 | issue = 7 | pages = 1371–4 | year = 1992 | pmid = 1620348 | doi = 10.1212/wnl.42.7.1371}}</ref> (An alternative explanation of this relationship is that the sleeper "dreams out the act": that the muscle impulse precedes the mental image. This explanation could also apply to normal sleepers whose commands to their muscles are suppressed.)<ref>Steriade & McCarley (1990), ''Brainstem Control of Wakefulness and Sleep", §13.3.2.3 (pp. 428–432).</ref> (Note that conventional [[sleepwalking]] takes place during slow-wave sleep.)<ref>Jouvet (1999), ''The Paradox of Sleep'', p. 102.</ref> [[Narcolepsy]] by contrast seems to involve excessive and unwanted REM atonia—i.e., [[cataplexy]] and [[excessive daytime sleepiness]] while awake, [[hypnagogic hallucinations]] before entering slow-wave sleep, or [[sleep paralysis]] while waking.<ref>Steriade & McCarley (1990), ''Brainstem Control of Wakefulness and Sleep", §13.1 (pp. 396–400).</ref> Other psychiatric disorders including depression have been linked to disproportionate REM sleep.<ref>Steriade & McCarley (1990), ''Brainstem Control of Wakefulness and Sleep", §13.2 (pp. 400–415).</ref> Patients with suspected sleep disorders are typically evaluated by [[polysomnogram]].<ref>{{cite journal | author = Koval'zon VM | title = [Central mechanisms of sleep-wakefulness cycle]. | journal = Fiziologiia cheloveka | volume = 37 | issue = 4 | pages = 124–34 | date = Jul–Aug 2011 | pmid = 21950094 }}</ref><ref>{{cite web|title=[Polysomnography].|url=http://www.nlm.nih.gov/medlineplus/ency/article/003932.htm|accessdate=2 November 2011}}</ref>
-Lesions of the pons to prevent atonia have induced functional “REM behavior disorder” in animals.<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', p. 87. “The open-loop mode of physiological regulation in REM sleep may restore the efficiency of the different neuronal networks of the brain stem by expressing also genetically coded patterns of instinctive behavior that are kept normally hidden from view by skeletal muscle atonia. Such behaviorally concealed neuronal activity was demonstrated by the effects of experimental lesions of specific pontine structures (Hendricks, 1982; Hendricks ''et al''., 1977, 1982; Henley and Morrison, 1974; Jouvet and Delorme, 1965; Sastre and Jouvet, 1979; Villablanca, 1996). Not only was the skeletal muscle atonia suppressed by also motor fragments of complex instinctive behaviors appeared, such as walking and attack, that were not externally motivated (see Morrison, 2005).”</ref>
-== Psychology ==
-=== Dreaming ===
-Rapid eye movement sleep (REM) has since its discovery been closely associated with [[dream]]ing. Waking up sleepers during a REM phase is a common experimental method for obtaining dream reports; 80% of neurotypical people can give some kind of dream report under these circumstances.<ref>Solms (1997), ''The Neuropsychology of Dreams'', pp. 10, 34.</ref> Sleepers awakened from REM tend to give longer more [[narrative]] descriptions of the dreams they were experiencing, and to estimate the duration of their dreams as longer.<ref name=HobsonEtAl2000>J. Alan Hobson, Edward F. Pace-Scott, & Robert Stickgold (2000), “Dreaming and the brain: Toward a cognitive neuroscience of conscious states”, ''Behavioral and Brain Sciences'' 23.</ref><ref name=Reinsel1992 /> [[Lucid dream]]s are reported far more often in REM sleep.<ref>Stephen LaBerge (1992), “Physiological Studies of Lucid Dreaming”, in Antrobus & Bertini (eds.), ''The Neuropsychology of Sleep and Dreaming''.</ref> (In fact these could be considered a hybrid state combining essential elements of REM sleep and waking consciousness.)<ref name=HobsonEtAl2000 /> The mental events which occur during REM most commonly have dream hallmarks including narrative structure, convincingness (experiential resemblance to waking life), and incorporation of instinctual themes.<ref name=HobsonEtAl2000 />
-Hobson and McCarley proposed that the PGO waves characteristic of “phasic” REM might supply the visual cortex and forebrain with electrical excitement which amplifies the hallucinatory aspects of dreaming.<ref name=Hobson2009 /><ref name=HobsonMcCarley1977 /> However, people woken up during sleep do not report significantly more bizarre dreams during phasic REMS, compared to tonic REMS.<ref name=Reinsel1992 /> Another possible relationship between the two phenomena could be that the higher threshold for sensory interruption during REM sleep allows the brain to travel further along unrealistic and peculiar trains of thought.<ref name=Reinsel1992 />
-Some dreaming can take place during non-REM sleep. “Light sleepers” can experience dreaming during stage 2 non-REM sleep, whereas “deep sleepers”, upon awakening in the same stage, are more likely to report “thinking” but not “dreaming”. Certain scientific efforts to assess the uniquely [[wikt:bizarre|bizarre]] nature of dreams experienced while asleep were forced to conclude that waking thought could be just as bizarre, especially in conditions of [[sensory deprivation]].<ref name=Reinsel1992>Ruth Reinsel, John Antrobus, & Miriam Wollman (1992), “Bizarreness in Dreams and Waking Fantasy”, in Antrobus & Bertini (eds.), ''The Neuropsychology of Sleep and Dreaming''.</ref><ref>Delphine Ouidette et al. (2012), “Dreaming without REM sleep”, ''Consciousness and Cognition'' 21.</ref> Because of non-REM dreaming, some sleep researchers have strenuously contested the importance of connecting dreaming to the REM sleep phase. The prospect that well-known neurological aspects of REM do not themselves cause dreaming suggests the need to re-examine the neurobiology of dreaming ''per se''.<ref>Solms (1997), ''The Neuropsychology of Dreams'', Chapter 6: “The Problem of REM Sleep” (pp. 54–57).”</ref> Some researchers (Dement, Hobson, Jouvet, for example) tend to resist the idea of disconnecting dreaming from REM sleep.<ref name=HobsonEtAl2000 /><ref>Jouvet (1999), ''The Paradox of Sleep'', p. 104. “I frankly support the theory that we do not dream all night, as do William Dement and Alan Hobson and most neurophysiologists. I am rather surprised that publications about dream recall during slow wave sleep increase in number each year. Further, the classic distinction established in the 1960s between 'poor' dream recall, devoid of color and detail, during slow wave sleep, and 'rich' recall, full of color and detail, during paradoxical sleep, is beginning to disappear. I believe that dream recall during slow wave sleep could be recall from previous paradoxical sleep.”</ref>
-=== Creativity ===
-After waking from REM sleep, the mind seems “hyperassociative”—more receptive to [[semantic priming]] effects. People awakened from REM have performed better on tasks like [[anagram]]s and creative problem solving.<ref name=RaschBorn2013>Rasch & Born (2013), “About Sleep's Role in Memory”, p. 688.</ref>
-Sleep aids the process by which [[creativity]] forms associative elements into new combinations that are useful or meet some requirement.<ref>{{cite journal |vauthors=Wagner U, Gais S, Haider H, Verleger R, Born J | title = Sleep inspires insight | journal = Nature | volume = 427 | issue = 6972 | pages = 352–5 | year = 2004 | pmid = 14737168 | doi = 10.1038/nature02223 }}</ref> This occurs in REM sleep rather than in NREM sleep.<ref name="Cai">{{cite journal |vauthors=Cai DJ, Mednick SA, Harrison EM, Kanady JC, Mednick SC | title = REM, not incubation, improves creativity by priming associative networks | journal = Proc Natl Acad Sci U S A | volume = 106 | issue = 25 | pages = 10130–10134 | year = 2009 | pmid = 19506253 | pmc = 2700890 | doi = 10.1073/pnas.0900271106 }}</ref><ref>{{cite journal |vauthors=Walker MP, Liston C, Hobson JA, Stickgold R | title = Cognitive flexibility across the sleep-wake cycle: REM-sleep enhancement of anagram problem solving | journal = Brain research. Cognitive brain research | volume = 14 | issue = 3 | pages = 317–24 | date = November 2002 | pmid = 12421655 | doi = 10.1016/S0926-6410(02)00134-9 }}</ref> Rather than being due to memory processes, this has been attributed to changes during REM sleep in [[cholinergic]] and [[noradrenergic]] [[Neuromodulation (biology)|neuromodulation]].<ref name="Cai"/> High levels of acetylcholine in the hippocampus suppress feedback from hippocampus to the [[neocortex]], while lower levels of acetylcholine and norepinephrine in the neocortex encourage the uncontrolled spread of associational activity within neocortical areas.<ref>{{cite journal | author = Hasselmo ME | title = Neuromodulation: acetylcholine and memory consolidation | journal = Trends in Cognitive Sciences | volume = 3 | issue = 9 | pages = 351–359 | date = September 1999 | pmid = 10461198 | doi = 10.1016/S1364-6613(99)01365-0 }}</ref> This is in contrast to waking consciousness, where higher levels of norepinephrine and acetylcholine inhibit recurrent connections in the neocortex. REM sleep through this process adds creativity by allowing "neocortical structures to reorganise associative hierarchies, in which information from the hippocampus would be reinterpreted in relation to previous semantic representations or nodes."<ref name="Cai"/>
-== Timing ==
-[[File:Sleep Hypnogram.svg|thumb|391px|Sample [[hypnogram]] (electroencephalogram of sleep) showing sleep cycles characterized by increasing paradoxical (REM) sleep.]]
-In the ''ultradian sleep cycle'' an organism alternates between deep sleep (slow, large, synchronized brain waves) and paradoxical sleep (faster, desynchronized waves). Sleep happens in the context of the larger [[circadian rhythm]], which influences sleepiness and physiological factors based on timekeepers within the body. Sleep can be distributed throughout the day or clustered during one part of the rhythm: in [[nocturnal]] animals, during the day, and in [[diurnality|diurnal]] animals, at night.<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', p. 9–11.</ref> The organism returns to homeostatic regulation almost immediately after REM sleep ends.<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', p. 17.</ref>
-During a night of sleep, humans usually experience about four or five periods of REM sleep; they are quite short at the beginning of the night and longer toward the end. Many animals and some people tend to wake, or experience a period of very light sleep, for a short time immediately after a bout of REM. The relative amount of REM sleep varies considerably with age. A newborn baby spends more than 80% of total sleep time in REM.<ref name="pmid10938176">{{cite journal |vauthors=Van Cauter E, Leproult R, Plat L | title = Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men | journal = JAMA | volume = 284 | issue = 7 | pages = 861–8 | year = 2000 | pmid = 10938176 | doi = 10.1001/jama.284.7.861 }}</ref> During REM, the activity of the brain's [[neuron]]s is quite similar to that during waking hours; for this reason, the REM-sleep stage may be called paradoxical sleep.<ref name="myers7e">{{cite book |last=Myers |first=David |authorlink=David Myers (academic) |title=Psychology |edition=7th |year=2004 |publisher=Worth Publishers |location=New York |isbn=0-7167-8595-1 |page=268 |url=https://books.google.com/?id=oYuBwPDsQZoC&lpg=PP1&dq=0716785951&pg=PA268 |accessdate=2010-01-09}}</ref>
-REM sleep typically occupies 20–25% of total sleep in adult humans: about 90–120 minutes of a night's sleep. The first REM episode occurs about 70 minutes after falling asleep. Cycles of about 90 minutes each follow, with each cycle including a larger proportion of REM sleep.<ref name=McCarley2007 />
-Infants spend more time in higher REM sleep than adults. The proportion of REM sleep then decreases significantly in childhood. Older people tend to sleep less overall but sleep in REM for about the same absolute time, and therefore spend a greater proportion of sleep in REM.<ref>Kazuo Mishima, Tetsuo Shimizu, & Yasuo Hishikawa (1999), "REM Sleep Across Age and Sex", in ''Rapid Eye Movement Sleep'' ed. Mallick & Inoué.</ref>
-Rapid eye movement sleep can be subclassified into tonic and phasic modes.<ref>{{cite book |vauthors=Kryger M, Roth T, Dement W |title=Principles & Practices of Sleep Medicine |publisher=WB Saunders Company |year=2000 |pages=1,572}}</ref> Tonic REM is characterized by theta rhythms in the brain; phasic REM is characterized by PGO waves and actual “rapid” eye movements. Processing of external stimuli is heavily inhibited during phasic REM and recent evidence suggests that sleepers  are more difficult to arouse from phasic REM than in slow-wave sleep.<ref name=ErmisEtAl>Ummehan Ermis, Karsten Krakow, & Ursula Voss (2010), “Arousal thresholds during human tonic and phasic REM sleep”, ''Journal of Sleep Research'' 19.</ref>
-==Effects of REM sleep deprivation==
-REM deprivation causes a significant increase in the number of attempts to go into REM stage while asleep. On recovery nights, an individual will most likely move to stage 3 and REM sleep more quickly and experience an [[REM rebound]], which refers to a great increase in the time spent in REM stage over normal levels.  These findings are consistent with the idea that REM sleep is biologically necessary.<ref>{{cite journal |vauthors=Endo T, Roth C, Landolt HP, Werth E, Aeschbach D, Achermann P, Borbély AA | title = Selective REM sleep deprivation in humans: Effects on sleep and sleep EEG | journal = The American journal of physiology | volume = 274 | issue = 4 Pt 2 | pages = R1186–R1194 | year = 1998 | pmid = 9575987 }}</ref><ref name=EllmanEtAl1991>Steven J. Ellman, Arthur J. Spielman, Dana Luck, Solomon S. Steiner, & Ronnie Halperin (1991), "REM Deprivation: A Review", in ''The Mind in Sleep'', ed. Ellman & Antrobus.</ref>
-After the deprivation is complete, mild psychological disturbances, such as anxiety, irritability, hallucinations, and difficulty concentrating may develop and appetite may increase. There are also positive consequences of REM deprivation. Some symptoms of depression are found to be suppressed by REM deprivation; aggression, and eating behavior may increase.<ref name=EllmanEtAl1991 /><ref name="Types of Sleep Deprivation">{{cite web |title=Types of Sleep Deprivation|url=http://www.macalester.edu/psychology/whathap/UBNRP/sleep_deprivation/intro04.html}}</ref> Higher noradrenaline is a possible cause of these results.<ref name=MallickEtAl /> Whether and how long-term REM deprivation has psychological effects remains a matter of controversy. Several reports have indicated that REM deprivation increases aggressive and sexual behavior in laboratory test animals.<ref name=EllmanEtAl1991 />
-It has been suggested that acute REM sleep deprivation can improve certain types of [[clinical depression|depression]] when depression appears to be related to an imbalance of certain neurotransmitters. Although sleep deprivation in general annoys most of the population, it has repeatedly been shown to alleviate depression, albeit temporarily.<ref>{{cite journal |vauthors=Ringel BL, Szuba MP | title = Potential mechanisms of the sleep therapies for depression | journal = Depression and Anxiety | volume = 14 | issue = 1 | pages = 29–36 | year = 2001 | pmid = 11568980 | doi = 10.1002/da.1044 }}</ref> More than half the individuals who experience this relief report it to be rendered ineffective after sleeping the following night. Thus, researchers have devised methods such as altering the sleep schedule for a span of days following a REM deprivation period<ref>{{cite journal |vauthors=Riemann D, König A, Hohagen F, Kiemen A, Voderholzer U, Backhaus J, Bunz J, Wesiack B, Hermle L, Berger M | title = How to preserve the antidepressive effect of sleep deprivation: A comparison of sleep phase advance and sleep phase delay | journal = European Archives of Psychiatry and Clinical Neuroscience | volume = 249 | issue = 5 | pages = 231–237 | year = 1999 | pmid = 10591988 | doi = 10.1007/s004060050092 }}</ref> and combining sleep-schedule alterations with pharmacotherapy<ref>{{cite journal |vauthors=Wirz-Justice A, Van den Hoofdakker RH | title = Sleep deprivation in depression: What do we know, where do we go? | journal = Biological Psychiatry | volume = 46 | issue = 4 | pages = 445–453 | year = 1999 | pmid = 10459393 | doi = 10.1016/S0006-3223(99)00125-0 }}</ref> to prolong this effect. Though most [[antidepressant]]s selectively inhibit REM sleep due to their action on monoamines, this effect decreases after long-term use. Sleep deprivation stimulates hippocampal neurogenesis much the same as antidepressants, but whether this effect is driven by REM sleep in particular is unknown.<ref>{{cite journal |vauthors=Grassi Zucconi G, Cipriani S, Balgkouranidou I, Scattoni R | title = 'One night' sleep deprivation stimulates hippocampal neurogenesis | journal = Brain Research Bulletin | volume = 69 | issue = 4 | pages = 375–381 | year = 2006 | pmid = 16624668 | doi = 10.1016/j.brainresbull.2006.01.009 }}</ref>
-Animal studies of REM deprivation are markedly different from human studies.  There is evidence that REM sleep deprivation in animals has more serious consequences than in humans.  This may be because the length of time animals have been REM deprived for is much longer (up to seventy days) or because the various experimental protocols used have been more uncomfortable and painful than those for humans.<ref name="Types of Sleep Deprivation"/> The “flower pot” method involves placing a laboratory animal above water on a platform so small that it falls off upon losing muscle tone. The naturally rude awakening which results may elicit changes in the organism which necessarily exceed the simple absence of a sleep phase.<ref>Rasch & Born (2013), “About Sleep's Role in Memory”, p. 686–687.</ref> Another method involves computer monitoring of brain waves, complete with automatic mechanized shaking of the cage when the test animal drifts into REM sleep.<ref>{{cite journal |author1=Feng Pingfu |author2=Ma Yuxian |author3=Vogel Gerald W | year = 2001 | title = Ontogeny of REM Rebound in Postnatal Rats | url = | journal = Sleep | volume = 24 | issue = 6 }}</ref>
-Evidence suggests that REM deprivation in rats impairs learning of new material, but does not affect existing memory.  In one study, rats did not learn to avoid a painful stimulus after REM deprivation as well as they could before the deprivation. No learning impairments have been found in humans undergoing one night of REM deprivation. REM deprivation in rats produces an increase in attempts to enter REM, and after deprivation, REM rebound.  In rats, as well as cats, REM sleep deprivation increased brain excitability (e.g. electrical amplification of sensory signals), and which lowered the threshold for waking seizures threshold.  This increase in brain excitability seems to be similar in humans.  One study also found a decrease in hindbrain sensory excitability.  The hindbrain was less receptive overall to information in the afferent pathway, because of the increase in the amplification of those pathways that it is receptive to.<ref name="Types of Sleep Deprivation"/>
-==REM sleep in animals==
-[[File:Ostriches-Sleep-like-Platypuses-pone.0023203.s003.ogv|thumb|[[Ostrich]]es sleeping, with REM and [[slow-wave sleep]] phases.<ref>{{Cite journal | last1 = Lesku | first1 = J. A. | last2 = Meyer | first2 = L. C. R. | last3 = Fuller | first3 = A. | last4 = Maloney | first4 = S. K. | last5 = Dell'Omo | first5 = G. | last6 = Vyssotski | first6 = A. L. | last7 = Rattenborg | first7 = N. C. | editor1-last = Balaban | editor1-first = Evan | title = Ostriches Sleep like Platypuses | doi = 10.1371/journal.pone.0023203 | journal = PLoS ONE | volume = 6 | issue = 8 | pages = e23203 | year = 2011 | pmid =  21887239| pmc =3160860 }}</ref>]]
-[[File:REM - Rapid eye movement sleep of a dog.webm|thumb|Rapid eye movement of a dog]]
-{{see also|Sleep (non-human)}}
-REM sleep occurs in all land [[mammals]] as well as in [[birds]]. Amount of REM sleep and cycling time vary among animals; predators enjoy more REM sleep than prey.<ref name=MallickEtAl /> Larger animals also tend to stay in REM for longer, possibly because higher [[thermal inertia]] of their brains and bodies allows them to tolerate longer suspension of thermoregulation.<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', pp. 13, 59–61. “In species with different body mass (e.g., rats, rabbits, cats, humans) the average duration of REM sleep episodes increases with the increase in body and brain weight, a determinant of the thermal inertia. Such inertia delays the changes in body core temperature so alarming as to elicit arousal from REM sleep. In addition, other factors, such as fur, food, and predator–prey relationships influencing REM sleep duration out to be mentioned here.”</ref> The period (full cycle of REM and non-REM) lasts for about 90 minutes in humans, 22 minutes in cats, and 12 minutes in rats.<ref>Steriade & McCarley (1990), ''Brainstem Control of Wakefulness and Sleep", §12.1 (p. 363).</ref>
-In utero, mammals spend more than half (50–80%) of a 24-hour day in REM sleep.<ref name=McCarley2007 />
-[[Mammal]]s and [[bird]]s were long thought to be the only animals to experience REM sleep. In 2016 however, researchers found that REM sleep could also be observed in [[lizard]]s. This suggest that REM sleep has a very ancient evolutionary origin and have probably evolved in the common ancestor of all [[amniote]]s.<ref>{{Cite journal|last=Shein-Idelson|first=Mark|last2=Ondracek|first2=Janie M.|last3=Liaw|first3=Hua-Peng|last4=Reiter|first4=Sam|last5=Laurent|first5=Gilles|date=2016-04-29|title=Slow waves, sharp waves, ripples, and REM in sleeping dragons|url=http://science.sciencemag.org/content/352/6285/590|journal=Science|language=en|volume=352|issue=6285|pages=590–595|doi=10.1126/science.aaf3621|issn=0036-8075|pmid=27126045}}</ref>
-==Hypotheses about the function(s) of REM sleep==
-While the function of REM sleep is not well understood, several theories have been proposed.
-===Memory===
-Sleep in general seems to aid memory. REM sleep may favor the preservation of certain types of [[memories]]: specifically, [[procedural memory]], [[spatial memory]], and [[emotional memory]]. REM sleep seems to increase following intensive learning in rats, especially several hours after, and sometimes for multiple nights after. Experimental REM deprivation has sometimes inhibited memory consolidation, especially regarding complex processes (e.g., how to escape from an elaborate maze).<ref>Rasch & Born (2013), “About Sleep's Role in Memory”, p. 686. Deprivation of REM sleep (mostly without simultaneous sleep recording) appeared to primarily impair memory for- mation on complex tasks, like two-way shuttle box avoidance and complex mazes, which encompass a change in the animals regular repertoire (69, 100, 312, 516, 525, 539, 644, 710, 713, 714, 787, 900, 903–906, 992, 1021, 1072, 1111, 1113, 1238, 1352, 1353). In contrast, long-term memory for simpler tasks, like one-way active avoidance and simple mazes, were less consistently affected (15, 249, 386, 390, 495, 558, 611, 644, 821, 872, 902, 907–909, 1072, 1091, 1334).”</ref> In humans, the best evidence for REM's improvement of memory pertains to learning of procedures—new ways of moving the body (such as trampoline jumping), and new techniques of problem solving. REM deprivation seemed to impair declarative (i.e., factual) memory only in more complex cases, such as memories of longer stories.<ref>Rasch & Born (2013), “About Sleep's Role in Memory”, p. 687.</ref> REM sleep apparently counteracts attempts to suppress certain thoughts.<ref name=RaschBorn2013 />
-According to the ''dual-process hypothesis'' of sleep and memory, the two major phases of sleep correspond to different types of memory. “Night half” studies have tested this hypothesis with memory tasks either begun before sleep and assessed in the middle of the night, or begun in the middle of the night and assessed in the morning.<ref>Rasch & Born (2013), “About Sleep's Role in Memory”, p. 689. “The dual process hypothesis assumes that different sleep stages serve the consolidation of different types of memories (428, 765, 967, 1096). Specifically it has been assumed that declarative memory profits from SWS, whereas the consolidation of nondeclarative memory is supported by REM sleep.” This hypothesis received support mainly from studies in humans, particularly from those employing the 'night half paradigm.'”</ref>  [[Slow-wave sleep]], part of non-REM sleep, appears to be important for [[declarative memory]]. Artificial enhancement of the non-REM sleep improves the next-day recall of memorized pairs of words.<ref name="pmid17086200">{{cite journal |vauthors=Marshall L, Helgadóttir H, Mölle M, Born J | title = Boosting slow oscillations during sleep potentiates memory | journal = Nature | volume = 444 | issue = 7119 | pages = 610–3 | year = 2006 | pmid = 17086200 | doi = 10.1038/nature05278 }}</ref> Tucker et al. demonstrated that a daytime nap containing solely  non-REM sleep enhances [[declarative memory]] but not [[procedural memory]].<ref name="Tucker et al.">{{cite journal |vauthors=Tucker MA, Hirota Y, Wamsley EJ, Lau H, Chaklader A, Fishbein W | title = A daytime nap containing solely non-REM sleep enhances declarative but not procedural memory | journal = Neurobiology of Learning and Memory | volume = 86 | issue = 2 | pages = 241–7 | year = 2006 | pmid = 16647282 | doi = 10.1016/j.nlm.2006.03.005 | url = http://web.mit.edu/dmalt/Public/9.10/newRun2.pdf | publisher = [[Elsevier]] | pages241-247 =  | accessdate = June 29, 2011 }}</ref> According to the ''sequential hypothesis'' the two types of sleep work together to consolidate memory.<ref>Rasch & Born (2013), “About Sleep's Role in Memory”, p. 690–691.</ref>
-[[Monoamine oxidase inhibitor|Monoamine oxidase (MAO) inhibitors]] and [[tricyclic antidepressants]] can suppress REM sleep and these drugs show no evidence of impairing memory. Some studies show MAO inhibitors ''improve'' memory. Moreover, one case study of an individual who had little or no REM sleep due to a shrapnel injury to the brainstem did not find the individual's memory to be impaired. (For a more detailed critique on the link between sleep and memory, see Ref.)<ref name=Siegel>{{cite journal |last=Siegel |first=Jerome M. |title=The REM Sleep-Memory Consolidation Hypothesis |url= http://www.semel.ucla.edu/publication/journal-article/siegel/2001/rem-sleep-memory-consolidation-hypothesis}}</ref>)
-Intimately related to views on REM function in memory consolidation, [[Graeme Mitchison]] and [[Francis Crick]] have proposed in 1983 that by virtue of its inherent spontaneous activity, the function of REM sleep "is to remove certain undesirable modes of interaction in networks of cells in the cerebral cortex", which process they characterize as "[[reverse learning|unlearning]]". As a result, those memories which are relevant (whose underlying neuronal substrate is strong enough to withstand such spontaneous, chaotic activation), are further strengthened, whilst weaker, transient, "noise" memory traces disintegrate.<ref>{{cite journal |vauthors=Crick F, Mitchison G | title = The function of dream sleep | journal = Nature | volume = 304 | issue = 5922 | pages = 111–14 | year = 1983 | pmid = 6866101 | doi = 10.1038/304111a0 }}</ref> Memory consolidation during paradoxical is specifically correlated with the periods of rapid eye movement, which do not occur continuously. One explanation for this correlation is that the PGO electrical waves, which precede the eye movements, also influence memory.<ref name=Datta /> REM sleep could provide a unique opportunity for “unlearning” to occur in basic neural networks involved in homeostasis, which are protected from this “synaptic downscaling” effect during deep sleep.<ref>Parmeggiani (2011), ''Systemic Homeostasis and Poikilostasis in Sleep'', p. 89. “In contrast to NREM sleep, downscaling of synapses would be produced in REM sleep by random bursts of neuronal firing (e.g., also bursts underlying ponto-geniculo-occipital waves) (see Tonioni and Cirelli, 2005). / This hypothesis is particularly enriched in functional significance by considering at this point the opposite nature, homeostatic and poikilostatic, of the systemic neural regulation of physiological functions in these sleep states. The important fact is that homeostasis if fully preserved in NREM sleep. This means that a systemic synaptic downcaling (slow-wave electroencephalographic activity) is practically limited to the relatively homogenous cortical structures of the telencephalon, while the whole brain stem, from diencephalon to medulla, is still exerting its basic functions of integrated homeostatic regulation of both somatic and autonomic physiological functions. In REM sleep, however, the necessary synaptic downscaling in the brain stem is instead the result of random neuronal firing.”</ref>
-===Stimulation of the central nervous system's development as a primary function===
-According to another theory, known as the Ontogenetic Hypothesis of REM sleep, this sleep stage (also known as [[active sleep]] in [[neonate]]s) is particularly important to the developing brain, possibly because it provides the neural stimulation that newborns need to form mature neural connections and for proper nervous system development.<ref>Marks et al. 1994</ref> Studies investigating the effects of active sleep deprivation have shown that deprivation early in life can result in behavioral problems, permanent sleep disruption, decreased brain mass,<ref name="pmid6850353">{{cite journal |vauthors=Mirmiran M, Scholtens J, van de Poll NE, Uylings HB, van der Gugten J, Boer GJ | title = Effects of experimental suppression of active (REM) sleep during early development upon adult brain and behavior in the rat | journal = Brain Res. | volume = 283 | issue = 2–3 | pages = 277–86 | year = 1983 | pmid = 6850353 | doi = 10.1016/0165-3806(83)90184-0 }}</ref> and result in an abnormal amount of neuronal cell death.<ref name="pmid15142640">{{cite journal |vauthors=Morrissey MJ, Duntley SP, Anch AM, Nonneman R | title = Active sleep and its role in the prevention of apoptosis in the developing brain | journal = Med. Hypotheses | volume = 62 | issue = 6 | pages = 876–9 | year = 2004 | pmid = 15142640 | doi = 10.1016/j.mehy.2004.01.014 }}</ref> Further supporting this theory is the fact that the amount of REM sleep in humans decreases with age, as well as data from other species (see below).
-One important theoretical consequence of the Ontogenetic Hypothesis is that REM sleep may have no essentially vital function in the mature brain, i.e., once the development of the central nervous system has completed. However, because processes of neuronal plasticity do not cease altogether in the brain,<ref>{{cite journal |vauthors=Bruel-Jungerman E, Rampon C, Laroche S | title = Adult hippocampal neurogenesis, synaptic plasticity and memory: facts and hypotheses | journal = Rev. Neurosci. | volume = 18 | issue = 2 | pages = 93–114 | year = 2006 | pmid = 17593874 | doi = 10.1515/REVNEURO.2007.18.2.93 }}</ref> REM sleep may continue to be implicated in neurogenesis in adults as a source of sustained spontaneous stimulation.
-===Defensive immobilization: the precursor of dreams===
-According to Tsoukalas (2012) REM sleep is an evolutionary transformation of a well-known defensive mechanism, the [[tonic immobility]] reflex. This reflex, also known as animal hypnosis or death feigning, functions as the last line of defense against an attacking predator and consists of the total immobilization of the animal so that it [[playing possum|appears dead]]. Tsoukalas argues that the neurophysiology and phenomenology of this reaction shows striking similarities to REM sleep; for example, both reactions exhibit brainstem control, paralysis, hypocampal theta rhythm, and thermoregulatory changes.<ref name=Tsoukalas>{{cite journal | author = Tsoukalas I | year = 2012 | title = The origin of REM sleep: A hypothesis | url = | journal = Dreaming | volume = 22 | issue = 4| pages = 253–283 | doi=10.1037/a0030790}}</ref><ref name=Vitelli2013>Vitelli, R. (2013). Exploring the Mystery of REM Sleep. ''Psychology Today'', On-line, March 25</ref>
-===Shift of gaze===
-According to "scanning hypothesis", the directional properties of REM sleep are related to a shift of gaze in dream imagery. Against this hypothesis is that such eye movements occur in those born [[blindness|blind]] and in [[fetuses]] in spite of lack of vision. Also, [[binocular vision|binocular]] REMs are non-conjugated (i.e., the two eyes do not point in the same direction at a time) and so lack a [[fixation point]]. In support of this theory, research finds that in goal-oriented dreams, eye gaze is directed towards the dream action, determined from correlations in the eye and body movements of REM sleep behavior disorder patients who enact their dreams.<ref name="Leclair-Visonneau">{{cite journal |vauthors=Leclair-Visonneau L, Oudiette D, Gaymard B, Leu-Semenescu S, Arnulf I | title = Do the eyes scan dream images during rapid eye movement sleep? Evidence from the rapid eye movement sleep behaviour disorder model | journal = Brain | volume = 133 | issue = 6 | pages = 1737–46 | year = 2010 | pmid = 20478849 | doi = 10.1093/brain/awq110 | url =  }}</ref>
-===Oxygen supply to cornea===
-Dr. [[David M. Maurice]] (1922-2002), an eye specialist and semi-retired adjunct professor at Columbia University, proposed that REM sleep was associated with oxygen supply to cornea when the animal was sleeping thus aqueous humor, the liquid between cornea and iris, was stagnant if not stirred ("stagnant aqueous humor hypothesis").<ref name=Maurice>{{cite journal |last=Maurice |first=David |title=The Von Sallmann Lecture 1996: An Ophthalmological Explanation of REM Sleep | journal = Experimental Eye Research | volume = 66 | issue =2 | pages = 139–145 | year = 1998 | pmid = 9533840 | doi = 10.1006/exer.1997.0444 |url = http://davidmaurice.com/papers/rem/rem.pdf}}</ref> Among the supportive evidences, he calculated that if aqueous humor was stagnant, oxygen from iris had to reach cornea by diffusion through aqueous humor, which was not sufficient. According to the theory, when the animal is awake, eye movement and/or cool environmental temperature make sure the aqueous humor is able to circulate. When the animal is sleeping, REM provides the much needed stir to aqueous humor. This theory is consistent with the observation that fetuses, as well as eye-sealed newborn animals, spend much time in REM sleep, and that during a normal sleep, a person's REM sleep episodes become progressively longer deeper into the night. However, owls have REM sleep (telling from EEG recording) but during REM sleep owls do not move their head more than Non-REM sleep. This observation can be derived from Figure S1 of a recently published research <ref name = Scriba>{{ cite journal |author1=Madeleine Scriba |author2=Anne-Lyse Ducrest |author3=Isabelle Henry |author4=Alexei L Vyssotski |author5=Niels C Rattenborg |author6=Alexandre Roulin | title = Linking melanism to brain development: expression of a melanism-related gene in barn owl feather follicles covaries with sleep ontogeny | journal = Frontiers in Zoology | volume = 10 | issue = 42 | year = 2013 | doi = 10.1186/1742-9994-10-42}}</ref> and it is well known that owls' eyes are nearly immobile.<ref>{{cite journal|pmc=1772283|author=Steinbach, M. J.|title=Owls’ eyes move|journal=The British Journal of Ophthalmology|volume=88|issue=8|year=2004|pages=1103|pmid=15258042|doi=10.1136/bjo.2004.042291}}</ref>
-===Other theories===
-Another theory suggests that [[monoamine]] shutdown is required so that the monoamine receptors in the brain can recover to regain full sensitivity. Indeed, if REM sleep is repeatedly interrupted, the person will compensate for it with longer REM sleep, "rebound sleep", at the next opportunity.
-Some researchers argue that the perpetuation of a complex brain process such as REM sleep indicates that it serves an important function for the survival of mammalian and avian species. It fulfills important physiological needs vital for survival to the extent that prolonged REM sleep deprivation leads to death in experimental animals. In both humans and experimental animals, REM sleep loss leads to several behavioral and physiological abnormalities. Loss of REM sleep has been noticed during various natural and experimental infections. Survivability of the experimental animals decreases when REM sleep is totally attenuated during infection; this leads to the possibility that the quality and quantity of REM sleep is generally essential for normal body physiology.<ref>Robert P. Vertes (1986), "A Life-Sustaining Function for REM Sleep: A Theory", ''Neuroscience and Behavioral Reviews'' 10.</ref>
-The ''sentinel hypothesis'' of REM sleep was put forward by Frederick Snyder in 1966. It is based upon the observation that REM sleep in several mammals (the rat, the hedgehog, the rabbit, and the rhesus monkey) is followed by a brief awakening. This does not occur for either cats or humans, although humans are more likely to wake from REM sleep than from NREM sleep. Snyder hypothesized that REM sleep activates an animal periodically, to scan the environment for possible predators. This hypothesis does not explain the muscle paralysis of REM sleep; however, a logical analysis might suggest that the muscle paralysis exists to prevent the animal from fully waking up unnecessarily, and allowing it to return easily to deeper sleep.<ref>{{cite book |title=The Mind in Sleep: Psychology and Psychophysiology |author1=Steven J. Ellman |author2=John S. Antrobus |chapter=Effects of REM deprivation |page=398 |year=1991 |publisher=John Wiley and Sons |isbn=0-471-52556-1}}</ref><ref>Jouvet (1999), ''The Paradox of Sleep'', pp. 122–124.</ref><ref>{{cite book |title=Understanding Sleep and sDreaming |author1=William H. Moorcroft |author2=Paula Belcher |chapter=Functions of REMS and Dreaming |page=290 |year=2003 |publisher=Springer |isbn=0-306-47425-5}}</ref>
-Jim Horne, a sleep researcher at Loughborough University, has suggested that REM in modern humans compensates for the reduced need for wakeful food [[foraging]].<ref name=Horne2013 />
-Other theories are that they lubricate the [[cornea]], warm the brain, stimulate and stabilize the [[neural circuit]]s that have not been activated during [[waking up|waking]], create internal stimulation to aid  development of the [[central nervous system|CNS]], or lack any purpose, being random creations of brain activation.<ref name="Leclair-Visonneau"/><ref name=Ruby2011 />
-==Discovery and further research==
-The German scientist Richard Klaue in 1937 first discovered a period of fast electrical activity in the brains of sleeping cats. In 1944, Ohlmeyer reported 90-minute ultradian sleep cycles involving male erections lasting for 25 minutes.<ref>Jouvet (1999), ''The Paradox of Sleep'', p. 32.</ref> At [[University of Chicago]] in 1952, [[Eugene Aserinsky]], [[Nathaniel Kleitman]], and [[William C. Dement]], discovered phases of rapid eye movement during sleep, and connected these to dreaming. Their article was published September 10, 1953.<ref>{{cite journal |vauthors=Aserinsky E, Kleitman N | title = Regularly Occurring Periods of Eye Motility, and Concomitant Phenomena, during Sleep | journal = Science | volume = 118 | issue = 3062 | pages = 273–274 | year = 1953 | pmid = 13089671 | doi = 10.1126/science.118.3062.273 }}</ref>
-William Dement advanced the study of REM deprivation, with experiments in which subjects were awoken every time their EEG indicated the beginning of REM sleep. He published "The Effect of Dream Deprivation" in June 1960.<ref>[[William Dement]], “The Effect of Dream Deprivation: The need for a certain amount of dreaming each night is suggested by recent experiments.” ''Science'' 131.3415, 10 June 1960.</ref> ("REM deprivation" has become the more common term following subsequent research indicating the possibility of non-REM dreaming.)
-Neurosurgical experiments by [[Michel Jouvet]] and others in the following two decades added an understanding of atonia and suggested the importance of the [[pontine tegmentum]] (dorsolateral [[pons]]) in enabling and regulating paradoxical sleep.<ref name=MallickEtAl /> Jouvet and others found that damaging the [[reticular formation]] of the brainstem inhibited this type of sleep.<ref name=LaiSiegel /> Jouvet coined the name “paradoxical sleep” in 1959 and in 1962 published results indicating that it could occur in a cat with its entire forebrain removed.<ref name=LuppiEtAl /><ref name=Ruby2011>Perrine M. Ruby (2011), “Experimental research on dreaming: state of the art and neuropsychoanalytic perspectives”, ''Frontiers in Psychology'' 2.</ref>
-==See also==
-* [[Sleep and learning]]
-* [[Neuroscience of sleep]]
-* [[Pedunculopontine nucleus]] (PPN)
-==References==
-{{reflist|2}}
-=== Sources ===
-* Antrobus, John S., & Mario Bertini (1992). ''The Neuropsychology of Sleep and Dreaming''. Hillsdale, NJ: Lawrence Erlbaum Associates. ISBN 0-8058-0925-2
-* {{cite journal |author1=Brown Ritchie E. |author2=Basheer Radhika |author3=McKenna James T. |author4=Strecker Robert E. |author5=McCarley Robert W. | year = 2012 | title = Control of Sleep and Wakefulness | journal = Physiological Review | volume = 92 | issue = | pages = 1087–1187 | doi=10.1152/physrev.00032.2011 | pmid=22811426 | pmc=3621793}}
-* Ellman, Steven J., & Antrobus, John S. (1991). ''The Mind in Sleep: Psychology and Psychophysiology''. Second edition. John Wiley & Sons, Inc. ISBN 0-471-52556-1
-* [[Michel Jouvet|Jouvet, Michel]] (1999). ''The Paradox of Sleep: The Story of Dreaming''. Originally ''Le Sommeil et le Rêve'', 1993. Translated by Laurence Garey. Cambridge: MIT Press. ISBN 0-262-10080-0
-* Mallick, B. N., & S. Inoué (1999). ''Rapid Eye Movement Sleep''. New Delhi: Narosa Publishing House; distributed in the Americas, Europe, Australia, & Japan by Marcel Dekker Inc (New York).
-* Monti, Jaime M., S. R. Pandi-Perumal, & Christopher M. Sinton (2008). ''Neurochemistry of Sleep and Wakefulness''. Cambridge University Press. ISBN 978-0-521-86441-1
-* Parmeggiani, Pier Luigi (2011). ''Systemic Homeostasis and Poikilostasis in Sleep: Is REM Sleep a Physiological Paradox?'' London: Imperial College Press. ISBN 978-1-94916-572-2
-* Rasch, Björn, & Jan Born (2013). “About Sleep's Role in Memory”. ''Physiological Review 93, pp. 681–766.
-* Solms, Mark (1997). ''The Neuropsychology of Dreams: A Clinico-Anatomical Study''. Mahwah, NJ: Lawrence Erlbaum Associates; ISBN 0-8058-1585-6
-* Steriade, Mircea, & Robert W. McCarley (1990). ''Brainstem Control of Wakefulness and Sleep''. New York: Plenum Press. ISBN 0-306-43342-7
-==Further reading==
-* {{cite journal | author = Snyder F | title = Toward an Evolutionary Theory of Dreaming | journal = American Journal of Psychiatry | volume = 123 | issue = 2 | pages = 121–142 | year = 1966 | pmid = 5329927 | doi=10.1176/ajp.123.2.121}}
-* {{cite book |title=Sleep and Dreaming: Scientific Advances and Reconsiderations |editor=Edward F. Pace-Schott |year=2003 |publisher=Cambridge University Press |isbn=0-521-00869-7}}
-* Koulack, D. To Catch A Dream: Explorations of Dreaming. New York, SUNY, 1991.
-* {{cite journal |vauthors=Nguyen TQ, Liang CL, Marks GA |title=GABA(A) receptors implicated in REM sleep control express a benzodiazepine binding site |journal=Brain Res. |volume=1527 |issue= |pages=131–40 |year=2013 |pmid=23835499 |pmc=3839793 |doi=10.1016/j.brainres.2013.06.037 |url=}}
-* {{cite journal |vauthors=Liang CL, Marks GA |title=GABAA receptors are located in cholinergic terminals in the nucleus pontis oralis of the rat: implications for REM sleep control |journal=Brain Res. |volume=1543 |issue= |pages=58–64 |year=2014 |pmid=24141149 |doi=10.1016/j.brainres.2013.10.019 |url=}}
-* {{cite journal |vauthors=Grace KP, Vanstone LE, Horner RL |title=Endogenous Cholinergic Input to the Pontine REM Sleep Generator Is Not Required for REM Sleep to Occur |journal=J. Neurosci. |volume=34 |issue=43 |pages=14198–209 |year=2014 |pmid=25339734 |doi=10.1523/JNEUROSCI.0274-14.2014 |url=}}
-* Carson III, Culley C., Kirby, Roger S., Goldstein, Irwin, editors, "Textbook of Erectile Dysfunction" Oxford, U.K.; Isis Medical Media, Ltd., 1999; Moreland, R.B. & Nehra, A.; Pathosphysiology of erectile dysfunction; a molecular basis, role of NPT in maintaining potency: pp.&nbsp;105–15.
-==External links==
-{{Wiktionary}}
-* [http://www.pbs.org/wgbh/nova/body/what-are-dreams.html PBS' NOVA episode "What Are Dreams?" Video and Transcript]
-* [http://lsdbase.org/category/states/rem-sleep LSDBase] - an open sleep research database with images of REM sleep recordings.
-{{Dreaming}}
-{{SleepSeries2}}
-{{Authority control}}
-{{DEFAULTSORT:Rapid Eye Movement Sleep}}
-[[Category:Dream]]
-[[Category:Sleep physiology]]
-[[Category:Neurophysiology]]
-[[Category:Articles containing video clips]]