Rapid eye movement sleep (REM sleep or REMS) is a unique phase of sleep in mammals (including humans) and birds, characterized by random rapid movement of the eyes, accompanied by low muscle tone throughout the body, and the propensity of the sleeper to dream vividly. The core body and brain temperatures increase during REM sleep and skin temperature decreases to lowest values.<ref>Template:Cite journal</ref>
The REM phase is also known as paradoxical sleep (PS) and sometimes desynchronized sleep or dreamy sleep,<ref name = "Hall_2010">Template:Cite book</ref> because of physiological similarities to waking states including rapid, low-voltage desynchronized brain waves. Electrical and chemical activity regulating this phase seem 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=BrownMcCarley /> Experiences of REM sleep are not transferred to permanent memory due to absence of norepinephrine.<ref name = "Hall_2010" />
REM sleep is physiologically different from the other phases of sleep, which are collectively referred to as non-REM sleep (NREM sleep, NREMS, synchronized sleep). The absence of visual and auditory stimulation (sensory deprivation) during REM sleep can cause hallucinations.<ref>Template:Cite book</ref>Template:Failed verificationTemplate:Page needed REM and non-REM sleep alternate within one sleep cycle, which lasts about 90 minutes in adult humans. As sleep cycles continue, they shift towards a higher proportion of REM sleep. The transition to REM sleep brings marked physical changes, beginning with electrical bursts called "ponto-geniculo-occipital waves" (PGO waves) originating in the brain stem. REM sleep occurs 4 times in a 7-hour sleep.<ref>Template:Cite book</ref> Organisms in REM sleep suspend central homeostasis, allowing large fluctuations in respiration, thermoregulation and circulation which do not occur in any other modes of sleeping or waking. The body abruptly loses muscle tone, a state known as REM atonia.<ref name=BrownMcCarley /><ref name=LaiSiegel />
In 1953, Professor Nathaniel Kleitman and his student Eugene Aserinsky defined rapid eye movement and linked it to dreams. REM sleep was further described by researchers, including William Dement and Michel Jouvet. Many experiments have involved awakening test subjects whenever they begin to enter the REM phase, thereby producing a state known as REM deprivation. Subjects allowed to sleep normally again usually experience a modest REM rebound. Techniques of neurosurgery, chemical injection, electroencephalography, positron emission tomography, and reports of dreamers upon waking have all been used to study this phase of sleep.<ref>Template:Cite journal</ref>
PhysiologyEdit
Electrical activity in the brainEdit
REM sleep is called "paradoxical" because of its similarities to wakefulness. Although the body is paralyzed, the brain acts as if it is somewhat awake, with cerebral neurons firing with the same overall intensity as in wakefulness.<ref name=MatarazzoEtAl2011>Template:Cite book</ref><ref name="myers7e">Template:Cite book</ref> Electroencephalography during REM sleep reveals fast, low amplitude, desynchronized neural oscillation (brainwaves) that resemble the pattern seen during wakefulness, which differ from the slow δ (delta) waves pattern of NREM deep sleep.<ref name=BrownMcCarley>Template:Cite book</ref><ref name="Steriade_2013">Template:Cite book</ref>Template:Rp An important element of this contrast is the 3–10 Hz theta rhythm in the hippocampus<ref name="Steriade_2013" />Template:Rp and 40–60 Hz gamma waves in the cortex; patterns of EEG activity similar to these rhythms are also observed during wakefulness.<ref name="Horne2013">Template:Cite journal</ref> The cortical and thalamic neurons in the waking and REM sleeping brain are more depolarized (fire more readily) than in the NREM deep sleeping brain.<ref name="Steriade_2013" />Template:Rp Human theta wave activity predominates during REM sleep in both the hippocampus and the cortex.<ref name="pmid26441373">Template:Cite journal</ref><ref name="pmid24596562">Template:Cite journal</ref>
During REM sleep, electrical connectivity among different parts of the brain manifests differently than during wakefulness. Frontal and posterior areas are less coherent in most frequencies, a fact which has been cited in relation to the chaotic experience of dreaming. However, the posterior areas are more coherent with each other; as are the right and left hemispheres of the brain, especially during lucid dreams.<ref>Template:Cite book</ref><ref name=EPS2011>Template:Cite book</ref>
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 />
Brain stemEdit
Neural activity during REM sleep seems to originate in the brain stem, especially the pontine tegmentum and locus coeruleus. REM sleep is punctuated and immediately preceded by PGO (ponto-geniculo-occipital) waves, bursts of electrical activity originating in the brain stem.<ref name="Steriade_2013" />Template:Rp (PGO waves have long been measured directly in cats but not in humans because of constraints on experimentation; however, comparable effects have been observed in humans during "phasic" events which occur during REM sleep, and the existence of similar PGO waves is thus inferred.)<ref name=EPS2011 /> These waves occur in clusters about every 6 seconds for 1–2 minutes during the transition from deep to paradoxical sleep.<ref name="Steriade_2013" /> 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>Template:Cite book</ref><ref name=ErmisEtAl /><ref name=HobsonEtAl2000 /> Other muscles may also contract under the influence of these waves.<ref name=Siegel2009 />
ForebrainEdit
Research in the 1990s using positron emission tomography (PET) confirmed the role of the brain stem and suggested that, within the forebrain, the limbic and paralimbic systems showed more activation than other areas.<ref name=MatarazzoEtAl2011 /> The areas activated during REM sleep are approximately inverse to those activated during non-REM sleep<ref name=HobsonEtAl2000 /> and display greater activity than in quiet waking. The "anterior paralimbic REM activation area" (APRA) includes areas linked with emotion, memory, fear and sex, and may thus relate to the experience of dreaming during REMS.<ref name=EPS2011 /><ref>Template:Cite journal</ref> More recent PET research has indicated that the distribution of brain activity during REM sleep varies in correspondence with the type of activity seen in the prior period of wakefulness.<ref name=MatarazzoEtAl2011 />
The superior frontal gyrus, medial frontal areas, intraparietal sulcus, and superior parietal cortex, areas involved in sophisticated mental activity, show equal activity in REM sleep as in wakefulness. The amygdala is also active during REM sleep and may participate in generating the PGO waves, and experimental suppression of the amygdala results in less REM sleep.<ref>Template:Cite book</ref> The amygdala may also regulate cardiac function in lieu of the less active insular cortex.<ref name=MatarazzoEtAl2011 />
Chemicals in the brainEdit
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 monoamine neurotransmitters have already been depleted.<ref name="BrownMcCarley"/><ref name=MallickEtAl>Template:Cite book.</ref><ref name=Hobson2009>Template:Cite journal</ref><ref name=AstonJonesEtAl>Template:Cite book</ref><ref>Template:Cite book</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>Template:Cite book</ref>
Unlike the abrupt transitions in electrical patterns, the chemical changes in the brain show continuous periodic oscillation.<ref name=McCarley2007>Template:Cite journal</ref>
Models of REM regulationEdit
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>Template:Cite journal</ref> They used Lotka–Volterra equations to describe this cyclical inverse relationship.<ref name="Steriade_2013" />Template:Rp 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>Template:Cite book</ref> The withdrawal of orexin and GABA may cause the absence of the other excitatory neurotransmitters;<ref name = "Parmeggiani_2011">Template:Cite book</ref>Template:Rp researchers in recent years increasingly include GABA regulation in their models.<ref>Template:Cite book</ref>
Eye movementsEdit
Most of the eye movements in "rapid eye movement" sleep are in fact less rapid than those normally exhibited by waking humans. They are also shorter in duration and more likely to loop back to their starting point. About seven such loops take place over one minute of REM sleep. In slow-wave sleep, the eyes can drift apart; however, the eyes of the paradoxical sleeper move in tandem.<ref name="Steriade_2013" />Template:Rp 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>Template:Cite journal</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 suggests that the functional purpose of REM sleep is for procedural memory processing, and the rapid eye movement is only a side effect of the brain processing the eye-related procedural memory.<ref>Template:Cite book</ref><ref>Template:Cite book</ref>
Circulation, respiration, and thermoregulationEdit
Generally speaking, the body suspends homeostasis during paradoxical sleep. Heart rate, cardiac pressure, cardiac output, arterial pressure, and breathing rate quickly become irregular when the body moves into REM sleep.<ref name = "Parmeggiani_2011" />Template:Rp 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 name = "Parmeggiani_2011" />Template:Rp
Erections of the penis (nocturnal penile tumescence or NPT) normally accompany REM sleep in rats and humans.<ref name = "Jouvet_1999">Template:Cite book</ref>Template:Rp 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>Template:Cite journal</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 breathe faster to regulate temperature during NREMS—but not during REMS.<ref name = "Parmeggiani_2011" />Template:Rp 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 name = "Parmeggiani_2011" />Template:Rp Neurons that 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 name = "Parmeggiani_2011" />Template:Rp
Consequently, hot or cold environmental temperatures can reduce the proportion of REM sleep, as well as amount of total sleep.<ref>Template:Cite book</ref><ref name = "Parmeggiani_2011" />Template:Rp 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 name = "Parmeggiani_2011" />Template:Rp This mechanism can be 'fooled' by artificially warming the brain.<ref name = "Parmeggiani_2011" />Template:Rp
MuscleEdit
REM atonia, an almost complete paralysis of the body, is accomplished through the inhibition of motor neurons. When the body shifts into REM sleep, motor neurons throughout the body undergo a process called hyperpolarization:<ref>Template:Cite journal</ref> 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 name="Steriade_2013" />Template:Rp The medulla oblongata, located between pons and spine, seems to have the capacity for organism-wide muscle inhibition.<ref name=LaiSiegel>Template:Cite book</ref> Some localized twitching and reflexes can still occur.<ref name = "Parmeggiani_2011" />Template:Rp Pupils contract.<ref name=Siegel2009>Template:Cite journal</ref>
Lack of REM atonia causes REM behavior disorder, where those affected physically act out their dreams,<ref name="pmid1620348">Template:Cite journal</ref> or conversely "dream out their acts", under an alternative theory on the relationship between muscle impulses during REM and associated mental imagery (which would also apply to people without the condition, except that commands to their muscles are suppressed).<ref name="Steriade_2013" />Template:Rp This is different from conventional sleepwalking, which takes place during slow-wave sleep, not REM.<ref name = "Jouvet_1999" />Template:Rp Narcolepsy, by contrast, seems to involve excessive and unwanted REM atonia: cataplexy and excessive daytime sleepiness while awake, hypnagogic hallucinations before entering slow-wave sleep, or sleep paralysis while waking.<ref name="Steriade_2013" />Template:Rp Other psychiatric disorders including depression have been linked to disproportionate REM sleep.<ref name="Steriade_2013" />Template:Rp Patients with suspected sleep disorders are typically evaluated by polysomnogram.<ref>Template:Cite journal</ref><ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>
Lesions of the pons to prevent atonia have induced functional "REM behavior disorder" in animals.<ref name = "Parmeggiani_2011" />Template:Rp
PsychologyEdit
DreamingEdit
Rapid eye movement sleep (REM) has since its discovery been closely associated with dreaming. Waking up sleepers during a REM phase is a common experimental method for obtaining dream reports; 80% of people can give some kind of dream report under these circumstances.<ref name = "Solms_1997">Template:Cite book</ref>Template:Rp<ref name=EPS2011 /> 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>Template:Cite journal</ref><ref name=Reinsel1992 /> Lucid dreams are reported far more often in REM sleep.<ref>Template:Cite book</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 (e.g., experiential resemblance to waking life), and incorporation of instinctual themes.<ref name=HobsonEtAl2000 /> Sometimes, they include elements of the dreamer's recent experience taken directly from episodic memory.<ref name=MatarazzoEtAl2011 /> By one estimate, 80% of dreams occur during REM.<ref name=Markov2012 />
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 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>Template:Cite book</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 name = "Solms_1997" />Template:Rp Some researchers (Dement, Hobson, Jouvet, for example) tend to resist the idea of disconnecting dreaming from REM sleep.<ref name=HobsonEtAl2000 /><ref name = "Jouvet_1999" />Template:Rp
Effects of SSRIsEdit
Previous research has shown that selective serotonin reuptake inhibitors (SSRIs) have an important effect on REM sleep neurobiology and dreaming.<ref name=":1">Template:Cite journal</ref> A study at Harvard Medical School in 2000 tested the effects of paroxetine and fluvoxamine on healthy young adult male and females for 31 days: a drug-free baseline week, 19 days on either paroxetine or fluvoxamine with morning and evening doses, and 5 days of absolute discontinuation.<ref name=":0">Template:Cite journal</ref> Results showed that SSRI treatment decreased the average amount of dream recall frequency in comparison to baseline measurements as a result of serotonergic REM suppression.<ref name=":0" /> Fluvoxamine increased the length of dream reporting, bizarreness of dreams as well as the intensity of REM sleep. These effects were the greatest during acute discontinuation compared to treatment and baseline days.<ref name=":0" /> However, the subjective intensity of dreaming increased<ref name=":0" /> and the proclivity to enter REM sleep was decreased during SSRI treatment compared to baseline and discontinuation days.<ref name=":0" />
CreativityEdit
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 anagrams and creative problem solving.<ref name="Rasch_2013">Template:Cite journal</ref>Template:Rp
Sleep aids the process by which creativity forms associative elements into new combinations that are useful or meet some requirement.<ref>Template:Cite journal</ref> This occurs in REM sleep rather than in NREM sleep.<ref name="Cai">Template:Cite journal</ref><ref>Template:Cite journal</ref> Rather than being due to memory processes, this has been attributed to changes during REM sleep in cholinergic and noradrenergic 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>Template:Cite journal</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"/>
TimingEdit
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 diurnal animals, at night.<ref name = "Parmeggiani_2011" />Template:Rp The organism returns to homeostatic regulation almost immediately after REM sleep ends.<ref name = "Parmeggiani_2011" />Template:Rp
During a night of sleep, humans usually experience about four or five periods of REM sleep; they are shorter (~15 min) at the beginning of the night and longer (~25 min) 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">Template:Cite journal</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 /> (The increased REM sleep later in the night is connected with the circadian rhythm and occurs even in people who did not sleep in the first part of the night.)<ref name=Aeschbach>Template:Cite book</ref><ref name=BarotKushida2011 />
In the weeks after a human baby is born, as its nervous system matures, neural patterns in sleep begin to show a rhythm of REM and non-REM sleep. (In faster-developing mammals, this process occurs in utero.)<ref name=Frank2011>Template:Cite book</ref> Infants spend more time in 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>Template:Cite book</ref><ref name=Markov2012 />
Rapid eye movement sleep can be subclassified into tonic and phasic modes.<ref>Template:Cite book</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>Template:Cite journal</ref>
Deprivation effectsEdit
Selective REMS deprivation causes a significant increase in the number of attempts to go into REM stage while asleep. On recovery nights, an individual will usually move to stage 3 and REM sleep more quickly and experience a REM rebound, which refers to an 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>Template:Cite journal</ref><ref name=EllmanEtAl1991>Template:Cite book</ref> However, the "rebound" REM sleep usually does not last fully as long as the estimated length of the missed REM periods.<ref name=Aeschbach />
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 may increase, and eating behavior may get disrupted.<ref name=EllmanEtAl1991 /><ref name="Types of Sleep Deprivation">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Higher norepinepherine 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 aggression and sexual behavior in laboratory test animals.<ref name=EllmanEtAl1991/> Rats deprived of paradoxical sleep die in 4–6 weeks (twice the time before death in case of total sleep deprivation). Mean body temperature falls continually during this period.<ref name=BarotKushida2011>Template:Cite book</ref>
It has been suggested that acute REM sleep deprivation can improve certain types of 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>Template:Cite journal</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>Template:Cite journal</ref> and combining sleep-schedule alterations with pharmacotherapy<ref>Template:Cite journal</ref> to prolong this effect. Antidepressants (including selective serotonin reuptake inhibitors, tricyclics, and monoamine oxidase inhibitors) and stimulants (such as amphetamine, methylphenidate and cocaine) interfere with REM sleep by stimulating the monoamine neurotransmitters which must be suppressed for REM sleep to occur. Administered at therapeutic doses, these drugs may stop REM sleep entirely for weeks or months. Withdrawal causes a REM rebound.<ref name=Markov2012>Template:Cite journal</ref><ref name=Siegel2001 /> Sleep deprivation stimulates hippocampal neurogenesis much as antidepressants do, but whether this effect is driven by REM sleep in particular is unknown.<ref>Template:Cite journal</ref>
In other animalsEdit
{{#invoke:Labelled list hatnote|labelledList|Main article|Main articles|Main page|Main pages}} Although it manifests differently in different animals, REM sleep or something like it occurs in all land mammals—as well as in birds. The primary criteria used to identify REM are the change in electrical activity, measured by EEG, and loss of muscle tone, interspersed with bouts of twitching in phasic REM.<ref name=RattenborgEtAl2011>Template:Cite book</ref>
The amount of REM sleep and cycling varies among animals; predators experience 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 name = "Parmeggiani_2011" />Template:Rp 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 name="Steriade_2013" />Template:Rp In utero, mammals spend more than half (50–80%) of a 24-hour day in REM sleep.<ref name=McCarley2007 />
Sleeping reptiles do not seem to have PGO waves or the localized brain activation seen in mammalian REM. However, they do exhibit sleep cycles with phases of REM-like electrical activity measurable by EEG.<ref name=RattenborgEtAl2011 /> A recent study found periodic eye movements in the central bearded dragon of Australia, leading its authors to speculate that the common ancestor of amniotes may therefore have manifested some precursor to REMS.<ref>Template:Cite journal</ref>
Observations of jumping spiders in their nocturnal resting position also suggest a REM sleep-like state characterized by bouts of twitching and retinal movements and hints of muscle atonia (legs curling up as a result of pressure loss caused by muscle atonia in the prosoma).<ref>Template:Cite journal</ref>
Sleep deprivation experiments on non-human animals can be set up differently than those on humans. 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 name="Rasch_2013" />Template:Rp This method also stops working after about 3 days as the subjects (typically rats) lose their will to avoid the water.<ref name=BarotKushida2011 /> 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>Template:Cite journal</ref>
Possible functionsEdit
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>Template:Cite journal</ref> Further, the existence of a "REM rebound" effect suggests the possibility of a biological need for REM sleep.
While the precise function of REM sleep is not well understood, several theories have been proposed.
MemoryEdit
Sleep in general aids memory. REM sleep may favor the preservation of certain types of memories: specifically, procedural memory, spatial memory, and emotional memory. In rats, REM sleep increases following intensive learning, especially several hours after, and sometimes for multiple nights. Experimental REM sleep deprivation has sometimes inhibited memory consolidation, especially regarding complex processes (e.g., how to escape from an elaborate maze).<ref name="Rasch_2013" />Template:Rp 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 name="Rasch_2013" />Template:Rp REM sleep apparently counteracts attempts to suppress certain thoughts.<ref name="Rasch_2013" />
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 name="Rasch_2013" />Template:Rp 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">Template:Cite journal</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.">Template:Cite journal</ref> According to the sequential hypothesis, the two types of sleep work together to consolidate memory.<ref name="Rasch_2013" />
Sleep researcher Jerome Siegel has observed that extreme REM deprivation does not significantly interfere with memory. 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. Antidepressants, which suppress REM sleep, show no evidence of impairing memory and may improve it.<ref name=Siegel2001>Template:Cite journal</ref>
Graeme Mitchison and Francis Crick 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"—a process they characterize as "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>Template:Cite journal</ref> Memory consolidation during paradoxical sleep 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 the basic neural networks involved in homeostasis, which are protected from this "synaptic downscaling" effect during deep sleep.<ref name = "Parmeggiani_2011" />Template:Rp
Neural ontogenyEdit
REM sleep prevails most after birth, and diminishes with age. According to the "ontogenetic hypothesis", REM (also known in neonates as active sleep) aids the developing brain by providing the neural stimulation that newborns need to form mature neural connections.<ref>Marks et al. 1994</ref> Sleep deprivation studies have shown that deprivation early in life can result in behavioral problems, permanent sleep disruption, and decreased brain mass.<ref name="pmid6850353">Template:Cite journal</ref><ref name=Frank2011 /> The strongest evidence for the ontogenetic hypothesis comes from experiments on REM deprivation, and from the development of the visual system in the lateral geniculate nucleus and primary visual cortex.<ref name=Frank2011 />
Defensive immobilizationEdit
Ioannis Tsoukalas of Stockholm University has hypothesized that 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 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, cholinergic neurotransmission, paralysis, hippocampal theta rhythm, and thermoregulatory changes.<ref name=Tsoukalas>Template:Cite journal</ref><ref name=Vitelli2013>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>
Shift of gazeEdit
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 blind and in fetuses in spite of lack of vision. Also, 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">Template:Cite journal</ref>
Oxygen supply to corneaEdit
Dr. David M. Maurice, an eye specialist and former adjunct professor at Columbia University, proposed that REM sleep was associated with oxygen supply to the cornea, and that aqueous humor, the liquid between cornea and iris, was stagnant if not stirred.<ref name=Maurice>Template:Cite journal</ref> Among the supportive evidence, he calculated that if aqueous humor was stagnant, oxygen from the iris had to reach the cornea by diffusion through aqueous humor, which was not sufficient. According to the theory, when the organism is awake, eye movement (or cool environmental temperature) enables the aqueous humor to circulate. When the organism 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 experience REM sleep, but do not move their head more than in non-REM sleep<ref name = Scriba>Template:Cite journal; see Fig. S1</ref> and it is well known that owls' eyes are nearly immobile.<ref>Template:Cite journal</ref>
Other theoriesEdit
Another theory suggests that monoamine shutdown is required so that the monoamine receptors in the brain can recover to regain full sensitivity.
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>Template:Cite book</ref><ref name = "Jouvet_1999" />Template:Rp<ref>Template:Cite book</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 REM sleep warms the brain, stimulates and stabilizes the neural circuits that have not been activated during waking, or creates internal stimulation to aid development of the CNS; while some argue that REM lacks any purpose, and simply results from random brain activation.<ref name="Leclair-Visonneau"/><ref name=Ruby2011>Template:Cite journal</ref>
Furthermore, eye movements are also theorized to play a role in certain psychotherapies such as eye movement desensitization and reprocessing (EMDR).
See alsoEdit
ReferencesEdit
Further readingEdit
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External linksEdit
- PBS' NOVA episode "What Are Dreams?" Video and Transcript
- LSDBase – an open sleep research database with images of REM sleep recordings.