Rapid eye movement ( REM sleep , REMS ) is the unique phase of sleep in mammals and birds, distinguished by random movements of the eye, accompanied by low muscle tone throughout the body, and a sleeping tendency to dream clearly.
The REM phase is also known as paradoxical sleep ( PS ) and sometimes desynchronized sleep due to physiological similarities with wake status, including fast, low-voltage brain waves that are not synchronized. The electrical and chemical activity that governs this phase appears to originate from the brainstem and is characterized primarily by the abundance of acetylcholine neurotransmitters, combined with the almost absence of monoamine histamine neurotransmitters, serotonin, and norepinephrine.
REM sleep is physiologically different from other sleep phases, which are collectively referred to as non-REM sleep (NREM sleep, NREMS, synchronized sleep). REM and non-REM sleep alternate in one sleep cycle, which lasts about 90 minutes in adult humans. As the sleep cycle continues, they move on to a higher proportion of REM sleep. The transition to REM sleep brings a marked physical change, beginning with a burst of electricity called the PGO wave coming from the brain stem. Organisms in REM sleep postpone central homeostasis, allowing large fluctuations in respiration, thermoregulation, and circulation that do not occur in other sleep or wake modes. The body suddenly loses muscle, a condition known as REM atonia.
Professor Nathaniel Kleitman and his pupil Eugene Aserinsky define rapid eye movements and relate them to dreams in 1953. REM sleep is further described by researchers including William Dement and Michel Jouvet. Many experiments have involved the test subjects as they begin to enter the REM phase, resulting in a state known as REM deprivation. Subjects that are allowed to sleep normally again usually experience a simple REM rebound. Neurosurgical techniques, chemical injections, electroencephalography, positron emission tomography, and dreamers' waking reports have all been used to study this sleep phase.
Video Rapid eye movement sleep
Physiology
Electricity activity in brain
REM sleep is a "paradox" because of its similarity to consciousness. Although the body is paralyzed, the brain acts somewhat awake, with the cerebral neurons firing with the same overall intensity as in consciousness. Electroencephalography during REM deep sleep reveals rapid, low amplitude, synchronization of nerve oscillations (brainwaves) that resemble patterns seen during awake different from slow? (delta) NREM wave pattern of deep sleep. An important element of this contrast is? (Theta) rhythm in the hippocampus that shows 40-60 gamma waves of Hz, in the cortex, as occurs when waking up. The cortical and thalamic neurons in the wake of sleep and REM sleep brain are more depolarized (fire easier) than in the NREM sleep brain.
During REM sleep, electrical connectivity between different parts of the brain manifests differently than when awake. The frontal and posterior areas are less coherent at most frequencies, a fact that has been cited in relation to a chaotic dream experience. However, the posterior area is more coherent with each other; such as right and left hemispheres, especially during clear dreams.
The use of brain energy in REM sleep, as measured by oxygen and glucose metabolism, equals or exceeds energy use when waking up. The levels in non-REM sleep are 11 - 40% lower.
Brainstem
Nerve activity during REM sleep seems to stem from the brain stem, especially pontine tegmentum and locus coeruleus. REM sleep is interspersed and immediately preceded by PGO (ponto-geniculo-occipital) waves, bursts of electrical activity originating from the brain stem. (PGO waves have long been measured directly in cats but not in humans due to experimental constraints, but comparable effects have been observed in humans during "phasic" events occurring during REM sleep, and the presence of similar PGO waves is thus concluded. in groups of about every 6 seconds for 1-2 minutes during transition from deep sleep to paradox They show the highest amplitude after moving to the visual cortex and are the cause of "rapid eye movement" in paradoxical sleep.Other muscles can also contract under the effects of these waves.
Forebrain
Research in the 1990s using positron emission tomography (PET) confirmed the role of the brain stem and suggested that, in the forebrain, the limbic and paralimbic systems show more activation than other regions. Areas activated during REM sleep are roughly the inverse of being activated during non-REM sleep and show greater activity than in a quiet wake. The "anterior paralimbic REM activation area" (APRA) includes areas related to emotion, memory, fear and sex, and may be associated with dreaming experiences during REMS. Recent PET research has shown that the distribution of brain activity during REM sleep varies in correspondence with the type of activity seen in previous periods of consciousness.
The superior frontal gyrus, the medial frontal area, the intraparietal sulcus, and the superior parietal cortex, the area involved in sophisticated mental activity, exhibit similar activity in REM sleep as in waking. The amygdala is also active during REM sleep and can participate in generating PGO waves, and the experimental emphasis of the amygdala results in less REM sleep. The amygdala can also function as the heart of the less active inactive cortex.
Chemicals in the brain
Compared to slow-wave sleep, both waking and sleeping paradoxes involve higher use of acotilcholine neurotransmitters, which can lead to brainwaves faster. Neurotransmitter monoamine norepinephrine, serotonin and histamine are completely unavailable. Injections of acetylcholinesterase inhibitors, which effectively increase the acetylcholine available, have been found to induce sleep paradox in humans and other animals already in slow-wave sleep. Carbachol, which mimics the effects of acetylcholine on neurons, has the same effect. In waking people, the same injections produce a paradoxical sleep only if the monoamine neurotransmitter is depleted.
Two other neurotransmitters, orexin and gamma-Aminobutyric acid (GABA), seem to promote awake, ease during deep sleep, and inhibit sleep paradox.
In contrast to the sudden transition in electrical patterns, chemical changes in the brain show continuous periodic oscillations.
Model REM rules
According to the synthesis-activation hypothesis proposed by Robert McCarley and Allan Hobson in 1975-1977, control over REM sleep involves the "REM-on" and "REM-off" neuron pathways in the brainstem. REM-on neurons are mainly cholinergic (ie, involving acetylcholine); REM-off neurons activate serotonin and noradrenaline, which are among other functions suppressing REM-on neurons. McCarley and Hobson suggest that REM-on neurons actually stimulate REM-off neurons, thus serving as a mechanism for cycling between REM and non-REM sleep. They used the Lotka-Volterra equation to illustrate this cyclical inverse relationship. Kayuza Sakai and Michel Jouvet proposed the same model in 1981. While acetylcholine manifests in the cortex simultaneously during awake and REM, it appears in higher concentrations in the brain stem during REM. Withdrawal of orexin and GABA may result in the absence of other excitatory neurotransmitters; researchers in recent years have increasingly covered GABA regulations in their models.
Eye movements
Most eye movements in "rapid eye movement" sleep are actually less rapid than those normally shown by human waking. They are also shorter in duration and more likely to roll back to their starting point. About seven of the loops lasted more than a minute of REM sleep. In slow-wave sleep the eyes can move away; However, the eyes of the sleeping paradox man move together. These eye movements follow a wave-geniculo ponto-occipital originating from the brain stem. The movement of the eye itself may be associated with a vision experienced in a dream, but a direct link remains to be clearly defined. Kongenit blind people, who usually have no visual imagery in their dreams, they move their eyes in REM sleep. An alternative explanation shows that the functional purpose of REM sleep is to process the procedural memory, and rapid eye movement is only a side effect of the brain that processes procedural memory associated with the eye.
circulation, respiration and thermoregulation
In general, the body delayed homeostasis during sleep paradox. Heart rate, heart pressure, cardiac output, arterial pressure, and rapid breathing rate become irregular as the body moves into REM sleep. In general, respiratory reflexes such as response to hypoxia are reduced. Overall, the brain gives less control over breathing; Electrical stimulation of areas of the brain associated with breathing does not affect the lungs, as is the case during non-REM sleep and in wake. Fluctuations in heart rate and arterial pressure tend to coincide with PGO waves and rapid eye movements, twitches, or sudden changes in breathing.
Penile erection (nocturnal penile tumescence or NPT) usually accompanies REM sleep in mice and humans. If a man has erectile dysfunction (ED) upon awakening, but has an episode of NPT during REM, it will show that ED is psychologically rather than a physiological cause. In women, clitoral erections (nocturnal clitoral tumescence or NCT) cause enlargement, accompanied by vaginal blood flow and transudation (ie lubrication). During a normal night's sleep the penis and clitoris can erect for a total time of one hour up to three and a half hours during REM.
Body temperature is not well regulated during REM sleep, and thus organisms become more sensitive to temperature outside their thermoneutral zone. Cats and other small furry mammals will shiver and breathe faster to regulate the temperature during NREMS but not during REMS. With the loss of muscle tone, the animals lose the ability to regulate temperature through body movement. (However, even cats with pontine lesions that prevent muscle atonia during REM do not regulate their temperature by shivering.) Neurons are usually active in response to cold temperatures - triggers for neurological thermoregulation - not burning during REM sleep, as they do in NREM sleep and get up.
As a result, hot or cold environmental temperatures can reduce the proportion of REM sleep, as well as the total amount of sleep. In other words, if at the end of the sleep phase, the organism's thermal indicator falls outside a certain range, then it will not enter paradoxical sleep, so the deregulation allows the temperature to move further than the desired value. This mechanism can be 'fooled' by artificially heating the brain.
Muscle
REM atonia , an almost complete paralysis of the body, is achieved by inhibition of motor neurons. As the body shifts to REM sleep, motor neurons throughout the body undergo a process called hyperpolarization: their already negative membrane potential is reduced by another 2-10 milivolts, thereby increasing the threshold that the stimulus must overcome to generate it. Muscle inhibition may result from the unavailability of monoamine neurotransmitters (retaining abundance of acetylcholine in the brain stem) and possibly from the mechanisms used in inhibition of built muscles. The medulla oblongata, located between the pons and the spine, appears to have a capacity for muscle-wide inhibition of organisms. Some local twitches and reflexes can still occur. Contract students.
The deficiency of REM atonia leads to REM behavior disorders, patients who physically acted their dreams, or otherwise "dreamed of their actions", under an alternative theory on the relationship between muscle impulses during REM and associated mental imagery (which would also apply to people without condition, except that the order for their muscles is suppressed). This is different from conventional sleepwalking, which occurs during slow wave sleep, not REM. On the other hand, narcolepsy seems to involve excessive and undesirable REM atony - that is, excessive daytime cataplexy and sleepiness, hypnagogic hallucinations before slow-wave sleep, or sleep paralysis on awakening. Other psychiatric disorders including depression have been associated with a disproportionate REM sleep. Patients with suspected sleep disorders are usually evaluated by polysomnograms.
Lesions in pons to prevent atony cause "REM behavior disorders" in animals.
Maps Rapid eye movement sleep
Psychology
Dreaming
Rapid eye movement sleep (REM) since its discovery is closely related to dreams. Waking up during the REM phase is a common experimental method for obtaining dream reports; 80% of neurotypical people can provide some sort of dream report in these situations. Sleepers awakening from REM tend to provide longer narrative descriptions of their dreams, and to estimate the duration of their dreams longer. Dirty dreams are reported much more often in REM sleep. (Even this can be regarded as a hybrid state that incorporates important elements of REM sleep and awakened awareness.) The mental events that occur during REM most often have dream features including narrative structures, convincing (similarity of experience to wake life), and merging instingtual theme. Sometimes they include elements of the dreamer's recent experiences taken directly from the episodic memory. With one estimate, 80% of dreams occur during REM.
Hobson and McCarley propose that the PGO wave of "phasic" REM characteristics may supply the visual cortex and the forebrain with electrical excitement that reinforce the hallucinatory aspects of dreaming. However, people who wake up during sleep do not report a more strange dream significantly during the REM phase basis, compared to REMS tonics. Another possible connection between these two phenomena is that a higher threshold for sensory disturbance during REM sleep allows the brain to travel further along unrealistic and strange thoughts.
Some dreams can occur during non-REM sleep. "Light sleepers" can experience dreams during stage 2 of non-REM sleep, while "deep sleep", after waking up at the same stage, are more likely to report "thinking" but not "dreaming". Certain scientific efforts to assess the unique nature of the unique dreams experienced during sleep are compelled to conclude that awakened minds can be just as strange, especially in conditions of sensory deficiency. Due to non-REM dreams, some researchers slept strongly to deny the importance of connecting dreams to the REM sleep phase. The prospect that the famous neurological aspects of REM do not cause dreams indicates the need to re-examine the neurobiology of dreams per se. Some researchers (Dement, Hobson, Jouvet, for example) tend to reject the idea of ​​deciding to dream of REM sleep.
Creativity
Upon awakening from REM sleep, thoughts appear "hyperassociative" - ​​more easily accept semantic priming effects. People who awaken from REM have done better on tasks such as anagrams and creative problem solving.
Sleep aids the process by which creativity forms associative elements into useful new combinations or meets certain requirements. It occurs in REM sleep rather than NREM sleep. Rather than due to the memory process, it has been associated with changes during REM sleep in cholinergic and noradrenergic neuromodulasi. High levels of acetylcholine in the hippocampus suppress feedback from the hippocampus to the neocortex, while lower levels of acetylcholine and norepinephrine in the neocortex encourage the spread of uncontrolled associative activity within the neocortex area. This is in contrast to awakening consciousness, in which higher levels of norepinephrine and acetylcholine inhibit recurrent connections in the neocortex. REM sleep through this process adds creativity by allowing "neocortical structures to reorganize associative hierarchies, where information from the hippocampus will be reinterpreted in relation to previous semantic representations or nodes."
Time
In the ultradian sleep cycle, an organism alternates between deep sleep (slow, large, synchronized brain waves) and paradoxical sleep (faster and less synchronized waves). Sleep occurs in the context of a larger circadian rhythm, which affects sleepiness and physiological factors based on time clocks in the body. Sleep can be distributed throughout the day or grouped during one part of the rhythm: in nocturnal animals, during the day, and in diurnal animals, at night. The organism returns to homeostatic regulation immediately after REM sleep ends.
During sleepless nights, humans usually experience about four or five periods of REM sleep; they are shorter (~ 15m) at the beginning of the night and longer (~ 25m) towards the end. Many animals and some people tend to wake up, or experience a very mild sleep period, for a short time immediately after REM attacks. The relative amount of REM sleep varies greatly with age. Newborns spend more than 80% of total sleep time on REM.
REM sleep typically occupies 20-25% of total sleep in adult humans: about 90-120 minutes of sleep a night. The first REM episode occurred about 70 minutes after falling asleep. A cycle of about 90 minutes each follows, with each cycle including a larger proportion of REM sleep. (Increased REM sleep at night is connected with circadian rhythms and occurs even in people who do not sleep in the first part of the night.)
In the weeks after the human baby is born, as the nervous system matures, the nervous pattern in sleep begins to show rhythm of REM and non-REM sleep. (In mammals that develop faster, this process occurs in the womb.) Babies spend more time in REM sleep than adults. The proportion of REM sleep subsequently decreased significantly in childhood. Older people tend to sleep less overall but sleep in REM for about the same absolute time, and therefore spend most of their sleep in REM.
Fast sleep eye movements can be subclassified into tonic and phasic mode. Tonic REM is characterized by theta rhythm in the brain; phasic REM is characterized by PGO waves and real "fast" eye movements. The processing of external stimuli is severely impeded during the REM phase, and recent evidence suggests that sleep is more difficult to evoke from the REM phase than in slow-wave sleep.
Influence of REM sleep deprivation
Selective REMS deposition leads to a significant increase in the number of attempts to enter the REM stage during sleep. On a recovery night, an individual will usually move to stage 3 and sleep REM faster and experience REM rebound, which refers to an increase in time spent in the REM stage above the normal level. This finding is consistent with the idea that REM sleep is biologically necessary. However, REM sleep "rebound" usually does not last fully for the estimated length of the missed REM period.
After 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 of the symptoms of depression are found suppressed by REM deprivation; aggression, and eating behavior may increase. Tall norepinepherine is the probable cause of this outcome. Whether and how long-term REM termination has a psychological effect remains a matter of controversy. Some reports indicate that REM deprivation increases aggression and sexual behavior in laboratory animal animals. Mice deprived of paradoxical sleep die within 4-6 weeks (twice before death if total sleep is lacking). The average body temperature continues to fall during this period.
It has been suggested that acute REM sleep deprivation may increase certain types of depression when depression appears to be associated with a particular neurotransmitter imbalance. Although sleep deprivation generally disrupts most of the population, it has been repeatedly proven to reduce depression, albeit temporarily. More than half of people who experienced this relief report became ineffective after sleeping the next night. Thus, researchers have devised methods such as changing sleep schedules for the day range after the REM deprivation period and incorporating sleep schedule changes with pharmacotherapy 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 monoamine neurotransmitters to be suppressed for REM sleep. Given on therapeutic doses, these medications can stop REM sleep completely for weeks or months. Withdrawal causes REM rebound. Sleep deprivation stimulates hippocampal neurogenesis such as antidepressants, but whether this effect is driven by REM sleep is specifically unknown.
REM sleep on other animals
Although it manifests differently in different animals, REM sleep or something like that happens in all land mammals as well as in birds. The main criteria used to identify REM are changes in electrical activity, measured by EEG, and loss of muscle tone, interspersed with twitch attacks in the REM phase. The amount of REM sleep and cycling varies among animals; predators enjoy more REM sleep than prey. Larger animals also tend to stay in longer REM, probably because higher thermal inertia of the brain and their body allows them to tolerate longer thermoregulation suspensions. The period (full REM and non-REM cycle) lasts for about 90 minutes in humans, 22 minutes in cats, and 12 minutes in mice. In the womb, mammals spend more than half (50-80%) of 24 hours a day in REM sleep.
Sleeping reptiles do not seem to have any PGO waves or local brain activations seen in REM mammals. Yet they show a sleep cycle with phases of REM electrical activity as can be measured by EEG. A recent study found a periodic eye movement on the central bearded dragon of Australia, leading to its authors speculating that the same amniotant ancestors may have manifested some predecessors for REMS.
Sleep-less experiments in non-human animals can be set differently than humans. The "flowerpot" method involves placing laboratory animals on water on a very small platform that falls after muscle loss. The natural revulsion that produces results in changes in organisms that certainly exceed the absence of the sleep phase. This method also stops working after about 3 days because the subject (usually a rat) loses his desire to avoid water. Another method involves brainwave computer monitoring, complete with mechanical automatic shuffling of the enclosure when the test animal enters REM sleep.
Possible function
Some researchers argue that the perpetuation of complex brain processes such as REM sleep suggests that it serves important for the survival of mammals and poultry species. It meets important physiological needs that are essential for survival to the extent that prolonged REM sleep disorders cause death in animal experiments. In humans and experimental animals, REM sleep disorders cause some behavioral and physiological abnormalities. REM sleep loss has been observed during various natural and experimental infections. The survival of experimental animals decreases when REM sleep is completely weakened during infection; this leads to the possibility that the quality and quantity of REM sleep is generally important for normal body physiology. Furthermore, the presence of the "REM rebound" effect suggests a possible biological need for REM sleep.
While the exact function of REM sleep is not well understood, several theories have been proposed.
Memory
Sleep generally helps memory. REM sleep can support the preservation of certain types of memory: specifically, procedural memory, spatial memory, and emotional memory. In mice, REM sleep increased after intensive study, especially a few hours later, and sometimes for several nights. Lack of experimental REM sleep sometimes inhibits memory consolidation, especially regarding complex processes (eg, how to escape from a complicated maze). In humans, the best evidence for REM repair in memory is related to learning procedures - new ways to move the body (such as trampoline jumps), and new troubleshooting techniques. REM deprivation seems to damage the declarative (ie, factual) memory only in more complex cases, such as longer story memories. REM sleep seems to negate attempts to suppress certain thoughts.
According to the dual-process hypothesis of sleep and memory, the two major phases of sleep are associated with different memory types. The "half-night" study has tested this hypothesis with good memory tasks beginning before bedtime and rated in the middle of the night, or starting at midnight and assessed in the morning. Slow wave sleep, part of non-REM sleep, seems important for declarative memory. An artificial increase in non-REM sleep improves the ability to remember the words remembered the next day. Tucker et al. shows that a nap that contains only non-REM sleep enhances declarative memory but not procedural memory. According to the sequential hypothesis two types of sleep work together to consolidate memory.
Sleep researcher Jerome Siegel has observed that extreme REM removal 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 brain stem did not find the individual memory to be disturbed. Antidepressants, which suppress REM sleep, show no evidence of damage to memory and can improve it.
Graeme Mitchison and Francis Crick proposed in 1983 that based on inherent spontaneous activity, REM sleep function "is to eliminate certain unwanted interaction modes within the tissue cells in the cerebral cortex", which their process characterizes as "unlearning". Consequently, the relevant memories (the neuronal substrate essentially strong enough to withstand spontaneity, chaotic activation) are further strengthened, while the "noise" memory footprint is weaker, while splitting. Consolidation of memory during sleep paradoxes is specifically correlated with periods of rapid eye movement, which does not occur continuously. One explanation for this correlation is that the PGO power wave, which precedes eye movements, also affects memory. REM sleep can provide a unique opportunity for "no learning" to occur in the basic neural tissues involved in homeostasis, which is protected from this "downscaling synaptic" effect during deep sleep.
nervous ontogeny
REM sleep occurs most often after birth, and decreases with age. According to the "ontogenetic hypothesis", REM (also known in neonates as active sleep) helps the development of the brain by providing the nerve stimulation that a newborn needs to establish a mature nerve connection. Lack of sleep has shown that early deprivation of life can lead to behavioral problems, permanent sleep disturbances, decreased brain mass, and produce abnormal amounts of nerve cell death. The strongest evidence for the ontogenetic hypothesis comes from experiments on REM deprivation and the development of visual systems in the Lateral geniculate nucleus and the primary visual cortex.
Defensive Immobilization
Ioannis Tsoukalas of the University of Stockholm has hypothesized that REM sleep is an evolutionary transformation of a well-known defense mechanism, a tonic immobility reflex. This reflex, also known as animal hypnosis or mock death, serves as the last line of defense against an invading predator and consists of total immobilization of the animal so that it looks dead. Tsoukalas argues that the neurophysiology and phenomenology of these reactions show striking similarity to REM sleep; for example, both reactions show brainstem control, paralysis, theta hippocampal rhythm, and thermoregulation changes.
Shift view
According to "hypothesis scanning", the directional nature of REM sleep is related to a shift in dream shadow. Against this hypothesis is that eye movement is like happening to those born blind and to the fetus despite the lack of vision. Also, binocular REM is not conjugated (ie, both eyes do not point in the same direction at a time) and so have no fixation points. To support this theory, the study found that in goal-oriented dreams, the eyes were directed at the actions of dreams, determined from the correlations in the eyes and body movements of REM sleep disorder patients imposing their dreams.
Supply of oxygen to the cornea
David M. Maurice (1922-2002), an eye specialist and assistant professor of semi-retirement at Columbia University, proposed that REM sleep was associated with oxygen supply to the cornea, and that aqueous humor, fluid between the cornea and iris, stagnant if not stirred. Among the supporting evidence, he calculated that if aqueous humor is stagnant, oxygen from the iris must reach the cornea by diffusion through aqueous humor, which is not enough. According to the theory, when animals are awake, eye movements (or cold temperatures) allow aqueous humor to circulate. When animals are asleep, REM provides a much-needed boost to watery humor. This theory is consistent with the observation that fetuses, as well as newborns with closed eyes, spend a lot of time in REM sleep, and that during normal sleep, a person's REM episode becomes progressively deeper in the night. However, owls have REM sleep, but do not move their heads more than on non-REM sleep and it is well known that owl eyes barely move.
Other theories
Another theory suggests that monoamine shutdown is required so that monoamine receptors in the brain can recover to regain full sensitivity.
The REM sleep sentinel hypothesis was proposed by Frederick Snyder in 1966. This is based on the observation that REM sleep in some mammals (rats, hedgehogs, rabbits, and rhesus monkeys) is followed by a brief resurrection. This does not happen to cats or humans, although humans are more likely to wake up from REM sleep than from NREM sleep. Snyder hypothesizes that REM sleep activates animals at regular intervals, to scan the environment for possible predators. This hypothesis does not explain the paralysis of REM sleep muscles; However, a logical analysis may indicate that muscle paralysis exists to prevent the animal from waking up completely unnecessarily, and allows it to return easily to deeper sleep.
Jim Horne, a sleep researcher at Loughborough University, has suggested that REM in modern humans compensates for the reduced need to look for food that is awake.
Another theory is that REM sleep warms the brain, stimulates and stabilizes neural circuits that have not been activated on waking, or creates internal stimuli to aid CNS development; while some argue that REM has no purpose whatsoever, and only the result of random brain activation.
Discovery and further research
The recognition of different types of sleep can be seen in ancient Indian and Roman literature. Observers have long noticed that sleeping dogs move and move but only at certain times.
The German scientist Richard Klaue in 1937 first discovered a period of rapid electrical activity in the sleeping cat's brain. In 1944, Ohlmeyer reported a 90-minute ultraman sleep cycle involving a male erection lasting 25 minutes. At the University of Chicago in 1952, Eugene Aserinsky, Nathaniel Kleitman, and William C. Dement, discovered the phase of rapid eye movement during sleep, and attributed it to dreams. Their article was published September 10, 1953. Aserinsky, then Kleitman, first observed eye movement and accompanied neuroelectrical activity in their own children.
William Dement advances the study of REM deprivation, with experiments in which the subject awakens whenever their EEG indicates the beginning of REM sleep. He published "The Effect of Dream Deprivation" in June 1960. ("REM deprivation" has become a more general term after subsequent research suggests the possibility of non-REM dreams.)
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