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The '''sentinel hypothesis''' of REM sleep was put forward by Frederic 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 non-REM 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.<ref>{{cite book|title=The Mind in Sleep: Psychology and Psychophysiology|author=Steven J. Ellman and John S. Antrobus|chapter=Effects of REM deprivation|pages=398|year=1991|publisher=John Wiley and Sons|isbn=0471525561}}</ref><ref>{{cite book|title=The Paradox of Sleep: The Story of Dreaming|author=Michel Jouvet|pages=123|others=Translated by Laurence Garey|year=2001|publisher=MIT Press|isbn=0262600404}}</ref><ref>{{cite book|title=Understanding Sleep and Dreaming|author=William H. Moorcroft and Paula Belcher|chapter=Functions of REMS and Dreaming|pages=290|year=2003|publisher=Springer|isbn=0306474255}}</ref>
The '''sentinel hypothesis''' of REM sleep was put forward by Frederic 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 non-REM 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.<ref>{{cite book|title=The Mind in Sleep: Psychology and Psychophysiology|author=Steven J. Ellman and John S. Antrobus|chapter=Effects of REM deprivation|pages=398|year=1991|publisher=John Wiley and Sons|isbn=0471525561}}</ref><ref>{{cite book|title=The Paradox of Sleep: The Story of Dreaming|author=Michel Jouvet|pages=123|others=Translated by Laurence Garey|year=2001|publisher=MIT Press|isbn=0262600404}}</ref><ref>{{cite book|title=Understanding Sleep and Dreaming|author=William H. Moorcroft and Paula Belcher|chapter=Functions of REMS and Dreaming|pages=290|year=2003|publisher=Springer|isbn=0306474255}}</ref>


==REM sleep in other BT animals==
==REM sleep in other animals==
{{Main|Sleep (non-human)}}
{{Main|Sleep (non-human)}}
REM sleep occurs in all [[mammal]]s (excluding the egg-laying [[monotremes]] of Australia)<ref>Winson, J. (1972),. Interspecies differences in the occurrences of theta. Behavioral Biology 7: 479–487</ref>.
REM sleep occurs in all [[mammal]]s (excluding the egg-laying [[monotremes]] of Australia)<ref>Winson, J. (1972),. Interspecies differences in the occurrences of theta. Behavioral Biology 7: 479–487</ref>.

Revision as of 20:46, 26 May 2009

For other uses, see Eye movement (disambiguation).
This article is about a phase of sleep. For the American rock band, see R.E.M.

Rapid eye movement (REM) sleep is a normal stage of sleep characterized by rapid movements of the eyes. REM sleep is classified into two categories: tonic and phasic.[1] It was identified and defined by Kleitman and Aserinsky in the early 1950s.

Criteria for REM sleep includes not only rapid eye movements, but also low muscle tone and a rapid, low voltage EEG -- these features are easily discernible in a polysomnogram, the sleep study typically done for patients with suspected sleep disorders.

REM sleep in adult humans typically occupies 20-25% of total sleep, about 90-120 minutes of a night's sleep. During a normal night of sleep, humans usually experience about 4 or 5 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.[2] During REM, the activity of the brain's neurons is quite similar to that during waking hours; for this reason, the sleep stage may be called paradoxical sleep. This means that there are no dominating brain waves during REM sleep.

REM sleep is physiologically different from the other phases of sleep, which are collectively referred to as non-REM sleep (NREM). Vividly recalled dreams mostly occur during REM sleep.

Physiology of REM sleep

Polysomnographic record of REM Sleep. EEG highlighted by red box. Eye movements highlighted by red line.

Physiologically, certain neurons in the brain stem, known as REM sleep-on cells, (located in the pontine tegmentum), are particularly active during REM sleep, and are probably responsible for its occurrence. The release of certain neurotransmitters, the monoamines (norepinephrine, serotonin and histamine), is completely shut down during REM. This causes REM atonia, a state in which the motor neurons are not stimulated and thus the body's muscles don't move. Lack of such REM atonia causes REM Behavior Disorder; sufferers act out the movements occurring in their dreams.

Heart rate and breathing rate are irregular during REM sleep, again similar to the waking hours. Body temperature is not well regulated during REM. Erections of the penis (Nocturnal Penile Tumescence or NPT) frequently accompany REM sleep and their presence in the case of someone suffering erectile dysfunction while awake may suggest its having a psychological rather than an organic cause. Clitoral enlargement, with accompanying vaginal blood flow and transudation (i.e. lubrication) is also present during REM.

In a study published in the journal Human Brain Mapping, participants who were in REM "dream" sleep were also monitored by special MRI imaging designed to visualize brain activity. The researchers found activity in areas of the brain that control sight, hearing, smell, touch, balance and body movements.[3][4]

The eye movements associated with REM are generated by the pontine nucleus with projections to the superior colliculus and are associated with PGO waves(Ponto-geniculo-occipital waves).

During dreaming, the primary visual cortex is inactive, while secondary areas are active. This is similar to when subjects are asked to imagine or recall a visual scene, and different from what happens when they are actually seeing the scene.[5]

See also: Dream

REM sleep disorders

REM sleep can occur within about 90 minutes of falling asleep, but in people with a sleep onset REM period, it may be as little as 15-25 minutes; this is considered a sign of narcolepsy.[6]

Rapid eye movement sleep behavior disorder (RBD) is a parasomnia that involves loss of atonia (paralysis) during otherwise intact REM sleep. The loss of motor inhibition leads to a wide spectrum of behavioral release during dreaming. This extends from simple limb twitches to more complex integrated movements where sufferers appear to be unconsciously acting out their dreams. One can have very vivid or life like dreams during REM. Also see lucid dreaming. This is where one is fully aware that he or she is sleeping and can control their dreams.

See also: Sleep disorder

Theories about the function(s) of REM sleep

The function of REM sleep is not well understood; several theories have been advanced.

According to one theory, certain memories are consolidated during REM sleep. Numerous studies have suggested that REM sleep is important for consolidation of procedural memory and spatial memory. (Slow-wave sleep, part of non-REM sleep, appears to be important for declarative memory.) A recent study[7] shows that artificial enhancement of the non-REM sleep improves the next-day recall of memorized pairs of words. Tucker et al.[8] demonstrated that a daytime nap containing solely non-REM sleep enhances declarative memory but not procedural memory. However, in people who have no REM sleep (because of brain damage), memory functions are not measurably affected.[9]

Intimately related to views on REM function in memory consolidation, Mitchison and Crick[10] have proposed 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 "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.

Stimulation in CNS 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 neonates) 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.[11] 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,[12] and result in an abnormal amount of neuronal cell death.[13] 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 Onthogenetic Hypothesis is that REM sleep may have no essentially vital function in the mature brain, i.e., once the development of CNS has completed. However, because processes of neuronal plasticity do not cease altogether in the adult brain,[14] REM sleep may continue to be implicated in neurogenesis in adults as a source of sustained spontaneous stimulation.

Other theories

Yet 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. The only way to cure it is to sleep early. 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. This however is not proven. As of yet, there is no known test that will prove the theory of chemical imbalance.[citation needed] Most antidepressants selectively inhibit REM sleep due to their effects on monoamines. However, this effect decreases after long-term use.

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.

The sentinel hypothesis of REM sleep was put forward by Frederic 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 non-REM 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.[15][16][17]

REM sleep in other animals

Main article: Sleep (non-human)

REM sleep occurs in all mammals (excluding the egg-laying monotremes of Australia)[18]. However the echidna does enter REM sleep, albeit only when the ambient temperature of its environment is around 25°C. At the temperatures of 15°C and 28°C, REMS is suppressed. Typical REM sleep has not been observed in cetaceans.

History

The phenomenon of REM sleep and its association with dreaming was discovered by Eugene Aserinsky and Nathaniel Kleitman with assistance from William C. Dement, a medical student at the time, in 1952 during their tenures at the University of Chicago. Kleitmann and Aserinsky's seminal article was published September 10, 1953.[19]

See also

References

  1. ^ Kryger M, Roth T, Dement W (2000). Principles & Practices of Sleep Medicine. WB Saunders Company. pp. 15, 724.{{cite book}}: CS1 maint: multiple names: authors list (link)
  2. ^ [1]
  3. ^ "fMRI evidence for multisensory recruitment associated with rapid eye movements during sleep". Human Brain Mappingdoi=10.1002/hbm.20635. 2008. doi:10.1002/hbm.20635. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |month= ignored (help); Unknown parameter |unused_data= ignored (help)
  4. ^ Rapid Eye Movement (REM) Study Shows Brain Functions Same Way Awake Or Asleep Newswise, Retrieved on November 2, 2008.
  5. ^ The Science Behind Dreams and Nightmares, Talk of the Nation, 30 Oct 2007
  6. ^ Sasaki Y (2000). "Sleep onset REM period appearance rate is affected by REM propensity in circadian rhythm in normal nocturnal sleep". Clin Neurophysiol. 111 (3): 428–33. doi:10.1016/S1388-2457(99)00254-0. PMID 10699402. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  7. ^ Marshall, Helgadóttir, Mölle & Born, 2006
  8. ^ Tucker; et al. (2006). "Neurobiology of Learning and Memory". 86 (2): 241–247. {{cite journal}}: Cite journal requires |journal= (help); Explicit use of et al. in: |author= (help)
  9. ^ Siegel, Jerome M. "The REM Sleep-Memory Consolidation Hypothesis". {{cite journal}}: Cite journal requires |journal= (help)
  10. ^ Mitchison & Crick (1984). "The function of dream sleep". Nature. 304 (5922): 111–4. doi:10.1038/304111a0.
  11. ^ Marks et al. 1995
  12. ^ Mirmiran et al. 1983
  13. ^ Morrissey, Duntley & Anch, 2004
  14. ^ Bruel-Jungerman E, Rampon C, Laroche S (2007). "Adult hippocampal neurogenesis, synaptic plasticity and memory: facts and hypotheses". Rev. Neurosci. 18 (2): 93–114.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ Steven J. Ellman and John S. Antrobus (1991). "Effects of REM deprivation". The Mind in Sleep: Psychology and Psychophysiology. John Wiley and Sons. p. 398. ISBN 0471525561.
  16. ^ Michel Jouvet (2001). The Paradox of Sleep: The Story of Dreaming. Translated by Laurence Garey. MIT Press. p. 123. ISBN 0262600404.
  17. ^ William H. Moorcroft and Paula Belcher (2003). "Functions of REMS and Dreaming". Understanding Sleep and Dreaming. Springer. p. 290. ISBN 0306474255.
  18. ^ Winson, J. (1972),. Interspecies differences in the occurrences of theta. Behavioral Biology 7: 479–487
  19. ^ Aserinsky E. and Kleitman N. (1953). "Regularly Occurring Periods of Eye Motility, and Concomitant Phenomena, during Sleep". Science. 118: 273–274. doi:10.1126/science.118.3062.273. PMID 13089671.

Further reading

  • Frederic Snyder (1966). "Toward an Evolutionary Theory of Dreaming". American Journal of Psychiatry. 123: 121–142.
  • Edward F. Pace-Schott, ed. (2003). Sleep and Dreaming: Scientific Advances and Reconsiderations. Cambridge University Press. ISBN 0521008697.

Koulack, D. To Catch A Dream: Explorations of Dreaming. New York, SUNY, 1991.

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