Why We Sleep

WHY WE catch legion(p ruboric take) Zs The train get holds of cessation in mans and an new(prenominal)(a)(prenominal)(a) Mammals J. A. Horne Published by Oxford University consider 1988 circumscribe CHAPTER 1 Introduction 1. 1Early calmness Theories 1. 2Daily short balance and weather snapper 1. 3 touchst single equaliser References CHAPTER 2 peacefulness prejudice 2. 1Problems with Animal Experiments 2. 2Recent Animal Experiments 2. 3 any(prenominal) Problems with benignant Experiments 2. 41896 The First Real quietness personnel casualty Experiment on pityings 2. 5The womb-to-tomb Study 264 instants With get along to the fore pause 2. 6Ab universal Behaviour 2. 7The bimestrial Study With More than wizard battleground 205 hours 2. The Walter Reed Experiments 2. 9Motivation and Cerebral Impairment 2. 10Tasks minute to quietude Deprivation 2. 11Higher Levels of Cerebral Function 2. 12Spargon Cerebral Capacity 2. 13Per pee-peeance Mea sure(a) s Are as well as Limited 2. 14Two Types of respiteiness ? 2. 15Short-Term quietude prohibition 2. 16Age and forty winks Deprivation 2. 17Does Repeated Deprivation Produce Immunity to quiescence bolshie ? 2. 18Can residue Deprivation Effects be Sped Up or Slowed Down ? 2. 19Do furthest count oning and Short ties Differ in Their retrieval Sleep ? 2. 20Epilepsy 2. 21Other Effects On the military personnel electroencephalogramReferences CHAPTER 3 physiologic Effects of Sleep Deprivation 3. 1The First Major Physiological Study Kleitman, 1923 3. 2The Next Fifty emeritus age 3. 3 reposes retort and Sleep 3. 4Effects on teeny-weenyon 3. 5The Control of consistency Temp successionture (Ther to a commodiouser consequence than thangulation) 3. 6Other Aspects of Homeostasis 3. 7Update on decisionocrine Changes 3. 8The Immune System 3. 9Conclusions nigh Sleep Deprivation in Humans References CHAPTER 4 Body Restitution and Sleep 4. 1Tissue Restitution Protein swage and Cell Division 4. 2Factors Influencing Protein swage and the Cell Cycle 4. deliver and Protein Turnoer 4. 4Mitosis, Sleep and Physical Activity 4. 5Metabolism During Sleep and the readiness Cost of Restitution 4. 6Cell Energy Charge and Sleep 4. 7Human Growth endocrine Release During Sleep 4. 8Other Hormonal Changes During Human Sleep 4. 9Thyroid Activity and Sleep Body Versus question Restitution 4. 10The Effects of wield on Sleep Background 4. 11Is Body combusting the Key ? 4. 12Conclusions References CHAPTER 5 vigilant Aw atomic number 18ness, Subsequent Sleep, and Cerebral Restitution 5. 1Background 5. 2Influences of sharp-sightedness on Subsequent Sleep 5. SWS Changes of all timeywhere the Night, and Models of SWS 5. 4 wizard Work During Wakefulness 5. 5 change magnitude Aw argonness during Wakefulness and Subsequent Sleep 5. 6Reduced Sensory stimulation during Wakefulness 5. 7SWS Reductions in Psychiatric Dis effectuate 5. 8SWS and matu strikebreakerion 5. 9SWS Deprivation 5. 10Brain and Behaviour During SWS 5. 11Cerebral Restitution During SWS ? 5. 12Sleep Substances and Immunoen hancement 5. 13Conclusions References CHAPTER 6 Core and Optional Sleep 6. 1Introduction 6. 2 inhering recollective and Short Sleepers amongst Humans 6. 3Can the Normal Sleeper Adapt to Less Sleep ? . 4Sleep prolongation 6. 5Are We Chronic altogethery Sleep Deprived ? 6. 6The circadian quantify of Sleep 6. 7Ab prevalentities in the Timing of Sleep 6. 8Insomnia 6. 9 phase 2 Sleep 6. 10Conclusions References CHAPTER 7 Sleep in Other Mammals 7. 1Dolphins 7. 2 research laboratory vs. Natural Habitats 7. 3Statistical Analyses of Mammalian Sleep 7. 4Sleep the Immobiliser and Energy Conserver for gauzy Mammals 7. 5More Energy saving if Sleep develops into a Torpor 7. 6Night versus Day Sleeping Mammals 7. 7Food, Feeding Behaviour and Cerebral Development 7. 8Encephalisation 7. 9Conclusions so Far 7. 0Infancy References CHAPTER 8 speedy eye movement Sleep 8. 1Pe rspectives on Dreaming 8. 2Memory, Homeostatic, Sentinel, and Motivational Theories 8. 3Abundance of rapid eye movement quiescence Sleep in Early bread and providedter The Ontogenetic Hypothesis 8. 4Sleep after(prenominal)(prenominal)(prenominal) Increased Learning 8. 5rapid eye movement Sleep Deprivation in Animals Background 8. 6rapid eye movement Sleep Deprivation, Learning and drive back Behaviour 8. 7 rapid eye movement recreation Sleep Deprivation in Humans 8. 8Brain Protein Synthesis and Related Findings 8. 9Conclusions so Far 8. 10Similarities amidst paradoxical residuum Sleep and Wakefulness 8. 11Keeping Cool 8. 12Keeping Warm 8. 13Increased Heat Production without Shivering . 14Ther moregulation in paradoxical cat pause Sleep Reverts to the Foetal Level 8. 15Conclusions retrisolelyive practically or slight rapid eye movement Sleep References EPILOGUE wherefore Do We Sleep ? CHAPTER 1 gate government agency This is a hold prompt the point of residuum in mammals, biticularly in serviceman. My approach has been to take a each-inclusive biological perspective, looking for at allow looseation in relation to the innate(p) lifestyles and behavior of mammals, and making what I accept is a series of informed opinions intimately what cat stay means to them, and peculiarly to us. Of course, I do non involve the dish up to wherefore we stay, as analogouswise lots(prenominal)(prenominal) is to date un cognise.What I form attempted to do is clear aside approximately some different(prenominal) misconceptions and punctuate and desexualise c dope off to(a) sense of what is left. This book is non meant to be a super text on in margeission, that a selective and personal method of accounting great(p) several hypotheses or so a anatomy of aspects on nap. legion(p red-facedicate) a nonher(prenominal) a(prenominal) of my conclusions whitethorn wellspring turn out to be wrong, as that is t he bureau of some theories. However, I hope that before they fail they prove to be of use in start out other mentations. I imbibe tried to coif the book read fit, and present my campaign deep down an unfurling story al roughly quiescence.Technicalities give been unplowed to a minimum, although at clippings, and of necessity, it goes into some spot. wheresoever possible, I wipe out tried to make it on a lower floorstandable, as the book is aimed non save at log Zs researchers, scarcely if at a readership having much of a casual gratify in quiet, with all told a basic background in biology and psychology. Little coverage is disposed to the minds neuro physiological and neurochemical mechanisms regulating rest. Whilst they help explain how residuum add ups, the fundamental questions active what they ar doing at that place in the root place, that is the melt down of kip, mollify mystify to be answered.Besides, thither atomic number 18 alread y excellent texts describing these mechanisms (e. g. ref. 1). Many rather a secondary recover that, disdain fifty old age of research, all we faecal matter conclude approximately the give way of eternal repose is that it over con plys quietusiness, and that the entirely bona fide run a ri clamberg from catnap wishing es hypothesises is that cessation dismissal makes us cessationy. such a forlorn outlook has been partly trus twainrthy for many calmness researchers turning forward from basic research to the more(prenominal)(prenominal) stimulating field of in bourneission disorders. Besides, is intimate why we peace such a life-sustaining question aft(prenominal)ward all ? workplace prospects argon furthest better in the atomic number 18a of resi referable disorders, and thither is the propitiation of world able to help or cure many patients. Numerous Sleep Disorders Centres have been established in the reach in States and Europe over the fail decade (alas, non in the UK), and this is by remote the greatest nonplusth argona in cessation research. Whilst it could rightly be argued that short peacefulness disorders is a uttermost-off more worthy bea for cessation research, unfortunately, corresponding the neurophysiological mechanisms of stay, it calm does not declaim us oft virtually why we quiescence.Certainly, it has hand overd worthy information round the neurophysiological mechanisms, and about the association amongst peacefulness and ventilating system (which is not in truth related to the function of recreation every). This is why the book contains infinitesimal about residuum disorders. Again, on that point atomic number 18 already several excellent accounts easy (e. g. refs. 2-4). The aim of this book is to show that we have not r severallyed a dead-end in our disposition about the functions of residual, hardly ahead, that we whitethorn have taken too a great deal for grante d.As go out be seen, this topic is keep mum an unk right offn and exciting entity, with many avenues silent to follow, and thither is lots work to be d nonp atomic number 18il. Writings about why we calm date back to before the eld of Aristotle. close couch the procedure of catch some Zs in terms of rest and retrieval from the wear and appoint of alerting. One keepnot actually argue with this idea as it makes so lots sense, and besides, we all know that we feel the worse for wear without stop, and so practically better by and by quietness. Neverthe flyspeck it is a vague idea what merely is regain ?This is ease a matter for sizingable confer, as testament be seen passim the book. It is comm completely thought that 7 8 hours forty winks a wickedness is requirement. This idea is reinforced from many buttockss. For lesson, by the democratic press (you must get your dish aerial kip), and by many GPs. postulation a patient how argon you quiescence ? , whitethorn unaccompanied be a stock phrase for helping the GP to establish rapport, but it cool off emphasises the take away for a intelligent wickednesss pause. The pigment symptom of insuffient or disturbed eternal rest is excessive pauseiness in the sidereal mean solar twenty- quadruple hour period age. sole(prenominal) if many insomniacs do not experience this, and a major reside is about not getting enough stay, and what whitethorn find oneself to their health as a consequence. However, we probably do not in reality need the go bad a couple of(prenominal) hours of a typical nights catch some Zs, and peacefulness dismissal is furthermost less harmful than about would think. Most of the theories about the function of tranquillity sign up on dreams or daydream sleep, immediately called rapid eye movement sleep (rapid eye movement sleep). Few look at the be sleep. Many people rely that we barg entirely go to sleep for the purpose of dreaming or ha ving paradoxical sleep sleep.Cl primal, dreams ar the n wee enjoyable and noticable part of sleep, but the richness of this sleep is probably overran ted. As get out be seen, a volumed voice of rapid eye movement sleep sleep is dispensable, without ill-effect. REM sleep effective occupies about one quarter of our nightly sleep, and to call the rest of sleep non-REM sleep, by describing it in terms of an absence seizure of REM sleep, not only debases the legal age of sleep, but overlooks what whitethorn losely be expound as the deeper part of non-REM sleep, called loosen up flap sleep (SWS) in humans.This form of sleep whitethorn well turn out to be the closely crucial for us. Nevertheless, despite the fact that no-one really knows what REM sleep does, or whether it is good for us, there is cephalalgia if it is dimimished. For example, if a sleeping tablet leaves REM sleep unchanged, or unconstipated increments it, hence this is often seen to be a exchange point for the drug, and secondary concern is ordinarily expressed if the drug impairs or alters non-REM sleep, which by the way, many of these tablets do to a perceptible close.This is not meant as a admonition of drug companies, as they have only been following the climate of opinion in sleep research. REM sleep has tralatitiously been viewed to be essential for the normal surgical procedure of the maven during watchfulness, trance non-REM sleep, curiously SWS, is for the rest of the torso. Rightly or wrongly so, the old idea of dualism, the consistence versus mind strife in biology has strongly influenced perspectives on sleep. However, as entrust be seen, this is too simple an explanation, as by from anything else, the functions of sleep have probably changed with mammalian evolution.For example, whereas sleep may well provide verbalise torso wander repair for the mouse, it is unconvincing that this is the cause for humans, where sleep seems especially honorable t o the cerebrum. On the other hand, for us, and perhaps fifty-fifty the mouse, REM sleep may generally be some form of transform for weather eye, property the psyche stimulated without having to brace the sleeper. Perhaps dreams themselves be just a cinema of the mind the mavins great entertainer to small-arm away the nighttime hours However, it is important not to fall into the trap of thinking about each grammatical case of sleep in isolation, each having its own distinct function, as pattern from any(prenominal) the other types of sleep argon doing. Sleep is a complex service and it is exchangeablely that disparate types of sleep act with one another to promote a var. of functions, veritable(a) though one type of sleep may be associated more with one function than another. The last troika paragraphs ar introductions to most of the discover themes of this book, which are essential a bitty more at the end of the abutting Section. for each one chapter expand s these themes shape up, and there are summaries at the end of most chapters. Each chapter is a sensibly self-contained unit, and does not have to be read in sequence, although this is recommended. A empyrean summary of all the main themes is inclined in the last chapter, why Do We Sleep, and the reader baron exemplificationised to take a preview of it. 1. 1 Early Sleep Theories Apart from showing sleep as some sort of reco genuinely process, most of the ahead of time theories only looked at the the mechanisms that produce sleep, preferably than what just sleep does.For example, believing it to be the dissolver of a build up of some substance in the brain during sleeplessness, that is immobile during sleep. Even Aristotle thought along these lines ii thousand old age adone for(p), and considered that sleep terminationed from cranky vapours rising from within the abdomen The evaporation attendant upon the process of upkeep .. naturally tends to move upward. This e xplains why fits of drowsiness are especially apt to come later meals. It a give care follows certain forms of tire out for scare off operates as a solvent, and the turn ( nimble) matter acts desire sustenance introductory to digestion.In the last ampere-second, with more advancements in the understanding of the brain, heart and vascular system, one educate of thought considered sleep to be ca employ by the congestion of the brain by livestock. This contrasted with another popular theory at the time, of rational anaemia, due to demarcation macrocosm drawn away from the brain and deviate elsewhere in the torso, especially to the gut. such(prenominal) ideas level(p) led to opposing beliefs about how to induce better sleep. Some propounded sleeping without pillows to encourage kindred flow to the head, and others promote the opposite use plenty of pillows to course the cable away. Behavioural theories were resemblingwise parkland in the 19th century, particularl y that sleep was due to an absence of out-of-door stimulation, with wakefulness only cosmosness possible if the existence was constantly stimulated. Take the stimulation away and the animate being allow fall dormant. To some extent this notion is true, as we crumb all testify, but it is not the answer. At the turn of the century another demeanoural theory became very popular, proposed by a Frenchman, Dr Eduard Claparede.He considered that sleep was not so much a passive reaction, but an active process bid an instinct, to keep down risqueigue glide byring we sleep not because we are shake up or exhausted, but in order to proscribe our becoming intoxicated or exhausted. For him, sleep ends when we have had enough. An kindle idea initially, but it has as much depth of understanding as maxim that we eat in order to pr eveningt ourselves from starving. The real purpose for eating is to provide nutrients, that undergo complex processes which consent to the ashes to live , grow, and repair itself.The bloodline of the 20th century besides produced many of what are termed humoral theories, whereby conf utilise sleep inducing substances put in in the brain. These ranged from known chemicals like lactic acid, carbon dioxide and cholesterol, to the vaguely described leucomaines and urotoxins. Nevertheless, by 1907 some headway began to be do when twain French researchers, Drs Rene Legendre and Henri Pieron, claimed to have obtained a substance they called hypnotoxin from sleep take brutes. This gave a queen-size boost to the humoral theories for the near twenty years or so, with much exertion by several groups of researchers.However, winner was hard to come by and interest dwindled. That is, until the 1960s, when great headway has since been do into sleep substances (see Section 5. 12). In those interim years most of the excitement came from advances in neurophysiology that could be related to sleep, and a spate of several(predicate) neura l inhibition theories for sleep progressed. Many had had their early impetus from Pavlovs views on cortical inhibition that sleep originated from a form of blocking within the rational hemispheres.Although Pavlov vehemently dismissed the alternative, of sleep inducing centres in more basic parts of the brain downstairs the cerebral lens cortex, these have since been gear up to exist, and have become the centre of one of the self-aggrandising fields of sleep research, especially, after the hu undressg in the late 1940s, of arousal centres in the reticular formation. Unfortunately though, sleep centres and humoral theories still do not tell us much about the purpose of sleep, in the very(prenominal) way that knowing about centres in the brain that act upon eating behaviour explain lowly about the purpose of eating.Hypotheses about the function of sleep have centred on heterogeneous types of recovery following the wear and tear of wakefulness, and come under the heading o f soda pop theories. In contrast, there are alternatives that disown this standpoint and claim that sleep is non-restorative just a form of instinct or non-behaviour for keeping us, as well as other mammals, out of harms way, and occupying the otherwise ho-hum and unproductive hours of darkness. Through this immobility, sleep go away in like manner prevent any fumble of zip finished needlessly contemptible about.Hence sleep is often seen as an vigour conserver. Whilst I believe that these restitutional and instinctive theories have their merits, they seem to fail because each is normally applied universally to all mammals. Why should the functions of sleep for a small nocturnal mammal like the mouse, with a poorly developed cerebral cortex, unable to slack during wakefulness, continually having to forage for nutrition and be on the lookout for predators, be on the dot the alike as that for humans, who are normally the opposite in all these view?One theme I shall be developing in this book is that these three aspects of sleep function restoration, elan vital conservation, and as an occupier of time, will alter as the evolutionary scale is ascended, depending on various interrelated circumstances of the mammal, particularly bole size, level of cerebral development, amount of relaxed wakefulness and type of diet. Furthermore, for most mammals including ourselves, the functions of sleep may well alter as each nights sleep progresses, initially serving more important purposes, and so changing to those of less benefit.Not only does this idea break with the traditional division of sleep into REM and non-REM sleep, but likewise means that the last part of sleep may be s toleratety in many mammals. For humans, this applies to the last 2 hours or so of the typical octette hours of nightly sleep. This is exchangeable to eating and drinking, where we dirty dog easily consume more than we really need, or do with a miniaturer less, without a ny ill- do, apart from some painless adjustment of dust burden, for example.My standpoints on sleep are approximately heretical, and argue once morest many commonly held ideas. But before get in this controversy, let me provide a poor background about some of the more common phenomena of sleep and how they are metrical. 1. 2 Daily Sleep and Wakefulness The lives of all mammals are very much influenced by internal biological pin grass under the pass off of centres within the brain that get not only the level of vigilance over the day, but the timing of sleep, wakefulness, and most other physiological functions.thither is much debate about whether these rhythms come under the bid of one, cardinal, or more central clock. At the moment it is thought that there may be two, one incorporateling sleep and wakefulness, and the other eubstance temperature and various aspects of general physiology. On the other hand, it is possible that two are part of some less well unders tood masterclock. However, assuming there to be two clocks, it seems that neither runs on the button at 24 hours, and the term circadian, from the latin circa diem (about a day) has been adopted to describe them.Human circadian rhythms are inclined to run a little gradual than 24 hours, more like 24. 5 hours, but they are keep back to 24 hours through the brain being aware of weak daily events in the surround. Such events are called zeitgeibers, a German word losely translated as time giver. For many mammals sun go and sunset are the main zeitgebers. If the zeitgeibers are re go, for example, by keeping an creature in an artificial environment under constant light, accordingly the carcass temperature clock free runs at its natural period (i. . 24. 5 hours in humans). But in the modern world of galvanising lighting, our internal clocks can no womb-to-tomb rely on daytime and darkness as a zeitgeiber, and instead, in some way use other regular cues such as meal time, and p erhaps morning waken by an alarm clock. downstairs normal everyday conditions our internal clocks are linked together, with body temperature and most physiological activities profit during wakefulness and declining during sleep. This is not hardly an effect of different levels of physical performance.For example, if sleep is scattered at night and taken in the day instead, as happens in shift work, the temperature rhythm pillows the same for several eld, still falling at night and rising by day. and so it flattens out, and eventually begins to re-shape itself to work up at night and fall by day. Full modification of the temperature rhythm may take two calendar weeks, and until this occurs, with the sleep-wakefulness rhythm completely resynchronised with it, the shiftworker experiences various discomforts such as sleepiness at work, indigestion, press release of appetite and headaches.These are not harmful, just annoying, and are in effect a worse form of jet lose, whe re the timing of sleep and wakefulness is also suddenly shifted in relation to body temperature and local time. Why Nature has given wights these circadian clocks is not take awayly clear, and the reason may vary somewhat from species to species. However, most brutes are very much at the mercy of daylight and darkness, regardless of whether they live diurnal or nocturnal lifestyles.One view of the function of the circadian clocks is that they preempt each part of the day by ensuring that sleep, wakefulness, alertness, and various physiological changes will be at their most suitable levels. Such preempting may be necessary as there is a time lag for these changes to occur, which might be too long if they did not begin until the external event arrived. For example, a warm brain works better than a chill one, but during the sleep period body and brain temperature fall a little. Some time is required for the brain to warm up, and if this did not begin until wakefulness then behavio ur could be impaired for a while.The circadian clock seems to anticipate wakefulness and starts the warm-up process a some hours beforehand, ensuring that the brain is at a good working temperature when wakefulness begins. 1. 3 Measuring Sleep If one simply watches a sleeping mammal, including humans, certain common features are seen A typical body perspective A specific site or nest for this behaviour Physical inertia A regular daily occurrence influenced by a circadian clock More stimulation is required to enkindle the wildcat than during wakefulness However, advanced mammals like ourselves can feign some of these haracteristics during wakefulness by resting with the look shut, and a more accurate regularity for measuring sleep is needed. Furthermore, as it is tedious to watch an animal sleeping for many hours at a time, some form of automatic transcription is desirable. The organ that shows the clearest changes during sleep compared with relaxed wakefulness is the brain, a nd this is particularly obvious in its galvanising military action. Concentrating on the brain in this way is eliminate in other mentions, as not only does it contain the fudge mechanisms of sleep, but of all the bodys organs it is for the brain and behaviour (i. . mainly the cerebral cortex) that sleep seems to be the most springy. Monitoring this electrical action in animals involves surgery and the placing of minute electrodes in the brain and other parts of the head. These are normally connected by supple wires to a junction box to a risqueer place the cage. This can restrict the animals movement, and if more freedom is wanted then a minature communicate transmitter can be intractable to the head instead. In humans, electrodes are only fixed to the surface of the scalp with a quick-drying sterile glue, easily removed by a solvent.Wires from the electrodes are plugged into a junction box, and the signals amplified by a work uniform to that use for animals. Such amp lifiers are technically very civilize as they have to boost the brains signals by about a million-fold, because the electrical activity of the brain is only at a a few(prenominal) millionths of a cinque. After amplification, the signals can be written out by mechanic ink pens on newspaper, or put down on magnetic tape. The human brain largely consists of the cerebral cortex (sometimes called the nous) surrounding the rest of the brain like the canopy of a mushroom about its stalk.As the electrodes are located preceding(prenominal) the cortex, the electrical activity they pick up is that of the cortex, rather than of deeper brain field of views. Hence the term electroencephalography (EEG for short) is utilise to describe this technique of scalp recording. The paper write-out is called an electroencephalogram (also called the EEG), and the ma lifte containing the amplifiers and pens, as an electroencephalograph. When electrodes are rigid in the cortex itself, as with anima ls, the electrical activity should strictly be called he electrocorticogram (ECoG). However, for simplicity, many people including myself, also refer to it as the EEG, even though this is incorrect. Much of sleep can be assessed from the EEG only when, but for the roundment of REM sleep, additional electrodes have to be placed well-nigh the eyes to detect the rapid eye movements, and over muscles in the lift or neck. For reasons that are not understood, in REM sleep these muscles pro arrangely relax (tonus is conf utilise), and this can be utilize as a further draw to REM sleep.Although muscles in the rest of the body do not lose their tonus, they are unable to move as there is also a type of paralysis going on during REM sleep that prevents voluntary movement. For many mammals the EEG of REM sleep is very much like that of a inflamed wakefulness, which is why REM sleep utilise to be called paradoxical sleep the animal is behaviourally asleep, but the brain seems to be wak e. So without knowing about the activities of the eyes and neck muscles, we could easily mistake REM sleep for wakefulness.For humans the EEG of REM sleep is very much like that of light non-REM sleep ( head 1 sleep), and then was once called format 1-REM sleep. Again, eye and neck muscle recordings are essential, to break-dance REM sleep from peak 1 sleep. The EEG consists of waves that can be measured in terms of AMPLITUDE The emf between the peak and the trough of a wave, and measured in millionths of a volt (microvolts uV). Amplitude jump ups as consciousness locomote from alert wakefulness, through drowsiness to deep sleep. FREQUENCY The number of complete waves or cycles occurring in one second, and expressed as hertz (hz cycles per second).The efficient range in the human EEG is from about 0. 5 hz to 25 hz. Generally speaking, frequencies above about 15 hz are quick waves, and frequencies of under about 3. 5 hz are slow waves these are the waves of slow wave sle ep (SWS). Whereas bounty aerodynamic lifts as sleep deepens, frequency falls. With the very advanced mammals, especially apes and humans, the EEG of both(prenominal)(prenominal) wakefulness and sleep is more complex, and enables further specific types of EEG to be set according to certain frequency bands. These are given greek letters, and going from high to low frequencies the MAIN divisions are as follows (there are some gaps)BETA is normally above 15 hz and consists of fast waves of low amplitude (under 10 uV) that occur when the cerebrum is alert or even anxious. of import is normally the range 8 11 hz, and is typical of relaxed wakefulness, and when there is little arousal to the eyes, especially when they are shut or staring at a clear wall. THETA is in the range of 3. 5 7. 5 hz and it reflects drowsiness and light sleep DELTA these are the slow waves of SWS, and have the last-place EEG frequency, of under 3. 5 hz. They are of a high amplitude, often over 100 uV, and increase in demeanor as sleep becomes deeper.There are some other, more transient EEG activities found only during sleep, such as eyeshade sharp waves occuring with theta activity at sleep onset, and spindles and K complexes that are most dramatic in spirit level 2 sleep (see Section 6. 9). only these EEG characteristics allow human non-REM sleep to be confused down further, and there are standard reference works for this purpose, one for infants (5) and the other for adults (6), describing in de back the EEG and other characteristics of REM sleep and of the four progressively deeper EEG gifts of non-REM sleep stages 1, 2, 3 and 4 sleep.However, the stage of non-REM sleep is arbitarily defined and still a matter for debate, particularly in the case of the elderly (7). Nevertheless, this sleep staging is generally accepted. Wakefulness is called stage 0, and is typified by alpha or beta activities. demo 1 is really a inflection stage from wakefulness or drowsiness to true sleep (stage 2 sleep or deeper), and ordinarily only occupies about 5% of the night. Stage 1 is typified by theta activity, a loss of alpha, and often some vertex sharp waves. There is also much eye rolling, as the eyelids easy open and shut a few times, with the eyes rolling upwardly and downwards.If one watches someone falling asleep, especially if they are also struggling to remain circumspect, then these movements of the eyes and eyelids can be clear seen. The bulk of human sleep, near 45 % of it, is make up of stage 2 sleep, containing a miscellanea of theta activity, sleep spindles, K complexes and a few delta waves. Stage 3 is more of a revolution phase from stage 2 to stage 4, and only constitutes about 7% of sleep in the childlike adult. It contains 20 50 % delta activity of a certain amplitude. When this activity goes beyond 50% then the deepest sleep, stage 4, is reached.This makes up about 13% of sleep in the young adult. SWS is the collective term for sta ges 3 and 4 sleep, where delta activity more and more predominates. The EEG characteristics of the various sleep stages are shown in Figure 1. REM sleep occurs regularly throughout sleep in nearly all mammals. The time from the solution of one episode of REM sleep to the beginning of the following is remarkably regular within any species, and seems to depend on the brain size of that species (8). The larger the brain, the lengthy this time interval. Whilst in humans it is about 90 minutes, for the rat it is only about 12 minutes.Interestingly, although REM sleep only makes up a small mass of entireness sleep in most mammal species, normally about 10 15%, humans have roughly double this value. However, for all of them, including humans, this declines with age (Figure 21), and as I have already mentioned, is much more evident in the newborn. REM sleep is discussed in de can in Chapter 8. Figure 1. 1 EEG of Human Sleep Stages Wakefulness shows alpha activity (subject relaxed) and beta activity (alert). Theta activity can be seen in Stage 1 sleep. Stage 2 sleep shows spindles and a K complex.Note the large slow waves (delta activity) of stage 4, also apparent to some extent in stage 3 sleep. Stages 3 and 4 together are slow wave sleep (SWS). The EEG of REM sleep resembles that of stage 1, and contains a mixture of beta and theta activities. To annul mistaking these two stages, recordings are make of eye movements and chin muscle tonus (see text). Usually, for humans each minute or one-half-minute of sleep is bewildered down into the sleep stages, and the results can be plotted out as a hypnogram. A simplify version is seen in Figure 2, and shows certain key features of sleep ) A rapid descent to stage 4 sleep currently after sleep onset. 2) A regular 90 minute cycling of REM sleep and other stages. 3) The prevalence of stages 3 and 4 sleep (SWS) in the initiative cycle, less in the second cycle, and only some stage 3 sleep in the third cycle. SWS is larg ely confined to the first half of sleep. 4) A great predomination of REM sleep and stage 2 sleep in the second half of the night. Figure 1. 2 A simplified hypnogram of sleep stage changes over the night in young human adults REFERENCES 1. McGinty D. J. , Drucker-Colin R. , Morrison A. & Parmeggiani P-L. (eds) Brain Mechanisms of Sleep, New York Raven Press (1985). 2. Williams R. L. , & Karacan I. (eds) Sleep Disorders, Diagnosis and Treatment, New York Wiley and Sons (1978). 3. Chase M. , & Weitzman, E. (eds) Sleep Disorders Basic and Clinical Research, New York MTP Press (1983) . 4. Parkes J. D. Sleep and Its Disorders, London W. B. Saunders Co (1985). 5. Anders T. , Emde R. , & Parmelee, A. A manual of Standardised Terminology, Techniques and Criteria for Scoring States of Sleep and Wakefulness in the Newborn Infant.Los Angeles UCLA Brain study Service (1971). 6. Rechtschaffen A. & Kales A. A Manual of Standardised Terminology, Techniques and Scoring System of Sleep Stages in Human Subjects. Los Angeles UCLA Brain Information Service (1968). 7. Webb W. B. & Drebelow L. M. A modified method for scoring slow wave sleep of older subjects. Sleep, 5, 195 199 (1982). 8. Zepelin H. , & Rechtschaffen A. Mammalian sleep, longevity and zero metabolism. Brain and Behavioural Evolution, 10, 425 470 (1974). CHAPTER 2 stop DEPRIVATION . 1. Problems with Animal Experiments One way of purpose out about the functions of sleep is through sleep expiration, and there have been many such investigations on animals and humans since the turn of the century. The general findings are, that although humans appear to cope fairly well, other mammals tend to come off worse. This does not ineluctably mean that humans have different sleep functions to those of animals, but that most of the animal experiments have introduced additional stresses which have been more eventful.With humans, we can ask for volunteers to go without sleep for a few geezerhood, and impress on them t hat they are free to withdraw whenever then want. Also, these volunteers are carefully looked after, their safety is delayd, and cipher harmful will be allowed to happen to them. However, none of these factors really apply to animals, as for example, we cannot communicate these assurances to them, and so to speak, put their minds at rest and allay apprehension. Their natural lifestyle is fallly disrupted, as they are unplowed awake at times of the day when they deliver to sleep, through methods they do not understand and have no promise over.Although sleep expiration in animals can be given for a longer time than for humans, implying that more interesting findings might be forthcoming, we can still be more confident that the results from human sleep neediness studies are less pretend by additional stresses. The first well-documented experiment of this type on animals was carried out in France during 1894 by a Dr M. de Manaceine, who kept puppies awake for 4-6 days by locomo te or handling them continually. By the end of this time their body temperatures had fallen by about 4C, and there was a nightfall in the number of red blood cells.Autopsies revealed many small haemorrhages in the cerebral cortex. These findings stimulated much interest and soon led to further studies by other laboratories, also on puppies. Again, falls in body temperature were found, and although changes in the cerebral cortex were also reported, these were more variable and of a different nature to those of Manaceines puppies. However, few of these experiments used a have group of animals, and it is presumable that some of the changes attributed to sleep loss may have been due simply to science laboratory techniques unrelated to the personnel casualty itself.Ideally a picture group would consist of littermates allowed to sleep normally, so that comparisons could be made with the take animals. Such a method was subsequently used in the substantive studies carried out by an American, Dr Nathaniel Kleitman, in the 1920s. Over the next 40 years he performed many more investigations into sleep in both animals and humans, and for these efforts he is unremarkably regarded as the father of sleep research. His great work, Sleep and Wakefulness (1), was for many years the textbook on sleep.In Kleitmans early experiments, puppies were kept awake for 2-7 days, by groups of assistants walking or playing with the animals. This technique was productive for up to 3-4 days of act wakefulness, with most of the animals feeding and drinking normally. Thereafter though, they would lose all interest in the surroundings. However, when they were compared with littermate tally animals that were not sleep strip, there was no greater fall in body temperature, nor any important change to vital functions.The only real finding was a confirmation of the earlier reports of a drivel in the number of red blood cells in the sleep disadvantaged animals. interrogative of the bra ins of all the animals showed uniform and clear abnormalities for both the groups. Whilst the true reasons for these latter effectuate are unknown, it is likely that the damage was done during autopsy, as the techniques used for preparing the brains for analysis were crude by todays standards. Other sleep loss experiments of this era used rabbits, but again, few used go steady groups. Probably the best known was by another American, Dr W G Crile, who kept rabbits awake for 4-5 days.A slight rise in body temperature and a retardant of respiration were found, but no fall in red blood cells. Autopsies revealed changes to the coloured and adrenal secreter gland gland, as well as to the cerebral cortex. Although Crile could not explain these findings, again it is likely that the autopsy procedure was to blame. These early studies simply relied on the experimenters claims that their animals remained awake, and it was not until the fifties that advances in EEG recording techniqu es made it possible to measure whether the animal was very asleep or awake.So until recent times, about the only way of making sure that the animal remained awake was to keep it continually moving, but this meant that one was now looking at the effects of physical activity plus sleep red ink. To some extent the influence of the physical activity alone could be subtracted by giving the same amount of case to a hear group allowed to sleep. However, it is possible that practice session interacts with sleep passing in a way not found in the make group, as for example, forced exercise when scatty to sleep may be more shewing to a sleep strip animal than to a refreshed experience animal.This is a problem that Kleitman readily acknowledged, even though he did use reserve groups. Nevertheless, this questioning about the impact of exercise may be rather theoretical, as it will be remembered that few of the early red experiments which used exercise found any serious abnormality in any event at to the lowest degree up to heptad days wakefulness, although using the limited and rather crude methods for determining an animals state of health. There is one more of the early sleep deprivation experiments that I must mention, carried out in 1946 by Drs J C R Licklider and M E Bunch, from Harvard and upper-case letter Universities (2).Their first aim was to determine the least amount of sleep that laboratory rats could exit on, as usually these animals slept around 12 hours a day. Animals were kept awake by forced walking on a treadmill. Very much to the experimenters credit, a variety of conquer groups were used. In an initial flee experiment, animals were divided into four groups no sleep, normal sleep, 8 hours sleep, and 4 hours sleep. They were kept like this for several weeks, or, as was to be the case for the on the whole sleep deprive group, until they died.This usually occurred after 3 14 days. To Licklider and Bunchs surprise, the four hour gro up seemed to prevail indefinitely. The only finding of note was that these animals were passing irritable and had to be handled with caution. Licklider and Bunchs next experiment, their major one, now looked in more de crap at the effects of four hours sleep per day, but this time on young (adolescent) animals, particularly, at their rate of growth and accomplishment baron. Control groups were again used.Although I will not go into de cigarettes, suffice to say that these tried to clarify the effects of the exercise itself, and other steadyial problems. Animals from the data-based and mastery groups were still growing, and all had access to food all of the time. Measurements were taken for 10 18 weeks. However, within a few days from the start, the growth rates of the 4 hour sleepers began to fall behind those of the view groups, and after a further 50 days their body clogs just levelled off whilst the others continued to grow.But according to the investigators the shorten ed sleepers seemed healthy enough, apart from irrit aptitude. Of great interest was that learning in these rats was certainly no worse than that of the control groups even marginally better. The most forward-looking studies of sleep deprivation using EEG methods also pair together sleep disadvantaged and control animals, so that when sleep onset occurs in the EEG of the sleep strip animal, it is stimulated into wakefulness. The control animal is interchangeablely stimulated irrespective of whether it is awake or asleep.Because both animals have similar circadian sleep and wake patterns, the likelihood of sleep is greater at certain times of the day, so whenever the sleep deprived animal is stimulated its companion may also be asleep. Consequently, the control animal also loses some sleep, but only about 20-30% of it, and is certainly not conglomerationly sleep deprived. For both animals these laboratory procedures are stressfull, and it is assumed that because one animal has hail sleep deprivation plus these stresses, and the other only partial sleep deprivation plus the stresses, any greater effects on the first animal are due to the larger sleep loss.These sophisticated studies are a great feeler on earlier ones where there was little or no control, but there is still the problem that the sleep deprived animal has a greater kerfuffle to its lifestyle as well as to its sleep. To be stimulated into wakefulness from drowiness or sleep, as is the case for the sleep deprived animal, may be more stressing than to be stimulated whilst already awake, as is the likelihood for the control animal.Although none of these animal experiments can be perfect, of course, they do have the great advantage over the human studies in that more searching measurements can be done, and autopsies carried out afterwards. Apart from changes in behaviour, one of the best signs of stress in both animals and humans is a marked increase in the output of certain hormones from the a drenal glands, particularly adrenaline and the corticosteroids, with the most notable example of the latter being hydrocortisone.Adrenaline (otherwise called epinephrin) is the main hormone produced in the upshot of the adrenals, the medulla, whereas the corticosteroids come from the outer layer, the cortex. Hence the more correct term for these latter hormones is the adrenocorticosteroids. Cortisol helps the body go for stress by protecting various tissues against excess damage, for example, by trim down inflammation. It combats jerk by making body nada reserves more available, and trying to ensure that the volume of the blood and blood nip can be maintain.The number of red cells in the blood falls, as more are switched to a reserve store so that fewer cells would be lost during any bleeding. For reasons that are not clear, it also depresses the immune system. Cortisol can affect the central nervous system and behaviour. Under non-stressful conditions hydrocortisone is r eleased in small amounts throughout the day, and has an obvious circadian rhythm, troughing at the beginning of a mammals daily sleep period, and peaking around the start of wakefulness.However, rapid increases can occur within a short while of a stressor occurring, and may be maintained for many days as the adrenal gland can soon grow in size to produce more of the hormone. Eventually though, the gland becomes exhausted and the animals ability to combat the stressing event fails. Death usually soon ensues. Whilst cortisol helps the organism to operate stress, especially if the animal is helpless and unable to avoid the underlying cause, adrenaline has a more rapid alerting effect, commonly called the fight or flight response, designed to help the animal quickly avoid the danger one way or another.Of the two hormones, adrenaline and cortisol, the sleep deprivation researcher usually prefers to measure the latter, because deprivation generally lasts for days, and this hormone is muc h easier to measure than is adrenaline. In the 1950s a Canadian, Dr Hans Selye, set three phases in the cortisol response to stress alarm, resistance and exhaustion (3), with the last one not usually occurring until many days have elapsed. Although Selyes interpretation is now thought to be too-simple an explanation for what is clearly a complex response, his approach is still reasonable for our purposes.Whilst injury and illness are major causes for the initial alarm response, it will also occur whenever the body is pushed to extremes, for example during heavy exercise or in very hot or chilly environments. More importantly, psychological factors such as apprehension and fear are potent triggers for this hormone. These can substantially add to the effects of more physical stimuli such as injury. Whilst animals usually show rises in cortisol during sleep deprivation, this tends not to be the case with humans.We can be sleepy, irritable and have a great desire to sleep, but providi ng we know that no harm will be allowed to come to us, and that we can leave out out of the experiment if necessary, then the deprivation will not necessarily be stressful. This suggests that some psychological factor in animals, such as fear, may be influencing their cortisol response to deprivation. It must be borne in mind that illness and tissue damage will also depart the alarm responses. So I cannot be clear about how much of the increase cortisol levels in sleep deprived animals is due to physical illness, fear alone, or fear as a result of the illness. . 2 Recent Animal Experiments The most elaborate sleep deprivation studies ever performed on animals are being run at the clams University Sleep Laboratory a premier sleep laboratory established 25 years ago by Dr. Allan Rechtschaffen, and still under his direction. Kleitman was also at Chicago University, but in another Department. He retired soon after Rechtschaffens arrival, and his sleep laboratory closed down. Rechts chaffens pioneering work along so many lines of sleep research has brought him a level of respect from sleep researchers that equals that accorded to Kleitman.Rechtschaffen and his team began their sleep deprivation experiments on rats in the early eighties (4 8). Two main types of study were performed (i) total sleep deprivation, and (ii) deprivation of REM sleep only. For each of these there were impressive control procedures using control animals. The centrepiece of this laboratorys equipment was the appliance for sleep deprivation a horizontal, bill rotating syllabus 45 centimeters in diameter, meet by shallow water. A straight barrier divided the platform into halves, allowing a sleep deprived animal to be confined to one side, and a control animal to the other.The platform could rotate slowly under the barrier. When this occurred, both animals had to move to avoid being gently propelled into the surrounding water. As rats dislike getting wet they would do their best to avoid falling in. Each animal had its EEG continuously monitored by a computer. When sleep was detected in the rat to be deprived of sleep, the platform would promptly rotate, causing the animal to rouse and move along the platform. Its partner, which might be awake or asleep at the time, had to move likewise, and to the same extent.Generally, control animals lost about 26% of their sleep, compared with about 92% for the observational group. Although this procedure was indeed stressful to sleep deprived animals, as shown by increases in adrenal gland weights and cortisol secretion, the control animals seemed to experience a similar amount of stress for most of the experimental period, as both these indices rose to similar extents in them as well. For REM sleep deprivation alone, the platform only moved when REM sleep was detected.The technique was kinda effective, as virtually all of REM sleep (99%) could be eliminated, whereas the control partner only lost about 4% of its REM sl eep. Although the experimental animals were still able to take most of their non-REM sleep (which makes up about 88% of sleep in the rat), there was some unavoidable loss of the deeper form of non-REM sleep. This was a problem of some concern to the investigators, and I will come back to this later. For both types of sleep deprivation, experimental and control animals were under constant light, and food always available.The environmental temperature was set at what is neutral for the rat. Total sleep deprivation caused general debility, weight loss and goal by about the 21st day. The control rats all survived the experience, although they became debilitated and lost weight to some extent. Post mortems were performed on all the animals. Examinations were carried out on the brain, liver, kidneys, spleen, lungs, duodenum, stomach, thyroid and thymus, with the pathologists not being told from which group each animal had come. Surprisingly, no significant dissimilitudes were found betw een the two groups for any of these organs.As the investigators pointed out, one of the remain possibilities was that expiration may have been due to undetected biochemical abnormalities. So far though, there is no sign of what, if any, these might be. In the total sleep deprivation procedure, both experimental and control animals ate much more food, whilst also losing weight. However, these effects were far more apparent in the experimental group. Calculations by the investigators on the efficacy obtained from digested food and from breakdown of the animals own body tissues, showed a very large rise in the readiness usage, to around 2. times the baseline levels for the experimental group, and to 1. 7 times these values for the control group. It seemed that such increases were being used to fuel a large rise in metabolism. Although most of this energy need was coming from voracious eating, particularly in the experimental animals, the fall in body weight showed that the animals own energy stores were being depleted. But this weight loss was probably not the cause of death in the sleep deprived animals, as at death their weight had only fallen to about 80% of the startle value.The investigators had shown that starved rats not sleep deprived can still survive at 70% of their original body weight. Sleep deprived animals were digesting their food normally, and there was no sign of diabetes or other illnesses that could account for weight loss and voracious eating. So what was contingency to all this energy, and was it all going to fuel increased metabolism? The gland that has a major effect on metabolic rate is the thyroid, but its hormones showed no changes. Could stress still have an answer?There were no noticable differences in the size of the adrenal glands between the two groups for most of the time, from the start of the deprivation until the death of the sleep deprived animal. However, there was a rise in adrenal weight a few days before death. To try and determine the stress responses further, the investigators made more detailed analyses of blood samples from both groups of animals, every few days. Apart from the measurement of cortisol and other blood constituents, assessments were also made of the hormone that controls cortisol release adrenocorticotrophic hormone (ACTH).Both the sleep deprived and control groups showed similar rises in these two hormones, with no significant differences between the two groups for either substance. Except of course, for the few days antecedent to the death of the experimental animal, when there was a greater rise in cortisol. The other blood constituents showed no notable differences between the groups, excerpt that the hormone noradrenaline (norepinephrine) was far higher(prenominal) in the experimental animals. The exact reasons for this were not really known.This hormone has many interesting actions, with several relating to metabolism and the enactment of foment loss from the body. For example, it limits light up loss from the hide by restricting blood flow to skin capillaries, also, it makes body fat supplies more easily available as an energy source for other tissues. One important character reference for noradrenaline is to stimulate special instigate producing organs called cook adipose tissue (BAT or browned fat) to burn up more energy for heating plant. However, this tissue is usually only found in infant animals and is gone by adulthood.It is not known if the rats used in the Chicago studies had any brown fat reserves. I shall cover the role of this tissue in more detail, in Section 8. 13. An important finding with the totally sleep deprived group was that body temperature fell during their last days, and this, together with the earlier increases in feeding and raised metabolism, suggests that something seriously happens to the ability of the animal to conserve its body heat that is, its thermoregulation becomes impaired. This state of affairs w as not so apparent in the control animals.What seems to be happening, although we cannot be certain, is that soon after sleep deprivation begins, experimental animals increasingly lose body heat, presumably through the skin, and compensate by burning more energy to increase metabolism and have more body heat. More and more food has to be eaten, but even this is not enough, as body energy reserves also have to be sacrificed on this metabolic fire. For the first two weeks, heat production matches heat loss, as body temperature stays normal.But then there is a deterioration, with heat loss olympian heat production, and body temperature falls. Although death follows a few days later, it is not yet known whether this is due directly to the bristle of thermoregulation, or just that this collapse is a symptom of something more subtle but nevertheless catastrophic, not yet understood. The control group did not reach this state, as their body temperature never fell, at least up to the tim e they were killed, when their experimental partners died.The physical shows of the sleep deprived animals changed in a characteristic way, apart from the weight loss. After about a week of total sleep deprivation their hair developed a yellowish tinge and became matted. The skin of the tail and paws developed small red inflamed compasss that eventually developed into often quite large lesions, very much like ulcers, but containing only a minor infection. These got worse as the deprivation progressed, and also began to appear in the control group, but at a slower rate of development.Surprisingly, all the animals seemed unconcerned about these sores and paid little attention to them. The lesions were only on the bare skin of the tail and feet, and were not found under the fur. timid examinations, by specialists in skin diseases, were made of the lesions, and it was concluded that these were not due to wetness, or pressure on the skin they remain a puzzle. Although there are suspi cions that a biochemical change in the skin may be the cause, perhaps even a vitamin deficiency, there is no show up of this, despite careful chemical analyses.To see whether the animals were becoming debilitated from infections, blood was analysed to find out if the immune system was functioning normally. Immunology is a highly complex athletic field (see Section 3. 8), and only a few tests could be performed. Nevertheless, such tests would have been discerning enough to pick up anything foreign going on but nothing remarkable was found. In fact, the remarkable finding was that there was nothing unusual, given the animals circumstances. What is happening to the sleep deprived rat so many blanks have been drawn?All that we apparently have so far is what seems to be a problem with thermoregulation, and the skin lesions neither of these seemed to be due to the animals getting wet through falling in the water, as this was also investigated. As far as can be seen, little else se ems to be going wrong. Rechtschaffen and colleagues are cautious over speculating over their findings. Although they believe that heat loss and thermoregulation lie at the crux of the demise of their animals, they emphasise that more conclusion is required.This would, for example, come from careful measurements of metabolic rate, which so far have been difficult to apply out in the sleep deprivation apparatus. Usually, animals would be put inside a calorimiter (a chamber for measuring body heat production), but a sleep deprived animal quickly falls asleep here, and sleep alters metabolic rate. Nevertheless, I would like to concentrate on thermoregulation a little more as I believe it to be a crucial factor. Firstly, let me give some more background, because even the normal and healthy rat has authority problems with its thermoregulation.Like other small mammals it has a relatively large body surface area in proportion to its weight. Simple geometry shows that as body weight dou bles, surface area only increases by about 60%. Keep on doubling size in this way until something of the mass of a human is produced, and the body surface becomes quite small in proportion to its weight. If there is any deterioration in the ability of the body surface to keep heat in, then this will become an increasing problem the smaller the mammal, with less body mass to generate heat in proportion to surface area. Body heat loss is less of a concern to humans than it is to rats, mainly ecause of our relatively large mass in proportion to surface area. But the animal usually has effective countermeasures physiological and behavioural. Both are by and large aimed at protecting its more open(a) body areas, the paws, and especially the large tail. Physiologically, blood flow to the skin is reduced here, and behaviourally, the animal can sit on its tail, or curl up into a ball. Now, it seems to be fairly certain that sleep deprived rats are losing a large amount of body heat, and p resumably, a major capableness route for this loss is through the tail and paws.Even though these animals are in a neutral environmental temperature, this is still below that of their body, and body heat can still be lost. Since food intake rises and weight falls as soon as deprivation begins, the apparent increase in heat loss seems to begin immediately. I suspect that a sleepy rat is less aware of this loss, and the animal may forget to sit on its tail to conserve body heat. It cannot curl up for long as the inevitable sleep and promp movement of the platform makes it wake up and walk. From what I have seen of sleep deprived rats, their tails are almost always exposed.If too much heat is being lost here, then one would expect the animal to protect its tail as much as possible but sleep deprived rats are not doing this. They still have the physiological countermeasure, of reducing the blood flow to the skin of the tail and feet. Whether or not the eventual appearance of ulcers in these areas is related to the problems of thermoregulation, or is just a coincidence, is an open question. Perhaps a prolonged restricted blood supply to the skin of the tail and feet, lasting for a week or so, promotes skin ulcers? large of this speculation of mine, and let us soften to some other fascinating findings from the Chicago Group. They had suspicions that the inevetable REM sleep loss during total sleep deprivation might have been a key factor in the deterioration of their animals, as REM sleep deprivaton alone, also led to death. But as the investigators noted, the difficulty with this idea is that death occurred much later during REM sleep deprivation, after an average of 37 days almost twice as long as for totally sleep deprived animals. REM sleep deprivation produced very similar ffects to total sleep deprivation, including the skin lesions, except that the course of events was spread over a longer time. Stress seemed slightly higher in the REM sleep deprived anim als than in their control partners, as cortisol and ACTH levels were somewhat higher, but this was not really apparent until about the week before death. The most dramatic difference was again a large increase in food intake, which began soon after the REM sleep deprivaton started. Calculations of the energy used by the REM sleep deprived animals showed a massive 3. times rise over that of the pre-deprivation levels, against a 1. 9 rise for the control group. Body temperature stayed normal for the first two weeks of REM sleep deprivation and then fell, but always remained permanent for the control animals. If REM sleep deprivation was the key to the death of the totally sleep deprived animals, why would REM sleep deprivation alone allow them to survive for twice as long? possibly REM sleep deprivation is of little relevance after all Instead, perhaps the fatal factor is not the type of sleep that is lost but the amount, of whatever type.Returning to my earlier line of thinking th e greater the sleep loss the more the sleepiness, and the greater the impairment to the behavioural countermeasures, etc. Remember, as REM sleep deprivation allows animals mo