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Sleep cycles

Sleep occurs in four stages that include varying degrees of wakefulness followed by deeper sleep throughout the sleep cycle. The stages in the sleep cycle fall into two... [Pg.238]

Other additional studies or pertinent information which lend support to this MRL Rats exposed to 1,000 ppm trichloroethylene for 3 days showed disturbed sleep cycles (Arito et al. 1993). Rats exposed to 250 ppm for less than 8 hours showed decreased electric shock avoidance and frequency of Skinner box lever press (Kishi et al. 1991). Humans exposed to 27 ppm trichloroethylene for up to 4 hours noted drowsiness, and headache was reported at 81 ppm (Nomiyama and Nomiyama 1977). Humans exposed for 8 hours to 110 ppm showed decreased performance on perception, memory, reaction time, and manual dexterity tests (Salvini et al. 1971). [Pg.304]

Rats exposed to 1,000 ppm TCE for 3 days had disturbed sleep cycles (Arito et al. 1993). Rats exposed to 1,000 ppm for 18 weeks showed increased latency in visual discrimination tasks (Kulig 1987). Sleep apnea has been observed in humans exposed to organic solvents (Edling et al. 1993 Monstad et al. 1987, 1992 Wise et al. 1983). Cardiac arrhythmia has been observed in humans exposed to trichloroethylene vapor (Dhuneretal. 1957 Hewer 1943 Milby 1968 Pembleton 1974 Thiersten et al. 1960). [Pg.305]

This sleep pattern, seen in adults, takes some time to develop and appears in infants only around 6 months to one year after birth. Instead, as new parents will testify, young babies have a sleep cycle that lasts only around 3-6 h. Further striking differences are that babies REM sleep accounts for as much as half the sleep cycle (compared with only a quarter in the adult) and is accompanied by increased motor activity with spasmodic movements of the limbs and facial muscles, rather than the muscle atonia seen in adults. In fact, the adult sleep cycle can take up to 20 years to stabilise and its pattern changes again in the elderly who show a reduction in the duration of SWS, an increase in the proportion of REM sleep, and increased daytime napping . [Pg.483]

The functions of these different phases of sleep are not at all clear but chronic sleep deprivation does eventually lead to death. It seems to be the slow-wave component of sleep (SWS) that is vital and it is thought to serve a restorative purpose. This would be consistent with its greater occurrence during the early stages of the sleep cycle when hormone secretion supports anabolic metabolism. If subjects are wakened every time they enter a period of REM sleep (evidenced by the EEG) there appears to be no overt harmful effect on their behaviour. In fact, REM sleep deprivation has even been used, with some claims of success, as a treatment for minor depression. However, there is an unproven belief that REM sleep is important for memory consolidation. [Pg.483]

It appears that the voltage waves recorded in the EEG represent the summation of synaptic potentials in the apical dendrites of pyramidal cells in the cortex. These cells generate sufficient extracellular current for it to reach, and be recorded from, the cranium and scalp. Although these waves originate from the cortex rather than the SCN, the distinctive REM and non-REM phases of sleep still remain after destruction of the SCN but they then occur randomly over the 24-h cycle. This is a further indication that the SCN is at least partly responsible for setting the overall circadian rhythm of the sleep cycle. [Pg.483]

Hobson, J. A., McCarley, R. W. Wyzinski, P. W. (1975). Sleep cycle oscillation reciprocal discharge by two brainstem neuronal groups. Science 189, 55-8. [Pg.50]

Steriade, M. (2004). Acetylcholine systems and rhythmic activities during the waking - sleep cycle. Prog. Brain Res. 145, 179-6. [Pg.56]

Feinberg, I. (1974). Changes in sleep cycle patterns with age. J. Psychiat. Res. 10, 283-306. [Pg.241]

One of us examined the timely use of three factors (melatonin treatment, exposure to light, physical exercise) to hasten the resynchronization of the sleep-wake cycle in a group of elite sports competitors after a transmeridian flight across 12 time zones (Cardinali et al. 2002). Outdoor light exposure and physical exercise were used to cover symmetrically the phase delay and the phase advance portions of the phase-response curve. Melatonin taken at local bedtime helped to resynchronize the circadian oscillator to the new time. Individual actograms taken from sleep log data showed that all subjects became synchronized in their sleep to the local time in 24-48 h, well in advance of what would be expected in the absence of any treatment (Cardinali et al. 2002). More recently, a retrospective analysis of the data obtained from 134 normal volunteers flying the Buenos Aires - Sydney transpolar route in the past 9 years was published this further supports such a role for exogenous melatonin in resynchronization of sleep cycles (Cardinal et al. 2006). [Pg.294]

Jewet R. E., Norton S. (1966). Effects of some stimulants and depressant drugs on the sleep cycle of the cat. Exp. Neurol 15, 463-74. [Pg.455]

Electrophysiology and neuroimaging Similar to LSD, peripheral injections of mescaline produce desynchronization of the EEG and increase arousal in the rat (Colasanti and Khazan 1975). This period asts for 2-3 hours, and is followed by a period of slow-wave and REM sleep with normal sleep cycles. [Pg.362]

Noradrenergic projections are involved in the modulation of sleep cycles, appetite, mood, and cognition by targeting the thalamus, limbic structures, and cortex. An increase in noradrenergic function appears to convey some of the therapeutic effect of antidepressants, although the exact mechanisms remain poorly understood (Charney, 1998 Anand and Charney, 2000 Frazer, 2000). [Pg.29]

Hobson JA, Lydic R, Baghdoyan HA Evolving concepts of sleep cycle generation from brain centers to neuronal populations. Behav Brain Sci 9 371-448, 1986... [Pg.658]

McCance SL, Cohen PR, Cowen PJ Dthium increases 5-HT-mediated prolactin release. Psychopharmacology 99 276-281, 1989 McCann U, Hatzidimitriou G, Ridenour A, et al Dexfenfluramine and serotonin neurotoxicity further prechnical evidence that chnical caution is indicated. J Pharmacol Exp Ther 269 792-798, 1994 McCarley RW REM sleep and depression common neurobiological control mechanisms. Am J Psychiatry 139 565-570, 1982 McCarley RW, Hobson JA Neuronal excitability modulation over the sleep cycle a structural and mathematical model. Science 189 58-60, 1975... [Pg.692]

Cataplexy A sudden muscle weakness and loss of tone that can prevent narcoleptics from achieving a normal sleep cycle. [Pg.129]

One of the most consistent findings is the sleep disturbance that often precedes and may even trigger a manic phase ( 46). Studies on circadian rhythms have demonstrated that many aspects of the sleep cycle are phase-advanced in mania (i.e., occur earlier than normal), and often these patterns resemble the free-running rhythms seen in normal individuals who are removed from all time cues. In addition, there is a blunting of amplitude and a doubling of the sleep-wake cycle up to 48 hours. Lithium is known to delay the sleep-wake cycle and often slow such free-running rhythms, which in turn are partly modulated by neurotransmitters such as NE, 5-HT, and acetylcholine. Further, manipulation of the sleep-wake cycle may prevent a manic episode or be used to treat the depressive phase (e.g., sleep deprivation therapy see also the section Experiments in Chapter 8). [Pg.191]


See other pages where Sleep cycles is mentioned: [Pg.530]    [Pg.1134]    [Pg.52]    [Pg.152]    [Pg.156]    [Pg.482]    [Pg.483]    [Pg.488]    [Pg.489]    [Pg.491]    [Pg.495]    [Pg.111]    [Pg.132]    [Pg.133]    [Pg.136]    [Pg.136]    [Pg.188]    [Pg.189]    [Pg.423]    [Pg.453]    [Pg.927]    [Pg.222]    [Pg.377]    [Pg.1137]    [Pg.355]   
See also in sourсe #XX -- [ Pg.6 , Pg.225 ]

See also in sourсe #XX -- [ Pg.504 , Pg.505 , Pg.506 , Pg.507 ]




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