The levels of urinary epinephrine during daytime REM sleep deprivation.

Urinary excretion of epinephrine during REM sleep deprivation in the daytime was examined in an attempt to determine whether epinephrine excretion during sleep is related to the structure of disturbed sleep. Six healthy males were subjected to two experimental conditions: 1) day sleep without interruption, as a control condition, and 2) day sleep with REM sleep deprivation. Under both conditions, epinephrine excretion levels of five of the subjects were found to be distributed along a basal regression line, expressing the relationship of epinephrine excretion and percent of waking time, as calculated in a previous study. The epinephrine levels of the one remaining subject exceeded the values predicted by the regression line. His sleep structure was not only distorted under REM deprivation conditions but also under control conditions as well. These results suggest that the basal regression line is useful for observing the existence of sleep disturbance; indeed, a subject with epinephrine excretion levels much higher than those predicted by the regression line was found to have spontaneously disturbed sleep. More study is needed to clarify the relationship between high epinephrine levels and disturbed sleep.     

Selective REM sleep deprivation during daytime. II. Muscle atonia in non-REM sleep

One of the hallmarks of rapid eye movement (REM) sleep is muscle atonia. Here we report extended epochs of muscle atonia in non-REM sleep (MAN). Their extent and time course was studied in a protocol that included a baseline night, a daytime sleep episode with or without selective REM sleep deprivation, and a recovery night. The distribution of the latency to the first occurrence of MAN was bimodal with a first mode shortly after sleep onset and a second mode 40 min later. Within a non-REM sleep episode, MAN showed a U-shaped distribution with the highest values before and after REM sleep. Whereas MAN was at a constant level over consecutive 2-h intervals of nighttime sleep, MAN showed high initial values when sleep began in the morning. Selective daytime REM sleep deprivation caused an initial enhancement of MAN during recovery sleep. It is concluded that episodes of MAN may represent an REM sleep equivalent and that it may be a marker of homeostatic and circadian REM sleep regulating processes. MAN episodes may contribute to the compensation of an REM sleep deficit.     

Tyrosine hydroxylase activity in rat brain following "REM" sleep deprivation

I n R ecent years biogenic amines have been implicated in the control mechanism for induction and maintenance of sleep processes (J ouvet , 1969). Investigators have looked for changes in the rate of synthesis of cerebral norepinephrine from [³H]tyrosine after REM sleep deprivation and reported increased rates of synthesis during REM sleep deprivation (M ark , H einer , M andel and G odin , 1969) and REM sleep rebound following 91 h of deprivation (P ujol , M ouret and G lowinski , 1968). Because tyrosine is thought to be the rate-limiting enzyme (U denfriend , 1966) in the synthetic pathways for norepinephrine and since the above-mentioned studies are suggestive of changes in the activity of the enzyme, we decided to measure tyrosine hydroxylase activity following REM sleep deprivation.     

Selective REM sleep deprivation during daytime I. Time course of interventions and recovery sleep

Although repeated selective rapid eye movement (REM) sleep deprivation by awakenings during nighttime has shown that the number of sleep interruptions required to prevent REM sleep increases within and across consecutive nights, the underlying regulatory processes remained unspecified. To assess the role of circadian and homeostatic factors in REM sleep regulation, REM sleep was selectively deprived in healthy young adult males during a daytime sleep episode (7-15 h) after a night without sleep. Circadian REM sleep propensity is known to be high in the early morning. The number of interventions required to prevent REM sleep increased from the first to the third 2-h interval by a factor of two and then leveled off. Only a minor REM sleep rebound (11.6%) occurred in the following undisturbed recovery night. It is concluded that the limited rise of interventions during selective daytime REM sleep deprivation may be due to the declining circadian REM sleep propensity, which may partly offset the homeostatic drive and the sleep-dependent disinhibition of REM sleep.     

Restricted sleep regime in rhesus monkeys: differential effect of one night's sleep loss and selective REM deprivation.

The differential effect of either one night's total sleep deprivation (TSD) or of selective REM deprivation (REMD) was examined on post-deprivation daytime EEG patterns with respect to control, in the same group of rhesus monkeys. TSD resulted in significantly decreased wakefulness and increased amounts of NREM and REM on the first day following TSD. In contrast, highly significant REM elevation without alteration of other EEG states occurred for 3 days after REMD. Post-deprivation behavioural and photic-induced neural changes were minor. The results obtained after sleep deprivation in simians are comparable with similar findings in human subjects.     

Effects of selective sleep deprivation on ventilation during recovery sleep in normal humans.

To assess the effects of selective sleep loss on ventilation during recovery sleep, we deprived 10 healthy young adult humans of rapid-eye-movement (REM) sleep for 48 h and compared ventilation measured during the recovery night with that measured during the baseline night. At a later date we repeated the study using awakenings during non-rapid-eye-movement (NREM) sleep at the same frequency as in REM sleep deprivation. Neither intervention produced significant changes in average minute ventilation during presleep wakefulness, NREM sleep, or the first REM sleep period. By contrast, both interventions resulted in an increased frequency of breaths, in which ventilation was reduced below the range for tonic REM sleep, and in an increased number of longer episodes, in which ventilation was reduced during the first REM sleep period on the recovery night. The changes after REM sleep deprivation were largely due to an increase in the duration of the REM sleep period with an increase in the total phasic activity and, to a lesser extent, to changes in the relationship between ventilatory components and phasic eye movements. The changes in ventilation after partial NREM sleep deprivation were associated with more pronounced changes in the relationship between specific ventilatory components and eye movement density, whereas no change was observed in the composition of the first REM sleep period. These findings demonstrate that sleep deprivation leads to changes in ventilation during subsequent REM sleep.     

REM sleep deprivation of rats induces acute phase response in liver

REM sleep is essential for maintenance of body physiology and its deprivation is fatal. We observed that the levels of ALT and AST enzymes and pro-inflammatory cytokines like IL-1β, IL-6 and IL-12 circulating in the blood of REM sleep deprived rats increased in proportion to the extent of sleep loss. But in contrast the levels of IFN-γ and a ∼200 kDa protein, identified by N-terminal sequencing to be alpha-1-inhibitor-3(A1I3), decreased significantly. Quantitative PCR analysis confirmed that REM sleep deprivation down regulates AII3 gene and up regulates IL1 β, IL6 and their respective receptors gene expression in the liver initiating its inflammation.     

Changes in the adrenal medulla of the rat during immobilization stress

A combined histofluorescent, light optic and electron microscopic investigation has been performed to study the medulla of the adrenals in intact rats (August strain) and immediately after immobilization for 30 h and 24 h after. In the intact animals heteromorphism of the medulla is demonstrated; this depends on the fact that adrenocytes are at different stages of the secretory cycle. Immobilization for 30 h results in synchronization of secretion; this is determined by adaptation of the adrenal system to immobilization. One day after immobilization restoration of heteromorphism in chromaffinocytes is demonstrated. The changes described are compensatory-adaptive reactions of the adrenal medulla to the stress in the animals survived.     

Changes occurring in cortical NO release and brain NO-synthases during a paradoxical sleep deprivation and subsequent recovery in the rat

Variations occurring in cortical nitric oxide (NO) release were analysed with a voltametric method in rats (i) placed in control conditions, (ii) while being paradoxical sleep deprived (PSD), or (iii) recovering from a PSD. Activities of neuronal (nNOS) and inducible (iNOS) NO-synthases as well as nNOS expression were also determined in several brain regions. In baseline conditions, circadian variations in nNOS expression and activity were maximal during the dark period and minimal during the light one for all the structures analysed (frontal cortex, pons and medulla). In the same way, cortical NO release occurred through a circadian rhythm exhibiting maxima and minima during dark and light periods, respectively. In the same experimental conditions, iNOS activity did not exhibit time-dependent changes. The correlative changes observed in baseline conditions between NO release, nNOS expression and activity within the frontal cortex were disrupted during PSD and subsequent recovery. Still again, iNOS activity remained unchanged. Results obtained point out that the tight coupling existing in control conditions between nNOS expression-activity and NO release is disrupted by a PSD and remains affected during the subsequent 24 h recovery. Their significance is discussed.     

快速眼动睡眠剥夺对大鼠线索性恐惧消退再现的影响

目的：研究RSD对大鼠线索性恐惧消退再现的影响。方法：1d大鼠适应环境;2d进行恐惧条件化;3d恐惧消退训练并进行RSD;4d进行恐惧消退再现检测。结果：在恐惧条件化及消退训练阶段,0-6hRSD组、6—12hRSD组与各自对照组大鼠的僵直水平组间差异都无显著性;在恐惧消退再现检测阶段,0-6hRSD组大鼠的僵直水平显著高于对照组,6-12hRSD组与对照组大鼠的僵直水平组间差异无显著性。结论：RSD损害消退记忆的再现,并且依赖于睡眠剥夺的时段。