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.

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II. Muscle atonia in non-REM sleep

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00466.2001 ◽

2002 ◽

Vol 283 (2) ◽

pp. R527-R532 ◽

Cited By ~ 20

Author(s):

Esther Werth ◽

Peter Achermann ◽

Alexander A. Borbély

Keyword(s):

Sleep Deprivation ◽

Rem Sleep ◽

Time Course ◽

Sleep Onset ◽

Rem Sleep Deprivation ◽

Sleep Episode ◽

Muscle Atonia ◽

Recovery Sleep ◽

Before And After ◽

Sleep Deficit

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.

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Selective REM sleep deprivation in humans: effects on sleep and sleep EEG

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.274.4.r1186 ◽

1998 ◽

Vol 274 (4) ◽

pp. R1186-R1194 ◽

Cited By ~ 19

Author(s):

Takuro Endo ◽

Corinne Roth ◽

Hans-Peter Landolt ◽

Esther Werth ◽

Daniel Aeschbach ◽

...

Keyword(s):

Sleep Deprivation ◽

Rem Sleep ◽

Power Spectra ◽

Sleep Regulation ◽

Compensatory Response ◽

Rem Sleep Deprivation ◽

Eeg Power Spectra ◽

Sleep Homeostasis ◽

Sleep Propensity

To investigate rapid eye movement (REM) sleep regulation, eight healthy young men were deprived of REM sleep for three consecutive nights. In a three-night control sleep deprivation (CD) session 2 wk later, the subjects were repeatedly awakened from non-REM sleep in an attempt to match the awakenings during the REM sleep deprivation (RD) nights. During the RD nights the number of sleep interruptions required to prevent REM sleep increased within and across consecutive nights. REM sleep was reduced to 9.2% of baseline (CD nights: 80.7%) and rose to 140.1% in the first recovery night. RD gave rise to changes in the EEG power spectra of REM sleep. Power in the 8.25- to 11-Hz range was reduced in the first recovery night, an effect that gradually subsided but was still present in the third recovery night. The rising REM sleep propensity, as reflected by the increase of interventions within and across RD nights, and the moderate REM sleep rebound during recovery can be accounted for by a compensatory response that serves REM sleep homeostasis. The changes in the electroencephalogram power spectra, which were observed during enhanced REM sleep propensity, may be a sign of an altered quality of REM sleep.

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REM sleep deprivation increases early morning pineal melatonin in castrated rats

Behavioral and Neural Biology ◽

10.1016/s0163-1047(89)90872-8 ◽

1989 ◽

Vol 51 (2) ◽

pp. 237-246 ◽

Cited By ~ 5

Author(s):

M. Peder ◽

T. Porkka-Heiskanen ◽

A. Alila ◽

M.-L. Laakso ◽

G. Johansson

Keyword(s):

Sleep Deprivation ◽

Rem Sleep ◽

Early Morning ◽

Rem Sleep Deprivation ◽

Pineal Melatonin

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REM sleep-dependent short-term and long-term hourglass processes in the ultradian organization and recovery of REM sleep in the rat

SLEEP ◽

10.1093/sleep/zsaa023 ◽

2020 ◽

Vol 43 (8) ◽

Author(s):

Adrián Ocampo-Garcés ◽

Alejandro Bassi ◽

Enzo Brunetti ◽

Jorge Estrada ◽

Ennio A Vivaldi

Keyword(s):

Sleep Deprivation ◽

Rem Sleep ◽

Transition Probability ◽

Nrem Sleep ◽

Short Term ◽

Rem Sleep Deprivation ◽

Sleep Episode ◽

Organization Of Sleep ◽

Sleep Transition

Abstract Study Objectives To evaluate the contribution of long-term and short-term REM sleep homeostatic processes to REM sleep recovery and the ultradian organization of the sleep wake cycle. Methods Fifteen rats were sleep recorded under a 12:12 LD cycle. Animals were subjected during the rest phase to two protocols (2T2I or 2R2I) performed separately in non-consecutive experimental days. 2T2I consisted of 2 h of total sleep deprivation (TSD) followed immediately by 2 h of intermittent REM sleep deprivation (IRD). 2R2I consisted of 2 h of selective REM sleep deprivation (RSD) followed by 2 h of IRD. IRD was composed of four cycles of 20-min RSD intervals alternating with 10 min of sleep permission windows. Results REM sleep debt that accumulated during deprivation (9.0 and 10.8 min for RSD and TSD, respectively) was fully compensated regardless of cumulated NREM sleep or wakefulness during deprivation. Protocol 2T2I exhibited a delayed REM sleep rebound with respect to 2R2I due to a reduction of REM sleep transitions related to enhanced NREM sleep delta-EEG activity, without affecting REM sleep consolidation. Within IRD permission windows there was a transient and duration-dependent diminution of REM sleep transitions. Conclusions REM sleep recovery in the rat seems to depend on a long-term hourglass process activated by REM sleep absence. Both REM sleep transition probability and REM sleep episode consolidation depend on the long-term REM sleep hourglass. REM sleep activates a short-term REM sleep refractory period that modulates the ultradian organization of sleep states.

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Cardiopulmonary regulation after rapid-eye-movement sleep deprivation

Journal of Applied Physiology ◽

10.1152/jappl.1992.72.3.970 ◽

1992 ◽

Vol 72 (3) ◽

pp. 970-976 ◽

Cited By ~ 16

Author(s):

S. DeMesquita ◽

G. A. Hale

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Sleep Deprivation ◽

Systolic Blood Pressure ◽

Respiratory Rate ◽

Eye Movement ◽

Rem Sleep ◽

Rem Sleep Deprivation ◽

Recovery Sleep ◽

Arterial Blood

Arterial blood pressure, chest movement, electroencephalogram, and electromyogram were monitored in six normotensive Sprague-Dawley rats for 4 h/day 3 days before and 4 days after 114 h of rapid-eye-movement (REM) sleep deprivation. During recovery sleep immediately after REM sleep deprivation (RD), there was a significant increase in the amount of time spent in REM sleep. During this rebound in REM sleep, there was a significant rise (26%) in heart rate in wakefulness, non-REM sleep, and REM sleep during the first 4 h after RD. Systolic blood pressure was also significantly elevated (14%) but only during wakefulness before recovery sleep. Rats with the greatest waking systolic blood pressure after RD had the lowest REM sleep rebound in the 4 h immediately after RD (r = -0.885, P less than 0.05). The rise in heart rate, systolic blood pressure, and REM sleep time evident on day 1 immediately after RD was absent on recovery days 2–4. The respiratory rate tended to be higher throughout the recovery period in every state of consciousness; however, these values never reached the level of significance. In the initial recovery sleep period, regulation of heart rate was more disrupted by REM sleep deprivation than either arterial blood pressure or respiratory rate.

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Neuronal activity in the preoptic hypothalamus during sleep deprivation and recovery sleep

Journal of Neurophysiology ◽

10.1152/jn.00504.2013 ◽

2014 ◽

Vol 111 (2) ◽

pp. 287-299 ◽

Cited By ~ 54

Author(s):

Md. Aftab Alam ◽

Sunil Kumar ◽

Dennis McGinty ◽

Md. Noor Alam ◽

Ronald Szymusiak

Keyword(s):

Sleep Deprivation ◽

Rem Sleep ◽

Preoptic Area ◽

Regulatory Elements ◽

Sleep Regulation ◽

Adenosine Receptor Antagonist ◽

Recovery Sleep ◽

Discharge Rates ◽

Baseline Values ◽

Extracellular Activity

The preoptic hypothalamus is implicated in sleep regulation. Neurons in the median preoptic nucleus (MnPO) and the ventrolateral preoptic area (VLPO) have been identified as potential sleep regulatory elements. However, the extent to which MnPO and VLPO neurons are activated in response to changing homeostatic sleep regulatory demands is unresolved. To address this question, we continuously recorded the extracellular activity of neurons in the rat MnPO, VLPO and dorsal lateral preoptic area (LPO) during baseline sleep and waking, during 2 h of sleep deprivation (SD) and during 2 h of recovery sleep (RS). Sleep-active neurons in the MnPO ( n = 11) and VLPO ( n = 13) were activated in response to SD, such that waking discharge rates increased by 95.8 ± 29.5% and 59.4 ± 17.3%, respectively, above waking baseline values. During RS, non-rapid eye movement (REM) sleep discharge rates of MnPO neurons initially increased to 65.6 ± 15.2% above baseline values, then declined to baseline levels in association with decreases in EEG delta power. Increase in non-REM sleep discharge rates in VLPO neurons during RS averaged 40.5 ± 7.6% above baseline. REM-active neurons ( n = 16) in the LPO also exhibited increased waking discharge during SD and an increase in non-REM discharge during RS. Infusion of A2A adenosine receptor antagonist into the VLPO attenuated SD-induced increases in neuronal discharge. Populations of LPO wake/REM-active and state-indifferent neurons and dorsal LPO sleep-active neurons were unresponsive to SD. These findings support the hypothesis that sleep-active neurons in the MnPO and VLPO, and REM-active neurons in the LPO, are components of neuronal circuits that mediate homeostatic responses to sustained wakefulness.

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

Journal of Applied Physiology ◽

10.1152/jappl.1992.72.1.100 ◽

1992 ◽

Vol 72 (1) ◽

pp. 100-109 ◽

Cited By ~ 11

Author(s):

J. B. Neilly ◽

N. B. Kribbs ◽

G. Maislin ◽

A. I. Pack

Keyword(s):

Sleep Deprivation ◽

Eye Movement ◽

Rem Sleep ◽

Minute Ventilation ◽

Nrem Sleep ◽

Rapid Eye Movement ◽

Rem Sleep Deprivation ◽

Sleep Period ◽

Recovery Sleep ◽

The Relationship

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.

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