Time-of-day modulation of homeostatic and allostatic sleep responses to chronic sleep restriction in rats

2012 ◽  
Vol 302 (12) ◽  
pp. R1411-R1425 ◽  
Author(s):  
S. Deurveilher ◽  
B. Rusak ◽  
K. Semba

To study sleep responses to chronic sleep restriction (CSR) and time-of-day influences on these responses, we developed a rat model of CSR that takes into account the polyphasic sleep patterns in rats. Adult male rats underwent cycles of 3 h of sleep deprivation (SD) and 1 h of sleep opportunity (SO) continuously for 4 days, beginning at the onset of the 12-h light phase (“3/1” protocol). Electroencephalogram (EEG) and electromyogram (EMG) recordings were made before, during, and after CSR. During CSR, total sleep time was reduced by ∼60% from baseline levels. Both rapid eye movement sleep (REMS) and non-rapid eye movement sleep (NREMS) during SO periods increased initially relative to baseline and remained elevated for the rest of the CSR period. In contrast, NREMS EEG delta power (a measure of sleep intensity) increased initially, but then declined gradually, in parallel with increases in high-frequency power in the NREMS EEG. The amplitude of daily rhythms in NREMS and REMS amounts was maintained during SO periods, whereas that of NREMS delta power was reduced. Compensatory responses during the 2-day post-CSR recovery period were either modest or negative and gated by time of day. NREMS, REMS, and EEG delta power lost during CSR were not recovered by the end of the second recovery day. Thus the “3/1” CSR protocol triggered both homeostatic responses (increased sleep amounts and intensity during SOs) and allostatic responses (gradual decline in sleep intensity during SOs and muted or negative post-CSR sleep recovery), and both responses were modulated by time of day.

1994 ◽  
Vol 77 (4) ◽  
pp. 1811-1818 ◽  
Author(s):  
C. P. O'Donnell ◽  
E. D. King ◽  
A. R. Schwartz ◽  
P. L. Smith ◽  
J. L. Robotham

The effect of sleep deprivation on sleep architecture and respiratory responses to repetitive airway obstruction during sleep was investigated in four chronically instrumented tracheostomized dogs during 12-h nocturnal experiments. A 24-h period of prior sleep deprivation increased (P < 0.05) the rate at which airway obstruction could be induced from 20 +/- 3 (SE) to 37 +/- 10 times/h compared with non-sleep-deprived dogs. During non-rapid-eye-movement sleep the duration of obstruction, minimum arterial hemoglobin saturation, and peak negative inspiratory effort at arousal were 20.5 +/- 1.0 s, 91.7 +/- 0.5%, and 28.4 +/- 1.8 mmHg, respectively, in non-sleep-deprived dogs. Sleep deprivation increased (P < 0.01) the duration of obstruction to 28.0 +/- 0.9 s, worsened (P < 0.05) the minimal arterial hemoglobin desaturation to 85.4 + 3.1%, and increased (P < 0.025) the peak negative inspiratory effort at arousal to 36.1 +/- 1.6 mmHg. Sleep deprivation also caused increases (P < 0.025) in total sleep time, rapid-eye-movement (REM) sleep time, and percentage of time in REM sleep in a 2-h recovery period without airway obstruction at the end of the study. We conclude that airway obstruction in the sleeping dog can reproduce the disturbances in sleep architecture and respiration that occur in obstructive sleep apnea and that prior sleep deprivation will increase apnea severity, degree of somnolence, and REM sleep rebound independent of change in upper airway collapsibility.


2010 ◽  
Vol 109 (4) ◽  
pp. 1053-1063 ◽  
Author(s):  
H. Schwimmer ◽  
H. M. Stauss ◽  
F. Abboud ◽  
S. Nishino ◽  
E. Mignot ◽  
...  

Sleep influences the cardiovascular, endocrine, and thermoregulatory systems. Each of these systems may be affected by the activity of hypocretin (orexin)-producing neurons, which are involved in the etiology of narcolepsy. We examined sleep in male rats, either hypocretin neuron-ablated orexin/ataxin-3 transgenic (narcoleptic) rats or their wild-type littermates. We simultaneously monitored electroencephalographic and electromyographic activity, core body temperature, tail temperature, blood pressure, electrocardiographic activity, and locomotion. We analyzed the daily patterns of these variables, parsing sleep and circadian components and changes between states of sleep. We also analyzed the baroreceptor reflex. Our results show that while core temperature and heart rate are affected by both sleep and time of day, blood pressure is mostly affected by sleep. As expected, we found that both blood pressure and heart rate were acutely affected by sleep state transitions in both genotypes. Interestingly, hypocretin neuron-ablated rats have significantly lower systolic and diastolic blood pressure during all sleep stages (non-rapid eye movement, rapid eye movement) and while awake (quiet, active). Thus, while hypocretins are critical for the normal temporal structure of sleep and wakefulness, they also appear to be important in regulating baseline blood pressure and possibly in modulating the effects of sleep on blood pressure.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A300-A300
Author(s):  
L Zhang ◽  
J Zhu

Abstract Introduction Impaired rapid eye movement sleep is common among patients with Parkinson’s disease (PD). However, information on rapid eye movement density (REM density) among PD patients is currently lacking. The current study sought to characterize REM density in PD patients and to examine the associations between REM density sleep parameters and clinical manifestations. Methods We retrospectively recruited 172 PD patients. All participants were assessed with a two-night polysomnography, and REM density was calculated. Clinical assessments were completed in PD patients before polysomnography. Results Rapid eye movement sleep behavior disorder (RBD) were observed in 93 patients (54.1%). The disease duration, UPDRS part III score, Hoehn and Yahr (H-Y) stage, and HAMA, HAMD, and PDQ-39 scores in the Parkinson’s disease patients with rapid eye movement sleep behavior disorder (RBD) were significantly higher than in the patients without RBD (P&lt;0.05). The REM density was also significantly higher in the RBD patients than in the patients without RBD (P&lt;0.05). NREM sleep stage 3 time (N3 time) and percentage of N3 time of total sleep time (N3%) were higher in patients without RBD. The forward binary logistic regression model showed that REM density, UPDRS-III score and N3 sleep time were associated with RBD in the PD patients. Conclusion Our results confirm the high prevalence of RBD in patients with PD. Increased REM density was the main risk factor of RBD. Support Special Funds of the Jiangsu Provincial Key Research and Development Projects (grant No. BE2018610)


2007 ◽  
Vol 293 (2) ◽  
pp. R922-R930 ◽  
Author(s):  
Éva Szentirmai ◽  
Tadanobu Yasuda ◽  
Ping Taishi ◽  
Mingxiang Wang ◽  
Lynn Churchill ◽  
...  

Growth hormone-releasing hormone (GHRH), its receptor (GHRHR), and other members of the somatotropic axis are involved in non-rapid eye movement sleep (NREMS) regulation. Previously, studies established the involvement of hypothalamic GHRHergic mechanisms in NREMS regulation, but cerebral cortical GHRH mechanisms in sleep regulation remained uninvestigated. Here, we show that unilateral application of low doses of GHRH to the surface of the rat somatosensory cortex ipsilaterally decreased EEG delta wave power, while higher doses enhanced delta power. These actions of GHRH on EEG delta wave power occurred during NREMS but not during rapid eye movement sleep. Further, the cortical forms of GHRH and GHRHR were identical to those found in the hypothalamus and pituitary, respectively. Cortical GHRHR mRNA and protein levels did not vary across the day-night cycle, whereas cortical GHRH mRNA increased with sleep deprivation. These results suggest that cortical GHRH and GHRHR have a role in the regulation of localized EEG delta power that is state dependent, as well as in their more classic hypothalamic role in NREMS regulation.


2019 ◽  
Vol 102 (6) ◽  
pp. 5458-5465 ◽  
Author(s):  
Emma Ternman ◽  
Emma Nilsson ◽  
Per Peetz Nielsen ◽  
Matti Pastell ◽  
Laura Hänninen ◽  
...  

1994 ◽  
Vol 77 (4) ◽  
pp. 1819-1828 ◽  
Author(s):  
C. P. O'Donnell ◽  
E. D. King ◽  
A. R. Schwartz ◽  
J. L. Robotham ◽  
P. L. Smith

The relationship between airway obstruction during sleep and changes in mean arterial pressure (MAP) was investigated in four chronically instrumented tracheostomized dogs during 12-h nocturnal experiments. The MAP response was determined 1) during experimental airway obstruction whenever sleep occurred, 2) over each 12-h experiment, and 3) during a 2-h recovery period at the end of each experiment. The effects of 24 h of sleep deprivation and changes in plasma levels of renin and atrial natriuretic peptide were assessed. In non-rapid-eye-movement sleep, a period of airway obstruction caused MAP to increase (P < 0.002) from 95 +/- 3 (SE) mmHg to 112 +/- 3 mmHg, and this difference was enhanced (P < 0.04) by sleep deprivation. There was an increase of 12 +/- 2 mmHg in the overall MAP over time (P < 0.001) in non-rapid-eye-movement sleep that was sustained in the 2-h recovery period. Plasma levels of renin and atrial natriuretic peptide were constant and unrelated to changes in MAP. We conclude that in the sleeping dog airway obstruction causes an increase in MAP that can be accentuated by prior sleep deprivation and that repetitive airway obstruction will cause an increase in MAP over time that is sustained for > or = 2 h when normal airway patency is restored.


2005 ◽  
Vol 57 (2) ◽  
pp. 277-282 ◽  
Author(s):  
Jessica Massicotte-Marquez ◽  
Julie Carrier ◽  
Anne Décary ◽  
Annie Mathieu ◽  
Mélanie Vendette ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Evgeny Yu. Bersenev ◽  
Yulia V. Ukraintseva ◽  
Gennadiy V. Kovrov ◽  
Yusef D. Yakhya ◽  
Galina Yu. Vassilieva ◽  
...  

Introduction: A decrease in sleep quality and duration during space missions has repeatedly been reported. However, the exact causes that underlie this effect remain unclear. In space, sleep might be impacted by weightlessness and its influence on cardiovascular function. In this study, we aimed at exploring the changes of night sleep architecture during prolonged, 21-day Dry Immersion (DI) as one of the ground-based models for microgravity studies and comparing them with adaptive changes in the cardiovascular system.Methods: Ten healthy young men were exposed to DI for 21 days. The day before (baseline, B-1), on the 3rd (DI3), 10th (DI10), and 19th (DI19) day of DI, as well as in the recovery period, 1 day after the end of DI (R + 1), they were subjected to overnight polysomnography (PSG) and ambulatory blood pressure monitoring.Results: On DI3, when the most severe back pain occurred due to the effects of DI on the spine and back muscles, the PSG data showed dramatically disorganized sleep architecture. Sleep latency, the number of awakenings, and the duration of wake after sleep onset (WASO) were significantly increased compared with the B-1. Furthermore, the sleep efficiency, duration of rapid eye movement sleep (REM), and duration of non-rapid eye movement stage 2 decreased. On DI10, subjective pain ratings declined to 0 and sleep architecture returned to the baseline values. On DI19, the REM duration increased and continued to rise on R + 1. An increase in REM was accompanied by rising in a nighttime heart rate (HR), which also shows the most significant changes after the end of DI. On DI19 and R + 1, the REM duration showed opposite correlations with the BP parameters: on DI19 it was negatively associated with the systolic BP (SBP), and on R + 1 it was positively correlated with the diastolic BP (DBP).Conclusion: An increase in REM at the end of DI and in recovery might be associated with regulatory changes in the cardiovascular system, in particular, with the reorganization of the peripheral and central blood flow in response to environmental changes.


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