scholarly journals Estradiol influences adenosinergic signaling and nonrapid eye movement sleep need in adult female rats

SLEEP ◽  
2021 ◽  
Author(s):  
Philip C Smith ◽  
Derrick J Phillips ◽  
Ana Pocivavsek ◽  
Carissa A Byrd ◽  
Shaun S Viechweg ◽  
...  
Keyword(s):  
Eye Movement ◽  
Adult Female ◽  
Nrem Sleep ◽  
Female Rats ◽  
Sleep Behavior ◽  
A2a Receptors ◽  
Recovery Sleep ◽  
And Gender ◽  
Physiological Markers ◽  
Adenosine Signaling

Abstract Gonadal steroids and gender are risk factors for sleep disruptions and insomnia in women. However, the relationship between ovarian steroids and sleep is poorly understood. In rodent models, estradiol (E2) suppresses sleep in females suggesting that E2 may reduce homeostatic sleep need. The current study investigates whether E2 decreases sleep need and the potential mechanisms that govern E2 suppression of sleep. Our previous findings suggest that the median preoptic nucleus (MnPO) is a key nexus for E2 action on sleep. Using behavioral, neurochemical, and pharmacological approaches, we tested whether (1) E2 influenced the sleep homeostat and (2) E2 influenced adenosine signaling in the MnPO of adult female rats. In both unrestricted baseline sleep and recovery sleep from 6-h sleep deprivation, E2 significantly reduced nonrapid eye movement (NREM) sleep-delta power, NREM-slow wave activity (NREM-SWA, 0.5–4.0 Hz), and NREM-delta energy suggesting that E2 decreases homeostatic sleep need. However, coordinated with E2-induced changes in physiological markers of homeostatic sleep was a marked increase in MnPO extracellular adenosine (a molecular marker of homeostatic sleep need) during unrestricted and recovery sleep in E2-treated but not oil control animals. While these results seemed contradictory, systemically administered E2 blocked the ability of CGS-21680 (adenosine A2A receptor agonist) microinjected into the MnPO to increase NREM sleep suggesting that E2 may block adenosine signaling. Together, these findings provide evidence that E2 may attenuate the local effects of the A2A receptors in the MnPO, which in turn may underlie estrogenic suppression of sleep behavior as well as changes in homeostatic sleep need.

scholarly journals Estradiol Influences Adenosinergic Signaling and NREM Sleep Need in Adult Female Rats

2021 ◽  
Author(s):  
Philip C Smith ◽  
Derrick J Phillips ◽  
Ana Pocivavsek ◽  
Carissa A Byrd ◽  
Shaun S Viechweg ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Adult Female ◽  
Dynamic Range ◽  
Fold Increase ◽  
Nrem Sleep ◽  
Female Rats ◽  
Control Treatment ◽  
Extracellular Adenosine ◽  
Recovery Sleep ◽  
Sleep Homeostat

Studies report estradiol (E2) suppresses sleep in females; however, the mechanisms of E2 action remain largely undetermined. Our previous findings suggest that the median preoptic nucleus (MnPO) is a key nexus for E2 action on sleep. Here, using behavioral, neurochemical and pharmacological approaches, we investigated whether E2 influenced the sleep homeostat as well as adenosinergic signaling in the MnPO of adult female rats. During the Light Phase, where rats accumulate the majority of sleep, E2 markedly reduced NREM-SWA (a measure of the homeostatic sleep need). Following 6-hours of sleep deprivation, levels of NREM-SWA were significantly increased compared to baseline sleep. However, the NREM-SWA levels were not different between E2 and control treatment despite a significant increase in wake at the expense of NREM sleep. Analysis of NREM-SWA differences between baseline and recovery sleep following sleep deprivation demonstrated that E2 induced a 2-fold increase in delta power compared to controls suggesting that E2 significantly expanded the dynamic range for the sleep homeostat. Correlated with E2-induced changes in physiological markers of homeostatic sleep was a marked increase in extracellular adenosine (a molecular marker of homeostatic sleep need) during unrestricted and recovery sleep following a 6-hour deprivation. Additionally, E2 blocked the ability of an adenosine A2A receptor agonist (CGS-21680) to increase NREM sleep compared to controls. Thus, taken together, the findings that E2 increased extracellular adenosine content, while blocking A2A signaling in the MnPO suggests a potential mechanism for how estrogens impact sleep in the female brain.

Arousal Characteristics in Patients with Parkinson’s Disease and Isolated Rapid Eye Movement Sleep Behavior Disorder

SLEEP ◽  
2021 ◽  
Author(s):  
Andreas Brink-Kjær ◽  
Matteo Cesari ◽  
Friederike Sixel-Döring ◽  
Brit Mollenhauer ◽  
Claudia Trenkwalder ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Eye Movement ◽  
Rem Sleep ◽  
Regression Models ◽  
Muscle Tone ◽  
Behavior Disorder ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Sleep Behavior

Abstract Study objectives Patients diagnosed with isolated rapid eye movement (REM) sleep behavior disorder (iRBD) and Parkinson’s disease (PD) have altered sleep stability reflecting neurodegeneration in brainstem structures. We hypothesize that neurodegeneration alters the expression of cortical arousals in sleep. Methods We analyzed polysomnography data recorded from 88 healthy controls (HC), 22 iRBD patients, 82 de novo PD patients without RBD and 32 with RBD (PD+RBD). These patients were also investigated at a 2-year follow-up. Arousals were analyzed using a previously validated automatic system, which used a central EEG lead, electrooculography, and chin electromyography. Multiple linear regression models were fitted to compare group differences at baseline and change to follow-up for arousal index (ArI), shifts in electroencephalographic signals associated with arousals, and arousal chin muscle tone. The regression models were adjusted for known covariates affecting the nature of arousal. Results In comparison to HC, patients with iRBD and PD+RBD showed increased ArI during REM sleep and their arousals showed a significantly lower shift in α-band power at arousals and a higher muscle tone during arousals. In comparison to HC, the PD patients were characterized by a decreased ArI in NREM sleep at baseline. ArI during NREM sleep decreased further at the 2-year follow-up, although not significantly Conclusions Patients with PD and iRBD present with abnormal arousal characteristics as scored by an automated method. These abnormalities are likely to be caused by neurodegeneration of the reticular activation system due to alpha-synuclein aggregation.

scholarly journals Nonrapid eye movement sleep electroencephalographic oscillations in idiopathic rapid eye movement sleep behavior disorder: a study of sleep spindles and slow oscillations

SLEEP ◽  
2020 ◽  
Author(s):  
Jun-Sang Sunwoo ◽  
Kwang Su Cha ◽  
Jung-Ick Byun ◽  
Jin-Sun Jun ◽  
Tae-Joon Kim ◽  
...  
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Rem Sleep Behavior Disorder ◽  
Behavior Disorder ◽  
Nrem Sleep ◽  
Sleep Spindles ◽  
Rapid Eye Movement ◽  
Sleep Behavior ◽  
Slow Oscillations ◽  
Lower Amplitude

Abstract Study Objectives We investigated electroencephalographic (EEG) slow oscillations (SOs), sleep spindles (SSs), and their temporal coordination during nonrapid eye movement (NREM) sleep in patients with idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD). Methods We analyzed 16 patients with video-polysomnography-confirmed iRBD (age, 65.4 ± 6.6 years; male, 87.5%) and 10 controls (age, 62.3 ± 7.5 years; male, 70%). SSs and SOs were automatically detected during stage N2 and N3. We analyzed their characteristics, including density, frequency, duration, and amplitude. We additionally identified SO-locked spindles and examined their phase distribution and phase locking with the corresponding SO. For inter-group comparisons, we used the independent samples t-test or Wilcoxon rank-sum test, as appropriate. Results The SOs of iRBD patients had significantly lower amplitude, longer duration (p = 0.005 for both), and shallower slope (p < 0.001) than those of controls. The SS power of iRBD patients was significantly lower than that of controls (p = 0.002), although spindle density did not differ significantly. Furthermore, SO-locked spindles of iRBD patients prematurely occurred during the down-to-up-state transition of SOs, whereas those of controls occurred at the up-state peak of SOs (p = 0.009). The phase of SO-locked spindles showed a positive correlation with delayed recall subscores (p = 0.005) but not with tonic or phasic electromyography activity during REM sleep. Conclusions In this study, we found abnormal EEG oscillations during NREM sleep in patients with iRBD. The impaired temporal coupling between SOs and SSs may reflect early neurodegenerative changes in iRBD.

scholarly journals A high-density electroencephalography study reveals abnormal sleep homeostasis in patients with rapid eye movement sleep behavior disorder

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Amandine Valomon ◽  
Brady A. Riedner ◽  
Stephanie G. Jones ◽  
Keith P. Nakamura ◽  
Giulio Tononi ◽  
...  
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Rem Sleep Behavior Disorder ◽  
Behavior Disorder ◽  
Nrem Sleep ◽  
High Density ◽  
Rapid Eye Movement ◽  
Sleep Behavior ◽  
Eeg Abnormalities ◽  
Beta Power

AbstractRapid eye movement (REM) sleep behavior disorder (RBD) is characterized by disrupting motor enactments during REM sleep, but also cognitive impairments across several domains. In addition to REM sleep abnormalities, we hypothesized that RBD patients may also display EEG abnormalities during NREM sleep. We collected all-night recordings with 256-channel high-density EEG in nine RBD patients, predominantly early-onset medicated individuals, nine sex- and age- matched healthy controls, and nine additional controls with matched medications and comorbidities. Power spectra in delta to gamma frequency bands were compared during both REM and NREM sleep, between phasic and tonic REM sleep, and between the first versus last cycle of NREM sleep. Controls, but not RBD patients, displayed a decrease in beta power during phasic compared to tonic REM sleep. Compared to controls, RBD patients displayed a reduced decline in SWA from early to late NREM sleep. Overnight changes in the distribution of the amplitude of slow waves were also reduced in RBD patients. Without suppression of beta rhythms during phasic REM sleep, RBD patients might demonstrate heightened cortical arousal, favoring the emergence of behavioral episodes. A blunted difference between REM sleep sub-stages may constitute a sensitive biomarker for RBD. Moreover, reduced overnight decline in SWA suggests a reduced capacity for synaptic plasticity in RBD patients, which may favor progression towards neurodegenerative diseases.

scholarly journals Estradiol Action at the Median Preoptic Nucleus is Necessary and Sufficient for Sleep Suppression in Female rats

2020 ◽  
Author(s):  
PC Smith ◽  
DM Cusmano ◽  
DJ Phillips ◽  
SS Viechweg ◽  
MD Schwartz ◽  
...  
Keyword(s):  
Eye Movement ◽  
Ovarian Hormones ◽  
Gonadal Steroids ◽  
Female Rats ◽  
Rapid Eye Movement ◽  
Preoptic Nucleus ◽  
Direct Infusion ◽  
Sleep Behavior ◽  
Median Preoptic Nucleus ◽  
Necessary And Sufficient

AbstractTo further our understanding of how gonadal steroids impact sleep biology, we sought to address the mechanism by which proestrus levels of cycling ovarian steroids, particularly estradiol (E2), suppress sleep in female rats. We showed that steroid replacement of proestrus levels of E2 to ovariectomized female rats, suppressed sleep to similar levels as those reported by endogenous ovarian hormones. We further showed that this suppression is due to the high levels of E2 alone, and that progesterone did not have a significant impact on sleep behavior. We found that E2 action within the Median Preoptic Nucleus (MnPN), which contains estrogen receptors (ERs), is necessary for this effect; antagonism of ERs in the MnPN attenuated the E2-mediated suppression of both non-Rapid Eye Movement (NREM) and Rapid Eye Movement (REM) sleep. Finally, we found E2 action at the MnPN is also sufficient for sleep suppression, as direct infusion of E2 into the MnPN suppressed sleep. Based on our findings, we predict proestrus levels of E2 alone, acting at the MnPN, mediate sex-hormone driven suppression of sleep in female rats.

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

1992 ◽  
Vol 72 (1) ◽  
pp. 100-109 ◽  
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.

Parasomnias

2020 ◽  
pp. 158-171
Author(s):  
Jessica Jung ◽  
Erik K. St. Louis
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Lewy Bodies ◽  
Rem Sleep Behavior Disorder ◽  
Behavior Disorder ◽  
Nrem Sleep ◽  
Sleep Behavior ◽  
Medical Disorders ◽  
Abnormal Movements ◽  
Psychological Comorbidities

Parasomnias are undesirable and abnormal movements, behaviors, emotions, perceptions, and dreams that occur during or immediately surrounding sleep. The parasomnias are categorized as nonrapid eye movement (NREM) sleep parasomnias, rapid eye movement (REM) sleep parasomnias, and other parasomnias. This chapter provides an overview to the epidemiology, clinical characteristics, differential diagnoses, diagnostic approach, and treatment of common parasomnias encountered in clinical practice. These common parasomnias include NREM parasomnias, considered to be disorders of arousal from NREM sleep and which include a heterogeneous spectrum of sleep behaviors encountered following arousal from NREM sleep exemplified by the phenotypes of sleep terrors, sleep walking, confusional arousals, sleep-related eating disorder, and sexsomnias; the REM parasomnias, including nightmare disorder, recurrent isolated sleep paralysis, and REM sleep behavior disorder, which is strongly associated with prodromal or overt alpha-synucleinopathy neurodegenerative disorders such as Parkinson disease and dementia with Lewy bodies; and other parasomnias, including a spectrum of “leftovers” that do not map well to NREM or REM sleep specifically such as exploding head syndrome, sleep-related hallucinations, sleep enuresis, and parasomnias ascribed to medical disorders, medication or substance use, or unspecified etiologies. It is important for a psychiatrist to be conversant with the complete range of parasomnias given the importance of effective management of frequent psychiatric and psychological comorbidities, which serve as drivers of the frequency and severity of nocturnal events, and to ensure timely referral for polysomnography or other necessary sleep diagnostics where appropriate.

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