scholarly journals Enduring effects of perinatal nicotine exposure on murine sleep in adulthood

2017 ◽  
Vol 313 (3) ◽  
pp. R280-R289 ◽  
Author(s):  
Jeremy C. Borniger ◽  
Reuben F. Don ◽  
Ning Zhang ◽  
R. Thomas Boyd ◽  
Randy J. Nelson
Keyword(s):  
Sleep Deprivation ◽  
Open Field ◽  
Spectral Power ◽  
Nrem Sleep ◽  
Nicotine Exposure ◽  
Smoking During Pregnancy ◽  
Percent Time ◽  
Baseline Recording ◽  
Male Specific ◽  
Reduced Mobility

The long-term consequences of early life nicotine exposure are poorly defined. Approximately 8–10% of women report smoking during pregnancy, and this may promote aberrant development in the offspring. To this end, we investigated potential enduring effects of perinatal nicotine exposure on murine sleep and affective behaviors in adulthood (~13–15 wk of age) in C57Bl6j mice. Mothers received a water bottle containing 200 µg/ml nicotine bitartrate dihydrate in 2% wt/vol saccharin or pH-matched 2% saccharin with 0.2% (vol/vol) tartaric acid throughout pregnancy and before weaning. Upon reaching adulthood, offspring were tested in the open field and elevated plus maze, as well as the forced swim and sucrose anhedonia tests. Nicotine-exposed male (but not female) mice had reduced mobility in the open field, but no differences were observed in anxiety-like or depressive-like responses. Upon observing this male-specific phenotype, we further assessed sleep-wake states via wireless EEG/EMG telemetry. Following baseline recording, we assessed whether mice exposed to nicotine altered their homeostatic response to 5 h of total sleep deprivation and whether nicotine influenced responses to a powerful somnogen [i.e., lipopolysaccharides (LPS)]. Males exposed to perinatal nicotine decreased the percent time spent awake and increased time in non-rapid eye movement (NREM) sleep, without changes to REM sleep. Nicotine-exposed males also displayed exaggerated responses (increased time asleep and NREM spectral power) to sleep deprivation. Nicotine-exposed animals additionally had blunted EEG slow-wave responses to LPS administration. Together, our data suggest that perinatal nicotine exposure has long-lasting effects on normal sleep and homeostatic sleep processes into adulthood.

scholarly journals The European starling (Sturnus vulgaris) shows signs of NREM sleep homeostasis but has very little REM sleep and no REM sleep homeostasis

SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Sjoerd J van Hasselt ◽  
Maria Rusche ◽  
Alexei L Vyssotski ◽  
Simon Verhulst ◽  
Niels C Rattenborg ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Rem Sleep ◽  
Spectral Power ◽  
Nrem Sleep ◽  
Sleep Time ◽  
European Starling ◽  
Dark Phase ◽  
Rapid Eye Movement ◽  
Sleep Homeostasis

Abstract Most of our knowledge about the regulation and function of sleep is based on studies in a restricted number of mammalian species, particularly nocturnal rodents. Hence, there is still much to learn from comparative studies in other species. Birds are interesting because they appear to share key aspects of sleep with mammals, including the presence of two different forms of sleep, i.e. non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. We examined sleep architecture and sleep homeostasis in the European starling, using miniature dataloggers for electroencephalogram (EEG) recordings. Under controlled laboratory conditions with a 12:12 h light–dark cycle, the birds displayed a pronounced daily rhythm in sleep and wakefulness with most sleep occurring during the dark phase. Sleep mainly consisted of NREM sleep. In fact, the amount of REM sleep added up to only 1~2% of total sleep time. Animals were subjected to 4 or 8 h sleep deprivation to assess sleep homeostatic responses. Sleep deprivation induced changes in subsequent NREM sleep EEG spectral qualities for several hours, with increased spectral power from 1.17 Hz up to at least 25 Hz. In contrast, power below 1.17 Hz was decreased after sleep deprivation. Sleep deprivation also resulted in a small compensatory increase in NREM sleep time the next day. Changes in EEG spectral power and sleep time were largely similar after 4 and 8 h sleep deprivation. REM sleep was not noticeably compensated after sleep deprivation. In conclusion, starlings display signs of NREM sleep homeostasis but the results do not support the notion of important REM sleep functions.

072 Sleep Spindle Harmonics in Insomnia

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A29-A30
Author(s):  
Michael Goldstein ◽  
Monika Haack ◽  
Janet Mullington
Keyword(s):  
Spectral Power ◽  
Nrem Sleep ◽  
Sleep Time ◽  
Sleep Spindle ◽  
Time Frequency ◽  
Insomnia Disorder ◽  
Spectral Peaks ◽  
Limited Application ◽  
Thalamic Relay Nuclei ◽  
Restorative Sleep

Abstract Introduction Prior research has reported NREM spectral EEG differences between individuals with insomnia and good-sleeper controls, including elevated high-frequency EEG power (beta/gamma bands, ~16-50Hz) and, to a lesser extent, elevations in sleep spindle parameters. However, the mechanisms driving these differences remain unclear. Harmonics have been observed in EEG data as spectral peaks at multiples of a fundamental frequency associated with an event (e.g., for a 14Hz spindle, the 2nd harmonic is expected to be a peak at 28Hz). Thus far, there has been very limited application of this idea of spectral harmonics to sleep spindles, even though these patterns can indeed be seen in some existing literature. We sought to build on this literature to apply spectral harmonic analysis to better understand differences between insomnia and good sleepers. Methods 15 individuals with insomnia disorder (DSM-5 criteria, 13 female, age 18–32 years) and 15 good-sleeper controls (matched for sex, age, and BMI) completed an overnight polysomnography recording in the laboratory and subsequent daytime testing. Insomnia diagnosis was determined by a board-certified sleep specialist, and exclusion criteria included psychiatric history within past 6 months, other sleep disorders, significant medical conditions, and medications with significant effects on inflammation, autonomic function, or other psychotropic effects. Results Consistent with prior studies, we found elevated sleep spindle density and fast sigma power (14-16Hz). Despite no difference in beta or gamma band power when averaged across NREM sleep, time-frequency analysis centered on the peaks of detected spindles revealed a phasic elevation in spectral power surrounding the 28Hz harmonic peak in the insomnia group, especially for spindles coupled with slow waves. We also observed an overall pattern of time-locked delay in the 28Hz harmonic peak, occurring approximately 40 msec after spindle peaks. Furthermore, we observed a 42Hz ‘3rd harmonic’ peak, not yet predicted by the existing modeling work, which was also elevated for insomnia. Conclusion In conjunction with existing mathematical modeling work that has linked sleep spindle harmonic peaks with thalamic relay nuclei as the primary generators of this EEG signature, these findings may enable novel insights into specific thalamocortical mechanisms of insomnia and non-restorative sleep. Support (if any) NIH 5T32HL007901-22

scholarly journals Sleep in Normal Aging, Homeostatic and Circadian Regulation and Vulnerability to Sleep Deprivation

2021 ◽  
Vol 11 (8) ◽  
pp. 1003
Author(s):  
Jacques Taillard ◽  
Claude Gronfier ◽  
Stéphanie Bioulac ◽  
Pierre Philip ◽  
Patricia Sagaspe
Keyword(s):  
Older Adults ◽  
Sleep Deprivation ◽  
Health Management ◽  
Nrem Sleep ◽  
Early Morning ◽  
Subcortical Structures ◽  
Wake Time ◽  
Adverse Health Outcomes ◽  
Neurobehavioral Function ◽  
Age Related

In the context of geriatric research, a growing body of evidence links normal age-related changes in sleep with many adverse health outcomes, especially a decline in cognition in older adults. The most important sleep alterations that continue to worsen after 60 years involve sleep timing, (especially early wake time, phase advance), sleep maintenance (continuity of sleep interrupted by numerous awakenings) and reduced amount of sigma activity (during non-rapid eye movement (NREM) sleep) associated with modifications of sleep spindle characteristics (density, amplitude, frequency) and spindle–Slow Wave coupling. After 60 years, there is a very clear gender-dependent deterioration in sleep. Even if there are degradations of sleep after 60 years, daytime wake level and especially daytime sleepiness is not modified with age. On the other hand, under sleep deprivation condition, older adults show smaller cognitive impairments than younger adults, suggesting an age-related lower vulnerability to extended wakefulness. These sleep and cognitive age-related modifications would be due to a reduced homeostatic drive and consequently a reduced sleep need, an attenuation of circadian drive (reduction of sleep forbidden zone in late afternoon and wake forbidden zone in early morning), a modification of the interaction of the circadian and homeostatic processes and/or an alteration of subcortical structures involved in generation of circadian and homeostatic drive, or connections to the cerebral cortex with age. The modifications and interactions of these two processes with age are still uncertain, and still require further investigation. The understanding of the respective contribution of circadian and homeostatic processes in the regulation of neurobehavioral function with aging present a challenge for improving health, management of cognitive decline and potential early chronobiological or sleep-wake interventions.

Sleep after arousal from hibernation is not homeostatically regulated

1999 ◽  
Vol 276 (2) ◽  
pp. R522-R529 ◽  
Author(s):  
Jennie E. Larkin ◽  
H. Craig Heller
Keyword(s):  
Sleep Deprivation ◽  
Brain Function ◽  
Extended Period ◽  
Nrem Sleep ◽  
Wave Activity ◽  
Ground Squirrels ◽  
Recovery Sleep ◽  
Sleep Homeostasis ◽  
Homeostatic Response ◽  
Periodic Arousals

Electroencephalographic slow-wave activity (SWA) in non-rapid eye movement (NREM) sleep is directly related to prior sleep/wake history, with high levels of SWA following extended periods of wake. Therefore, SWA has been thought to reflect the level of accumulated sleep need. The discovery that euthermic intervals between hibernation bouts are spent primarily in sleep and that this sleep is characterized by high and monotonically declining SWA has led to speculation that sleep homeostasis may play a fundamental role in the regulation of the timing of bouts of hibernation and periodic arousals to euthermia. It was proposed that because the SWA profile seen after arousal from hibernation is strikingly similar to what is seen in nonhibernating mammals after extended periods of wakefulness, that hibernating mammals may arouse from hibernation with significant accumulated sleep need. This sleep need may accumulate during hibernation because the low brain temperatures during hibernation may not be compatible with sleep restorative processes. In the present study, golden-mantled ground squirrels were sleep deprived during the first 4 h of interbout euthermia by injection of caffeine (20 mg/kg ip). We predicted that if the SWA peaks after bouts of hibernation reflected a homeostatic response to an accumulated sleep need, sleep deprivation should simply have displaced and possibly augmented the SWA to subsequent recovery sleep. Instead we found that after caffeine-induced sleep deprivation of animals just aroused from hibernation, the anticipated high SWA typical of recovery sleep did not occur. Similar results were found in a study that induced sleep deprivation by gentle handling (19). These findings indicate that the SWA peak immediately after hibernation does not represent homeostatic regulation of NREM sleep, as it normally does after prolonged wakefulness during euthermia, but instead may reflect some other neurological process in the recovery of brain function from an extended period at low temperature.

NREM delta stimulation following MK-801 is a response of sleep systems

1996 ◽  
Vol 76 (6) ◽  
pp. 3714-3720 ◽  
Author(s):  
I. G. Campbell ◽  
I. Feinberg
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Time Course ◽  
Sleep Onset ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Mk 801 ◽  
Regulatory Systems ◽  
Sleep Centers ◽  
Electroencephalogram Eeg

1. We have previously shown that noncompetitive blockade of the N-methyl-D-aspartate (NMDA)-gated cation channel with ketamine or Dizocilpine maleate (MK-801) increases the intensity of non-rapid-eye-movement (NREM) delta during subsequent sleep. This delta increase [measured as integrated amplitude (IA) in 1- to 4-Hz electroencephalogram (EEG)] occurs in the 12-h period following intraperitoneal injection. However, the 12 h after drug injection is also the period in which these drugs induce neurotoxic changes, raising the possibility that the increased delta represents toxic EEG slowing rather than an increase in the physiological delta waves of NREM sleep. 2. We hypothesized that the time course of delta stimulation could be separated from the time course of neurotoxicity. We tested this hypothesis by injecting 0.3 mg/kg MK-801 at the start of the dark period (DP) and depriving rats of sleep until the onset of the light period (LP) 12 h later. 3. There were two control groups: one received MK-801 at the start of the DP with no further manipulation, and the second received a saline injection at DP onset followed by 12 h of sleep deprivation. The dependent variable was the amount of delta IA in the LP, whose onset was 12 h after MK-801 injection. Total IA in the LP was significantly greater in rats that received MK-801 followed by sleep deprivation than in rats that received sleep deprivation alone or MK-801 alone. 4. This finding indicates that delta stimulation by MK-801 is maintained over 12 h of waking, indicating that the delta increase is not due to toxic EEG slowing or persisting MK-801. Instead, NMDA channel blockade by MK-801 increases the homeostatic need for delta or else directly alters sleep regulatory systems. We speculate that these effects are mediated by hypothalamic sleep centers through control of neuroendocrine pulses that produce both NREM and rapid-eye-movement sleep. 5. Imposing a period of waking between drug administration and sleep onset may prove a generally useful strategy for determining whether a drug affects the homeostatic need for sleep or acutely stimulates sleep systems. This strategy can also help distinguish between toxic and physiological increases in delta EEG.

scholarly journals 0789 Decreased Sigma Band Power During NREM Sleep in REM Sleep Behavior Disorder

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A300-A300
Author(s):  
Y Lee ◽  
B Lee
Keyword(s):  
Rem Sleep ◽  
Spectral Power ◽  
Rem Sleep Behavior Disorder ◽  
Behavior Disorder ◽  
Nrem Sleep ◽  
Control Group ◽  
Sleep Behavior ◽  
Band Power ◽  
Potential Biomarker ◽  
Obstructive Sleep

Abstract Introduction REM sleep Behavior Disorder (RBD) is characterized by dream enacting behaviors and a loss of atonia during REM sleep. Early detection of RBD is important because it is considered premonitory symptoms neurodegenerative disorders. In this study, we investigated the slow and fast sigma band power of patients with RBD using frequency analysis. Methods Twenty patients who were diagnosed as RBD according to the ICSD-3 criteria and 20 age-matched controls who underwent polysomnography (PSG) for other sleep disorders (insomnia, snoring) and showed normal to mild obstructive sleep apnea (OSA). NREM sleep EEG data was extracted and N1 sleep data was excluded to minimize arousal artifact. Fast Fourier transform-based spectral power analysis was used to compute the power spectral densities of the EEG in the MATLAB environment. The sigma bands were divided into 2 discrete bands: slow sigma (11 to 13 Hz) and- fast sigma (13 to 15 Hz). Mann-Whitney U test by SPSS was used. Results RBD patients (61.9 ± 7.1 years old; 12 men) had a significantly lower sigma band power than the control group (61.5 ± 1.1 years old; 11 men) in central region (p = 0.028). Particularly, the slow sigma band power showed a bigger difference in all regions except O1 (F3 = 0.017, F4 = 0.027, C3 = 0.004, C4 = 0.009, O2 = 0.017). Conclusion Sigma power was lower in the RBD patients than in the control. It suggests that RBD has impaired cortical activity. Thus, decreased spindle activity during NREM sleep may be a potential biomarker of RBD. Support  

Total sleep deprivation in the rat transiently abolishes the delta amplitude response to darkness: implications for the mechanism of the “negative delta rebound”

1993 ◽  
Vol 70 (6) ◽  
pp. 2695-2699 ◽  
Author(s):  
I. Feinberg ◽  
I. G. Campbell
Keyword(s):  
Sleep Deprivation ◽  
Rem Sleep ◽  
Nrem Sleep ◽  
Sleep Research ◽  
Amplitude Response ◽  
Total Sleep Deprivation ◽  
Sleep Physiology ◽  
Total Failure ◽  
Delta Sleep ◽  
Homeostatic Model

1. The homeostatic model of delta sleep has provided a useful framework for basic sleep research. This model is based on the relation of delta EEG to the duration of prior waking in man, a relation highlighted by the marked increase (rebound) in the delta EEG of nonrapid eye movement (NREM) sleep that follows total sleep deprivation (TSD). The generality of this model is severely challenged by the response to TSD in the rat. In the 12-h light period (LP) that immediately follows TSD, the rat shows a massive increase in REM sleep but only a modest increase in NREM delta EEG. Although this initial delta increase does not nearly compensate for the delta lost during deprivation, the rat then exhibits a depressed rate of delta production (the “negative delta rebound”). This robust and reproducible reaction worsens the delta deficit. 2. Using rats with chronic electrode implantations, we deprived them of all sleep for 24 h by handling them gently when they became inactive. We found that the negative delta rebound entails a transient, near-total failure of delta amplitude to increase normally in response to the onset of darkness. This loss of the rat's EEG response to darkness suggests a disruption of basic sleep physiology and raises the possibility that the negative rebound is also a pathological response. 3. We hypothesize that the negative rebound is maladaptive, and is caused by the massive increase in REM sleep that precedes it; this hypothesis can be tested experimentally.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Caffeine and sleep-deprivation mediated changes in open-field behaviours, stress response and antioxidant status in mice

Sleep Science ◽  
2016 ◽  
Vol 9 (3) ◽  
pp. 236-243 ◽  
Author(s):  
J. Olakunle Onaolapo ◽  
Y. Adejoke Onaolapo ◽  
A. Moses Akanmu ◽  
Gbola Olayiwola
Keyword(s):  
Stress Response ◽  
Sleep Deprivation ◽  
Open Field ◽  
Antioxidant Status
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