scholarly journals Budgerigars have complex sleep structure similar to that of mammals

PLoS Biology ◽  
2020 ◽  
Vol 18 (11) ◽  
pp. e3000929
Author(s):  
Sofija V. Canavan ◽  
Daniel Margoliash
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Mammalian Species ◽  
Parallel Evolution ◽  
Bird Species ◽  
Sleep Architecture ◽  
Sleep Structure ◽  
Lighting Conditions ◽  
Order Of Magnitude ◽  
Electroencephalogram Eeg

Birds and mammals share specialized forms of sleep including slow wave sleep (SWS) and rapid eye movement sleep (REM), raising the question of why and how specialized sleep evolved. Extensive prior studies concluded that avian sleep lacked many features characteristic of mammalian sleep, and therefore that specialized sleep must have evolved independently in birds and mammals. This has been challenged by evidence of more complex sleep in multiple songbird species. To extend this analysis beyond songbirds, we examined a species of parrot, the sister taxon to songbirds. We implanted adult budgerigars (Melopsittacus undulatus) with electroencephalogram (EEG) and electrooculogram (EOG) electrodes to evaluate sleep architecture, and video monitored birds during sleep. Sleep was scored with manual and automated techniques, including automated detection of slow waves and eye movements. This can help define a new standard for how to score sleep in birds. Budgerigars exhibited consolidated sleep, a pattern also observed in songbirds, and many mammalian species, including humans. We found that REM constituted 26.5% of total sleep, comparable to humans and an order of magnitude greater than previously reported. Although we observed no spindles, we found a clear state of intermediate sleep (IS) similar to non-REM (NREM) stage 2. Across the night, SWS decreased and REM increased, as observed in mammals and songbirds. Slow wave activity (SWA) fluctuated with a 29-min ultradian rhythm, indicating a tendency to move systematically through sleep states as observed in other species with consolidated sleep. These results are at variance with numerous older sleep studies, including for budgerigars. Here, we demonstrated that lighting conditions used in the prior budgerigar study—and commonly used in older bird studies—dramatically disrupted budgerigar sleep structure, explaining the prior results. Thus, it is likely that more complex sleep has been overlooked in a broad range of bird species. The similarities in sleep architecture observed in mammals, songbirds, and now budgerigars, alongside recent work in reptiles and basal birds, provide support for the hypothesis that a common amniote ancestor possessed the precursors that gave rise to REM and SWS at one or more loci in the parallel evolution of sleep in higher vertebrates. We discuss this hypothesis in terms of the common plan of forebrain organization shared by reptiles, birds, and mammals.

scholarly journals P120 The Relationship Between Sleep Architecture And Cognition In Late-Life Depression

2021 ◽  
Vol 2 (Supplement_1) ◽  
pp. A60-A60
Author(s):  
A Ricciardiello ◽  
L Mowszowski ◽  
H LaMonica ◽  
F Kumfor ◽  
R Wassing ◽  
...  
Keyword(s):  
Executive Function ◽  
Depressive Symptoms ◽  
Older People ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Depression Scale ◽  
Sleep Architecture ◽  
Late Life Depression ◽  
Significant Group ◽  
Rem Density

Abstract Introduction Depression in older people is associated with changes in sleep, however associations between sleep architecture and cognition have not yet been delineated. We examined sleep architecture in older people with and without depressive symptoms, and relationships with neuropsychological performance. Methods Adults over 50 years underwent overnight polysomnography and memory and executive function tests. Depression and controls groups were defined by a Geriatric Depression Scale-15 cut off score of 6. Sleep architectural outcomes included amount of slow wave sleep (SWS), rapid eye movement (REM) sleep, REM onset latency (ROL), NREM slow wave activity (SWA, 0.5–4 Hz), N2 sleep spindle density and REM density. Results The sample comprised of 71 participants with depressive symptoms and 101 controls (mean age both groups = 64, mean GDS-15 dep= 9.3, con= 1.8). There were no significant group differences in time spent in SWS, REM, REM density or SWA. Those with depressive symptoms had later ROL (p=.008) and less N2 sleep spindles (p=.03) compared to controls. A differential association was observed with less SWS being associated with poor memory recall in the depression group only (z=.342, p=0.008). No associations between sleep and executive function performance were observed. Discussion The link between less time in SWS and poorer memory in those with depressive symptoms could suggest that SWS is particularly pertinent for cognition in depression or that both sleep and cognition mechanisms are influenced by depressive state. Further studies are needed to determine if changes in sleep are linked with underlying neurobiological changes.

scholarly journals Continuous Spike-Wave during Slow Wave Sleep and Related Conditions

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Nilika Shah Singhal ◽  
Joseph E. Sullivan
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Treatment Strategies ◽  
Epileptic Encephalopathy ◽  
Related Condition ◽  
Age Related ◽  
Hormonal Therapies ◽  
Electroencephalogram Eeg ◽  
International League ◽  
Spike Wave

Continuous spike and wave during slow wave sleep (CSWS) is an epileptic encephalopathy that presents with neurocognitive regression and clinical seizures, and that demonstrates an electroencephalogram (EEG) pattern of electrical status epilepticus during sleep, as defined by the Commission on Classification and Terminology of the International League Against Epilepsy 1989. CSWS is an age-related condition, typically presenting in children around 5 years of age, with clinical seizures which progress within 2 years to a severe epileptic encephalopathy. The pathophysiology of CSWS is not completely understood, but the corticothalamic neuronal network involved in sleep patterns is thought to be involved. Genetic predisposition and injury in early development are thought to play etiological roles. Treatment strategies have involved traditional anticonvulsants, hormonal therapies, and other newer techniques. Outcomes are fair, and the thought is that earlier diagnosis and intervention preserve neurocognitive development, as in the case of other epileptic encephalopathies. Further understanding of the mechanisms of CSWS may lead to improved therapeutic options and thus outcomes of children with CSWS.

Ghrelin promotes slow-wave sleep in humans

2003 ◽  
Vol 284 (2) ◽  
pp. E407-E415 ◽  
Author(s):  
J. C. Weikel ◽  
A. Wichniak ◽  
M. Ising ◽  
H. Brunner ◽  
E. Friess ◽  
...  
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Wave Activity ◽  
Sleep Eeg ◽  
Endogenous Ligand ◽  
Plasma Gh ◽  
Electroencephalogram Eeg ◽  
Inverse Pattern ◽  
Ghs Receptor

Ghrelin, an endogenous ligand of the growth hormone (GH) secretagogue (GHS) receptor, stimulates GH release, appetite, and weight gain in humans and rodents. Synthetic GHSs modulate sleep electroencephalogram (EEG) and nocturnal hormone secretion. We studied the effect of 4 × 50 μg of ghrelin administered hourly as intravenous boluses between 2200 and 0100 on sleep EEG and the secretion of plasma GH, ACTH, cortisol, prolactin, and leptin in humans ( n = 7). After ghrelin administration, slow-wave sleep was increased during the total night and accumulated δ-wave activity was enhanced during the second half of the night. Rapid-eye-movement (REM) sleep was reduced during the second third of the night, whereas all other sleep EEG variables remained unchanged. Furthermore, GH and prolactin plasma levels were enhanced throughout the night, and cortisol levels increased during the first part of the night (2200–0300). The response of GH to ghrelin was most distinct after the first injection and lowest after the fourth injection. In contrast, cortisol showed an inverse pattern of response. Leptin levels did not differ between groups. Our data show a distinct action of exogenous ghrelin on sleep EEG and nocturnal hormone secretion. We suggest that ghrelin is an endogenous sleep-promoting factor. This role appears to be complementary to the already described effects of the peptide in the regulation of energy balance. Furthermore, ghrelin appears to be a common stimulus of the somatotropic and hypothalamo-pituitary-adrenocortical systems. It appears that ghrelin is a sleep-promoting factor in humans.

062 Sex Differences in Slow Wave Sleep Following Evening Binge Alcohol Consumption

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A26-A26
Author(s):  
Ian Greenlund ◽  
Jeremy Bigalke ◽  
Anne Tikkanen ◽  
Jennifer Nicevski ◽  
Carl Smoot ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Slow Wave ◽  
Repeated Measures ◽  
Slow Wave Sleep ◽  
Pearson Correlation ◽  
Sleep Architecture ◽  
Alcohol Content ◽  
Men And Women ◽  
Percent Change ◽  
Alcohol Dose

Abstract Introduction Binge alcohol consumption alters normal sleep architecture, often via increased slow wave sleep (SWS) and decreased rapid eye movement (REM) sleep. Women may be more susceptible to the sedative effects of alcohol during blood alcohol content (BAC) decrease as they report higher subjective sleepiness scores prior to bedtime. The purpose of the present study was to examine changes in SWS between men and women following binge alcohol consumption and determine the relation between BAC change at lights out and subsequent sleep architecture. Methods Twenty-three participants (11 men, 12 women) between the ages of 21–45 years were tested twice, once after evening binge alcohol consumption and once after fluid control (randomized, cross-over design). The alcohol dose was based on body weight and sex (1g/kg in men, 0.85g/kg in women) and served as a 4–5 drink equivalent consumed over two hours. Breath alcohol content (BrAC) was monitored in 15-minute increments from first drink consumption to lights out. Overnight polysomnography (PSG) was recorded in each individual and scored by a board-certified sleep physician. Statistical analysis consisted of repeated measures ANOVA and Pearson correlation (p>0.05). Results Age (24±4 vs. 26±6 years) and BMI (27±4 vs. 27±4 kg/m2) were similar between men and women. Peak BrAC (0.10±0.02% vs. 0.10±0.02%) and percent change (-19±11% vs. -19±11%) in BrAC from peak to lights out were also similar between the sexes. Peak BrAC was significantly correlated to the percentage of SWS in women (r=-0.71; p=0.01), but not men (r=-0.25; p=0.45). Similarly, the percent change in BrAC from peak to lights out was significantly correlated to the percentage of SWS in women (r=-0.66; p=0.02), but not men (r=-0.40; p=0.22). The SWS and REM latencies were not associated with either peak or lights out BrAC in both men and women. Conclusion Peak BrAC, and the rate of BrAC clearance prior to lights out, appear to impact SWS differently in men and women. Specifically, women appear to have more SWS in response to high BrAC than their male counterparts, suggesting a stronger depressor impact with regards to SWS in women. Support (if any) National Institutes of Health (AA-024892; U54GM115371; P20GM103474).

Sleep-electroencephalography and the secretion of cortisol and growth hormone in normal controls

1987 ◽  
Vol 116 (1) ◽  
pp. 36-42 ◽  
Author(s):  
A. Steiger ◽  
T. Herth ◽  
F. Holsboer
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Sleep Onset ◽  
Cell Activity ◽  
Cortisol Concentration ◽  
Sleep Stages ◽  
Sleep Structure ◽  
Endocrine Activity ◽  
Normal Controls

Abstract. Sleep-electroencephalography, and the nocturnal secretion of cortisol and GH were investigated simultaneously in a sample of 25 male normal controls (27.1 ± 1.3 years) in order further to examine interaction between sleep structure and concurrent endocrine activity. Slow wave sleep activity was increased during the first part of the night, whereas cortisol concentration was low and GH output reached maximal levels. The second half of the night was characterized by a relative preponderance of REM-sleep, low GH-concentration, and an increase in cortisol. However, no distinct reciprocal interaction between cortisol and GH concentration was noted. In all subjects, a pronounced GH surge between 22.00 and 02.00 h was recorded which occurred independently of the presence of slow wave sleep. Six out of the 25 subjects showed nocturnal GH increases even before sleep onset. These data indicate that somatotropic cell activity during night is less dependent upon the sleeping state or specific conventially defined sleep stages than originally reported.

Time course of EEG power density during long sleep in humans

1990 ◽  
Vol 258 (3) ◽  
pp. R650-R661 ◽  
Author(s):  
D. J. Dijk ◽  
D. P. Brunner ◽  
A. A. Borbely
Keyword(s):  
Slow Wave ◽  
Process Model ◽  
Time Course ◽  
Slow Wave Sleep ◽  
Nrem Sleep ◽  
Sleep Stages ◽  
Base Line ◽  
Sleep Regulation ◽  
Recovery Sleep ◽  
Electroencephalogram Eeg

In nine subjects sleep was recorded under base-line conditions with a habitual bedtime (prior wakefulness 16 h; lights off at 2300 h) and during recovery from sleep deprivation with a phase-advanced bedtime (prior wakefulness 36 h; lights off at 1900 h). The duration of phase-advanced recovery sleep was greater than 12 h in all subjects. Spectral analysis of the sleep electroencephalogram (EEG) revealed that slow-wave activity (SWA; 0.75-4.5 Hz) in non-rapid-eye-movement (NREM) sleep was significantly enhanced during the first two NREM-REM sleep cycles of displaced recovery sleep. The sleep stages 3 and 4 (slow-wave sleep) and SWA decreased monotonically over the first three and four NREM-REM cycles of, respectively, base-line and recovery sleep. The time course of SWA in base-line and recovery sleep could be adequately described by an exponentially declining function with a horizontal asymptote. The results are in accordance with the two-process model of sleep regulation in which it is assumed that SWA rises as a function of the duration of prior wakefulness and decreases exponentially as a function of prior sleep. We conclude that the present data do not provide evidence for a 12.5-h sleep-dependent rhythm of deep NREM sleep.

scholarly journals Evidence That Homeostatic Sleep Regulation Depends on Ambient Lighting Conditions during Wakefulness

2019 ◽  
Vol 1 (4) ◽  
pp. 517-531 ◽  
Author(s):  
Christian Cajochen ◽  
Carolin Reichert ◽  
Micheline Maire ◽  
Luc J. M. Schlangen ◽  
Christina Schmidt ◽  
...  
Keyword(s):  
Slow Wave ◽  
White Light ◽  
Slow Wave Sleep ◽  
Age Groups ◽  
Sleep Regulation ◽  
Older Volunteers ◽  
Lighting Conditions ◽  
Ambient Lighting ◽  
Sleep Homeostasis ◽  
Subjective Sleepiness

We examined whether ambient lighting conditions during extended wakefulness modulate the homeostatic response to sleep loss as indexed by. slow wave sleep (SWS) and electroencephalographic (EEG) slow-wave activity (SWA) in healthy young and older volunteers. Thirty-eight young and older participants underwent 40 hours of extended wakefulness [i.e., sleep deprivation (SD)] once under dim light (DL: 8 lux, 2800 K), and once under either white light (WL: 250 lux, 2800 K) or blue-enriched white light (BL: 250 lux, 9000 K) exposure. Subjective sleepiness was assessed hourly and polysomnography was quantified during the baseline night prior to the 40-h SD and during the subsequent recovery night. Both the young and older participants responded with a higher homeostatic sleep response to 40-h SD after WL and BL than after DL. This was indexed by a significantly faster intra-night accumulation of SWS and a significantly higher response in relative EEG SWA during the recovery night after WL and BL than after DL for both age groups. No significant differences were observed between the WL and BL condition for these two particular SWS and SWA measures. Subjective sleepiness ratings during the 40-h SD were significantly reduced under both WL and BL compared to DL, but were not significantly associated with markers of sleep homeostasis in both age groups. Our data indicate that not only the duration of prior wakefulness, but also the experienced illuminance during wakefulness affects homeostatic sleep regulation in humans. Thus, working extended hours under low illuminance may negatively impact subsequent sleep intensity in humans.

Selective slow-wave sleep suppression affects glucose tolerance and melatonin secretion. The role of sleep architecture

2020 ◽  
Vol 67 ◽  
pp. 171-183
Author(s):  
Yu.V. Ukraintseva ◽  
K.M. Liaukovich ◽  
K.A. Saltykov ◽  
D.A. Belov ◽  
А.N. Nizhnik
Keyword(s):  
Glucose Tolerance ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Sleep Architecture ◽  
Melatonin Secretion

Lighting conditions alter Candida albicans-induced sleep responses in rabbits

1995 ◽  
Vol 269 (6) ◽  
pp. R1441-R1447 ◽  
Author(s):  
L. A. Toth ◽  
J. M. Krueger
Keyword(s):  
Candida Albicans ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Constant Darkness ◽  
Dark Phase ◽  
Circadian Period ◽  
Delta Wave ◽  
Lighting Conditions ◽  
Before And After ◽  
Sleep Alterations

To evaluate the influence of light on sleep patterns after microbial challenge, we studied rabbits housed in 12:12-h light-dark (LD), constant light (LL), or constant darkness (DD) before and after intravenous Candida albicans inoculation. Compared with the LD group, uninoculated LL rabbits sporadically increased slow-wave sleep and delta-wave amplitudes during the circadian period previously associated with the dark phase. In contrast, uninfected DD rabbits showed reduced sleep during the circadian period previously associated with the light phase. Inoculation of LD rabbits with Candida approximately 2 h after light onset increased slow-wave sleep and delta-wave amplitudes during hours 4-8 postinoculation and reduced these parameters during hours 20-46. In contrast, Candida-inoculated LL rabbits demonstrated increased slow-wave sleep for up to 28 h after inoculation, with little subsequent reduction; delta-wave amplitudes were similar to those of LD rabbits. Candida-inoculated DD rabbits demonstrated attenuated increases in slow-wave sleep and delta-wave amplitudes, but the suppression phase was not altered. We conclude that lighting conditions modulate microbially induced sleep alterations.

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