scholarly journals The Effects of Daytime Psilocybin Administration on Sleep: Implications for Antidepressant Action

2020 ◽  
Vol 11 ◽  
Author(s):  
Daniela Dudysová ◽  
Karolina Janků ◽  
Michal Šmotek ◽  
Elizaveta Saifutdinova ◽  
Jana Kopřivová ◽  
...  

Serotonergic agonist psilocybin is a psychedelic with antidepressant potential. Sleep may interact with psilocybin’s antidepressant properties like other antidepressant drugs via induction of neuroplasticity. The main aim of the study was to evaluate the effect of psilocybin on sleep architecture on the night after psilocybin administration. Regarding the potential antidepressant properties, we hypothesized that psilocybin, similar to other classical antidepressants, would reduce rapid eye movement (REM) sleep and prolong REM sleep latency. Moreover, we also hypothesized that psilocybin would promote slow-wave activity (SWA) expression in the first sleep cycle, a marker of sleep-related neuroplasticity. Twenty healthy volunteers (10 women, age 28–53) underwent two drug administration sessions, psilocybin or placebo, in a randomized, double-blinded design. Changes in sleep macrostructure, SWA during the first sleep cycle, whole night EEG spectral power across frequencies in non-rapid eye movement (NREM) and REM sleep, and changes in subjective sleep measures were analyzed. The results revealed prolonged REM sleep latency after psilocybin administration and a trend toward a decrease in overall REM sleep duration. No changes in NREM sleep were observed. Psilocybin did not affect EEG power spectra in NREM or REM sleep when examined across the whole night. However, psilocybin suppressed SWA in the first sleep cycle. No evidence was found for sleep-related neuroplasticity, however, a different dosage, timing, effect on homeostatic regulation of sleep, or other mechanisms related to antidepressant effects may play a role. Overall, this study suggests that potential antidepressant properties of psilocybin might be related to changes in sleep.

SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Sjoerd J van Hasselt ◽  
Maria Rusche ◽  
Alexei L Vyssotski ◽  
Simon Verhulst ◽  
Niels C Rattenborg ◽  
...  

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.


2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 8526-8526 ◽  
Author(s):  
K. P. Parker ◽  
D. L. Bliwise ◽  
J. Dalton ◽  
W. Harris ◽  
S. Jain ◽  
...  

8526 Background: We explored the effects of polysomnographic measures of nocturnal sleep on depression and pain in advanced cancer patients taking opioids. Methods: The sample included 72 subjects (solid tumor, Stages III/IV) with a mean age of 55.9 (9.1); 39 were male. All were taking opioids. Subjects underwent ambulatory polysomnography for 48 hours in their homes. Nocturnal sleep parameters included total sleep time (minutes); sleep efficiency (SE; %); sleep latency (SL; minutes); rapid-eye-movement sleep latency (REML; minutes); the percentages (%) of non-rapid eye movement (NREM) Stages 1, 2, and slow wave sleep (SWS, 3 & 4), and REM sleep; and the number of awakenings > 60 seconds. Subjects kept an opioid diary, data from which were converted into a mean hourly morphine equivalent dose (HMED). Subjects also completed the Brief Pain Inventory (BPI) and the Beck Depression Inventory (BDI). Descriptive, correlation, and regression procedures were used for data analysis. Results: Subjects had a mean nocturnal sleep period of 400.1 ± 97.4 minutes. The SL was normal at 26.5 ± 42.6 minutes but the SE was low (77.5 ± 13.2%). Most sleep was light NREM Stages 1 and 2 with decreased amounts of deep SWS (0.3 ± 2.7%) and REM sleep (14.4 ± 8.5%). The REML was prolonged at 149.1 ± 105.1 minutes. The mean BPI scores for pain intensity and interference were 4.4 ± 1.4 and 5.0 ± 2.1, respectively. The mean BDI score was 13.7 ± 7.9. The average HMED was .59 ± .1. Controlling for age and gender, regression analyses revealed that SWS and REM sleep moderated the relationship between depression and pain. Those with more SWS had lower depression levels in spite of higher pain intensity (t = -2.8, p = .007) while those with more REM sleep had lower depression levels despite higher pain interference (t = -2.0, p = .045). Controlling for pain intensity and interference, HMED was positively associated with Stage 1 % (r = .36, p = .001) and the number of nocturnal awakenings > 60 seconds (r = .28, p = .019). Conclusions: Opioids may lighten and disrupt sleep altering sleep cycle progression. The resulting decrements in SWS and REM sleep may lead to increased depression and enhanced pain. Consideration of the timing and dosing of opioids in relationship to nocturnal sleep may decrease depression and subsequently optimize pain management. No significant financial relationships to disclose.


2020 ◽  
pp. 1-12
Author(s):  
Sue Llewellyn

Dreaming happens during sleep. When we aren’t interacting with the world, our minds turn inwards. We dream. These dreams differ. Rapid eye movement (REM) dreams are visual, vivid, bizarre, emotional, and highly associative with embodied narratives, whereas non-rapid eye movement (NREM) dreams tend to be shorter and more thought-like. During REM dreams, the brain is as active, or even more active, than it is during wakefulness. In some dreams, during REM sleep, the dreamer is lucid—they become aware they are dreaming and can, sometimes control the dream content. These different types of dream happen at different times in the sleep cycle. Across the night, we experience NREM sleep (including light sleep and deep sleep) and REM sleep in a fixed sequence. The night isn’t a uniform period of rest. This introductory chapter explains these basic issues about sleep and dreams.


2015 ◽  
Author(s):  
Sudhansu Chokroverty

Recent research has generated an enormous fund of knowledge about the neurobiology of sleep and wakefulness. Sleeping and waking brain circuits can now be studied by sophisticated neuroimaging techniques that map different areas of the brain during different sleep states and stages. Although the exact biologic functions of sleep are not known, sleep is essential, and sleep deprivation leads to impaired attention and decreased performance. Sleep is also believed to have restorative, conservative, adaptive, thermoregulatory, and consolidative functions. This review discusses the physiology of sleep, including its two independent states, rapid eye movement (REM) and non–rapid eye movement (NREM) sleep, as well as functional neuroanatomy, physiologic changes during sleep, and circadian rhythms. The classification and diagnosis of sleep disorders are discussed generally. The diagnosis and treatment of the following disorders are described: obstructive sleep apnea syndrome, narcolepsy-cataplexy sydrome, idiopathic hypersomnia, restless legs syndrome (RLS) and periodic limb movements in sleep, circadian rhythm sleep disorders, insomnias, nocturnal frontal lobe epilepsy, and parasomnias. Sleep-related movement disorders and the relationship between sleep and psychiatric disorders are also discussed. Tables describe behavioral and physiologic characteristics of states of awareness, the international classification of sleep disorders, common sleep complaints, comorbid insomnia disorders, causes of excessive daytime somnolence, laboratory tests to assess sleep disorders, essential diagnostic criteria for RLS and Willis-Ekbom disease, and drug therapy for insomnia. Figures include polysomnographic recording showing wakefulness in an adult; stage 1, 2, and 3 NREM sleep in an adult; REM sleep in an adult; a patient with sleep apnea syndrome; a patient with Cheyne-Stokes breathing; a patient with RLS; and a patient with dream-enacting behavior; schematic sagittal section of the brainstem of the cat; schematic diagram of the McCarley-Hobson model of REM sleep mechanism; the Lu-Saper “flip-flop” model; the Luppi model to explain REM sleep mechanism; and a wrist actigraph from a man with bipolar disorder. This review contains 14 highly rendered figures, 8 tables, 115 references, and 5 MCQs.


2015 ◽  
Author(s):  
Sudhansu Chokroverty

Recent research has generated an enormous fund of knowledge about the neurobiology of sleep and wakefulness. Sleeping and waking brain circuits can now be studied by sophisticated neuroimaging techniques that map different areas of the brain during different sleep states and stages. Although the exact biologic functions of sleep are not known, sleep is essential, and sleep deprivation leads to impaired attention and decreased performance. Sleep is also believed to have restorative, conservative, adaptive, thermoregulatory, and consolidative functions. This review discusses the physiology of sleep, including its two independent states, rapid eye movement (REM) and non–rapid eye movement (NREM) sleep, as well as functional neuroanatomy, physiologic changes during sleep, and circadian rhythms. The classification and diagnosis of sleep disorders are discussed generally. The diagnosis and treatment of the following disorders are described: obstructive sleep apnea syndrome, narcolepsy-cataplexy sydrome, idiopathic hypersomnia, restless legs syndrome (RLS) and periodic limb movements in sleep, circadian rhythm sleep disorders, insomnias, nocturnal frontal lobe epilepsy, and parasomnias. Sleep-related movement disorders and the relationship between sleep and psychiatric disorders are also discussed. Tables describe behavioral and physiologic characteristics of states of awareness, the international classification of sleep disorders, common sleep complaints, comorbid insomnia disorders, causes of excessive daytime somnolence, laboratory tests to assess sleep disorders, essential diagnostic criteria for RLS and Willis-Ekbom disease, and drug therapy for insomnia. Figures include polysomnographic recording showing wakefulness in an adult; stage 1, 2, and 3 NREM sleep in an adult; REM sleep in an adult; a patient with sleep apnea syndrome; a patient with Cheyne-Stokes breathing; a patient with RLS; and a patient with dream-enacting behavior; schematic sagittal section of the brainstem of the cat; schematic diagram of the McCarley-Hobson model of REM sleep mechanism; the Lu-Saper “flip-flop” model; the Luppi model to explain REM sleep mechanism; and a wrist actigraph from a man with bipolar disorder. This review contains 14 highly rendered figures, 8 tables, 115 references, and 5 MCQs.


SLEEP ◽  
2021 ◽  
Author(s):  
Andreas Brink-Kjær ◽  
Matteo Cesari ◽  
Friederike Sixel-Döring ◽  
Brit Mollenhauer ◽  
Claudia Trenkwalder ◽  
...  

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.


SLEEP ◽  
2020 ◽  
Author(s):  
Jun-Sang Sunwoo ◽  
Kwang Su Cha ◽  
Jung-Ick Byun ◽  
Jin-Sun Jun ◽  
Tae-Joon Kim ◽  
...  

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.


SLEEP ◽  
2019 ◽  
Vol 42 (7) ◽  
Author(s):  
Sarah L Appleton ◽  
Andrew Vakulin ◽  
Angela D’Rozario ◽  
Andrew D Vincent ◽  
Alison Teare ◽  
...  

AbstractStudy ObjectivesQuantitative electroencephalography (EEG) measures of sleep may identify vulnerability to obstructive sleep apnea (OSA) sequelae, however, small clinical studies of sleep microarchitecture in OSA show inconsistent alterations. We examined relationships between quantitative EEG measures during rapid eye movement (REM) and non-REM (NREM) sleep and OSA severity among a large population-based sample of men while accounting for insomnia.MethodsAll-night EEG (F4-M1) recordings from full in-home polysomnography (Embletta X100) in 664 men with no prior OSA diagnosis (age ≥ 40) were processed following exclusion of artifacts. Power spectral analysis included non-REM and REM sleep computed absolute EEG power for delta, theta, alpha, sigma, and beta frequency ranges, total power (0.5–32 Hz) and EEG slowing ratio.ResultsApnea–hypopnea index (AHI) ≥10/h was present in 51.2% (severe OSA [AHI ≥ 30/h] 11.6%). In mixed effects regressions, AHI was positively associated with EEG slowing ratio and EEG power across all frequency bands in REM sleep (all p < 0.05); and with beta power during NREM sleep (p = 0.06). Similar associations were observed with oxygen desaturation index (3%). Percentage total sleep time with oxygen saturation <90% was only significantly associated with increased delta, theta, and alpha EEG power in REM sleep. No associations with subjective sleepiness were observed.ConclusionsIn a large sample of community-dwelling men, OSA was significantly associated with increased EEG power and EEG slowing predominantly in REM sleep, independent of insomnia. Further study is required to assess if REM EEG slowing related to nocturnal hypoxemia is more sensitive than standard PSG indices or sleepiness in predicting cognitive decline.


1998 ◽  
Vol 84 (1) ◽  
pp. 253-256 ◽  
Author(s):  
David Megirian ◽  
Jacek Dmochowski ◽  
Gaspar A. Farkas

Megirian, David, Jacek Dmochowski, and Gaspar A. Farkas. Mechanism controlling sleep organization of the obese Zucker rat. J. Appl. Physiol. 84(1): 253–256, 1998.—We tested the hypothesis that the obese ( fa/fa) Zucker rat has a sleep organization that differs from that of lean Zucker rats. We used the polygraphic technique to identify and to quantify the distribution of the three main states of the rat: wakefulness (W), non-rapid-eye-movement (NREM), and rapid-eye-movement (REM) sleep states. Assessment of states was made with light present (1000–1600), at the rats thermoneutral temperature of 29°C. Obese rats, compared with lean ones, did not show significant differences in the total time spent in the three main states. Whereas the mean durations of W and REM states did not differ statistically, that of NREM did ( P = 0.046). However, in the obese rats, the frequencies of switching from NREM sleep to W, which increased, and from NREM to REM sleep, which decreased, were statistically significantly different ( P = 0.019). Frequency of switching from either REM or W state was not significantly different. We conclude that sleep organization differs between lean and obese Zucker rats and that it is due to a disparity in switching from NREM sleep to either W or REM sleep and the mean duration of NREM sleep.


1994 ◽  
Vol 76 (6) ◽  
pp. 2326-2332 ◽  
Author(s):  
S. T. Kuna ◽  
J. S. Smickley ◽  
C. R. Vanoye ◽  
T. H. McMillan

Previous investigators reported that cricothyroid (CT) muscle usually exhibits phasic inspiratory activity in normal adult humans during wakefulness. The purpose of this study was to determine respiratory-related CT activity in normal adult humans during sleep. Nighttime polysomnograms were performed in 16 subjects. Hooked-wire electrodes were percutaneously implanted in CT with 21-gauge needle-catheter unit that allowed artifact-free monopolar recordings during electrode placement. During wakefulness, CT was usually phasically active on inspiration, with tonic activity throughout the respiratory cycle. Phasic inspiratory activity was present throughout sleep in all subjects, even those without respiratory-related CT activity during wakefulness. Compared with non-rapid-eye-movement (NREM) sleep, phasic CT activity uniformly increased in rapid-eye-movement (REM) sleep. No differences were apparent in height of phasic CT activity between phasic and tonic REM sleep. Application of nasal continuous positive pressure in stage 3/4 NREM sleep was associated with a decrease in phasic CT activity. Passively induced hypocapnia with positive-pressure ventilation via a nose mask in stage 3/4 NREM sleep was associated with a disappearance of phasic CT activity. Cessation of positive-pressure ventilation under hypocapnic conditions frequently resulted in apnea. Phasic CT activity remained absent during apnea but reappeared coincident with or soon after resumption of spontaneous respiration. In summary, CT′s phasic inspiratory activity and respiratory-related response to various stimuli during sleep were very similar to those of posterior cricoarytenoid muscle, the principal vocal cord abductor.


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