scholarly journals Galanin neurons in the hypothalamus link sleep homeostasis, body temperature and actions of the α2 adrenergic agonist dexmedetomidine

2019 ◽  
Author(s):  
Ying Ma ◽  
Giulia Miracca ◽  
Xiao Yu ◽  
Edward C. Harding ◽  
Andawei Miao ◽  
...  
Keyword(s):  
Body Temperature ◽  
Sleep Deprivation ◽  
Core Body Temperature ◽  
Neuronal Cell ◽  
Nrem Sleep ◽  
Temperature Characteristic ◽  
Adrenergic Agonist ◽  
Delta Power ◽  
Recovery Sleep ◽  
Sleep Homeostasis

AbstractSleep deprivation induces a characteristic rebound in NREM sleep accompanied by an immediate increase in the power of delta (0.5 - 4 Hz) oscillations, proportional to the prior time awake. To test the idea that galanin neurons in the mouse lateral preoptic hypothalamus (LPO) regulate this sleep homeostasis, they were selectively genetically ablated. The baseline sleep architecture of LPO-ΔGal mice became heavily fragmented, their average core body temperature permanently increased (by about 2°C) and the diurnal variations in body temperature across the sleep-wake cycle also markedly increased. Additionally, LPO-ΔGal mice showed a striking spike in body temperature and increase in wakefulness at a time (ZT24) when control mice were experiencing the opposite - a decrease in body temperature and becoming maximally sleepy (start of “lights on”). After sleep deprivation sleep homeostasis was largely abolished in LPO-ΔGal mice: the characteristic increase in the delta power of NREM sleep following sleep deprivation was absent, suggesting that LPO galanin neurons track the time spent awake. Moreover, the amount of recovery sleep was substantially reduced over the following hours. We also found that the α2 adrenergic agonist dexmedetomidine, used for long-term sedation during intensive care, requires LPO galanin neurons to induce both the NREM-like state with increased delta power and the reduction in body temperature, characteristic features of this drug. This suggests that dexmedetomidine over-activates the natural sleep homeostasis pathway via galanin neurons. Collectively, the results emphasize that NREM sleep and the concurrent reduction in body temperature are entwined at the circuit level.SignificanceCatching up on lost sleep (sleep homeostasis) is a common phenomenon in mammals, but there is no circuit explanation for how this occurs. We have discovered that galanin neurons in the hypothalamus are essential for sleep homeostasis as well as for the control of body temperature. This is the first time that a neuronal cell type has been identified that underlies sleep homeostasis. Moreover, we show that activation of these galanin neurons are also essential for the actions of the α2 adrenergic agonist dexmedetomidine, which induces both hypothermia together with powerful delta oscillations resembling NREM sleep. Thus, sleep homeostasis, temperature control and sedation by α2 adrenergic agonists can all be linked at the circuit level by hypothalamic galanin neurons.

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.

scholarly journals Genetic lesioning of histamine neurons increases sleep–wake fragmentation and reveals their contribution to modafinil-induced wakefulness

SLEEP ◽  
2019 ◽  
Vol 42 (5) ◽  
Author(s):  
Xiao Yu ◽  
Ying Ma ◽  
Edward C Harding ◽  
Raquel Yustos ◽  
Alexei L Vyssotski ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Knockout Mice ◽  
Histidine Decarboxylase ◽  
Nrem Sleep ◽  
Delta Power ◽  
Adult Mice ◽  
Sleep Homeostasis ◽  
Normal Sleep ◽  
Wake State

Abstract Acute chemogenetic inhibition of histamine (HA) neurons in adult mice induced nonrapid eye movement (NREM) sleep with an increased delta power. By contrast, selective genetic lesioning of HA neurons with caspase in adult mice exhibited a normal sleep–wake cycle overall, except at the diurnal start of the lights-off period, when they remained sleepier. The amount of time spent in NREM sleep and in the wake state in mice with lesioned HA neurons was unchanged over 24 hr, but the sleep–wake cycle was more fragmented. Both the delayed increase in wakefulness at the start of the night and the sleep–wake fragmentation are similar phenotypes to histidine decarboxylase knockout mice, which cannot synthesize HA. Chronic loss of HA neurons did not affect sleep homeostasis after sleep deprivation. However, the chronic loss of HA neurons or chemogenetic inhibition of HA neurons did notably reduce the ability of the wake-promoting compound modafinil to sustain wakefulness. Thus, part of modafinil’s wake-promoting actions arise through the HA system.

scholarly journals Probiotic bacteria and bile acid profile are modulated by prebiotic diet and associate with facilitated diurnal clock/sleep realignment after chronic disruption of rhythms

2021 ◽  
Author(s):  
Robert S. Thompson ◽  
Michelle K Gaffney ◽  
Shelby Hopkins ◽  
Tel Kelley ◽  
Antonio Gonzalez ◽  
...  
Keyword(s):  
Bile Acid ◽  
Body Temperature ◽  
Core Body Temperature ◽  
Nrem Sleep ◽  
Diurnal Rhythms ◽  
Shotgun Metagenomics ◽  
Relative Abundances ◽  
Negative Impacts ◽  
Bile Acid Profiles ◽  
Core Body

Chronic disruption of rhythms (CDR) impacts sleep and can result in circadian misalignment of physiological systems, which in turn is associated with increased disease risk. Exposure to repeated or severe stressors also disturbs sleep and diurnal rhythms. Prebiotic nutrients produce favorable changes in gut microbial ecology, the gut metabolome, and reduce several negative impacts of acute severe stressor exposure, including disturbed sleep, core body temperature rhythmicity, and gut microbial dysbiosis. This study tested the hypothesis whether prebiotics can also reduce the negative impacts of CDR by facilitating light/dark realignment of sleep/wake, core body temperature, and locomotor activity; and whether prebiotic-induced changes in bacteria and bile acid profiles are associated with these effects. Male, Sprague Dawley rats were fed diets enriched in prebiotic substrates or calorically matched control chow. After 5 weeks on diet, rats were exposed to CDR (12h light/dark reversal, weekly for 8 weeks) or remained on undisturbed normal light/dark cycles (NLD). Sleep EEG, core body temperature, and locomotor activity were recorded via biotelemetry in freely moving rats. Fecal samples were collected on experimental days -33, 0 (day of onset of CDR), and 42. Taxonomic identification and relative abundances of gut microbes were measured in fecal samples using 16S rRNA gene sequencing and shotgun metagenomics. Fecal primary, bacterially-modified secondary, and conjugated bile acids were measured using liquid chromatography with tandem mass spectrometry (LC-MS/MS). Prebiotic diet produced rapid and stable increases in the relative abundances of Parabacteroides distasonis and Ruminiclostridium 5. Shotgun metagenomics analyses confirmed reliable increases in relative abundances of Parabacteroides distasonis and Clostridium leptum, a member of the Ruminiclostridium genus. Prebiotic diet also modified fecal bile acid profiles; and based on correlational and step-wise regression analyses, Parabacteroides distasonis and Ruminiclostridium 5 were positively associated with each other and negatively associated with secondary and conjugated bile acids. Prebiotic diet, but not CDR, impacted beta diversity. Measures of alpha diversity evenness were decreased by CDR and prebiotic diet prevented that effect. Rats exposed to CDR while eating prebiotic, compared to control diet, more quickly realigned NREM sleep and core body temperature (ClockLab) diurnal rhythms to the altered light/dark cycle. Finally, both cholic acid and Ruminiclostridium 5 prior to CDR were associated with time to realign CBT rhythms to the new light/dark cycle after CDR; whereas both Ruminiclostridium 5 and taurocholic acid prior to CDR were associated with NREM sleep recovery after CDR. These results suggest that ingestion of prebiotic substrates is an effective strategy to increase the relative abundance of health promoting microbes, alter the fecal bile acid profile, and facilitate the recovery and realignment of sleep and diurnal rhythms after circadian disruption.

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.

008 ARC Genotype Modulates Slow Wave Sleep Following Total Sleep Deprivation

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A4-A4
Author(s):  
Brieann Satterfield ◽  
Darian Lawrence-Sidebottom ◽  
Michelle Schmidt ◽  
Jonathan Wisor ◽  
Hans Van Dongen
Keyword(s):  
Individual Differences ◽  
Sleep Deprivation ◽  
Slow Wave ◽  
Molecular Mechanisms ◽  
Slow Wave Sleep ◽  
Early Gene ◽  
Total Sleep Deprivation ◽  
Recovery Sleep ◽  
Sleep Homeostasis ◽  
Arc Gene

Abstract Introduction The activity-regulated cytoskeleton associated protein (ARC) gene is an immediate early gene that is involved in synaptic plasticity. Recent evidence from a rodent model suggests that Arc may also be involved in sleep homeostasis. However, little is known about the molecular mechanisms regulating the sleep homeostat. In humans, sleep homeostasis is manifested by a marked increase in slow wave sleep (SWS) following acute total sleep deprivation (TSD). There are large, trait individual differences in the magnitude of this SWS rebound effect. We sought to determine whether a single nucleotide polymorphism (SNP) of the ARC gene is associated with individual differences in SWS rebound following TSD. Methods 64 healthy normal sleepers (ages 27.2 ± 4.8y; 32 females) participated in one of two in-laboratory TSD studies. In each study, subjects had a baseline day with 10h sleep opportunity (TIB 22:00–08:00) which was followed by 38h TSD. The studies concluded with 10h recovery sleep opportunity (TIB 22:00–08:00). Baseline and recovery sleep were recorded polysomnographically and scored visually by a trained technician. Genomic DNA was extracted from whole blood. The ARC c.*742 + 58C>T non-coding SNP, rs35900184, was assayed using real-time PCR. Heterozygotes and T/T homozygotes were combined for analysis. The genotype effect on time in SWS was assessed using mixed-effects ANOVA with fixed effects for ARC genotype (C/C vs. T carriers), night (baseline vs. recovery), and their interaction, controlling for study. Results The genotype distribution in this sample – C/C: 41; C/T: 17; T/T: 6 – did not vary significantly from Hardy-Weinberg equilibrium. There was a significant interaction between ARC genotype and night (F1,62=7.27, p=0.009). Following TSD, T allele carriers exhibited 47.6min more SWS compared to baseline, whereas C/C homozygotes exhibited 62.3min more SWS compared to baseline. There was no significant difference in SWS between genotypes at baseline (F1,61=0.69, p=0.41). Conclusion ARC T allele carriers exhibited an attenuated SWS rebound following TSD compared to those homozygous for the C allele. This suggests that the ARC SNP is associated with trait individual differences related to sleep homeostasis, and may thus influence molecular mechanisms involved in long-term memory. Support (if any) ONR N00014-13-1-0302, NIH R21CA167691, and USAMRDC W81XWH-18-1-0100.

scholarly journals Elevated body temperature during sleep in orexin knockout mice

2006 ◽  
Vol 291 (3) ◽  
pp. R533-R540 ◽  
Author(s):  
Takatoshi Mochizuki ◽  
Elizabeth B. Klerman ◽  
Takeshi Sakurai ◽  
Thomas E. Scammell
Keyword(s):  
Locomotor Activity ◽  
Body Temperature ◽  
Heat Loss ◽  
Core Body Temperature ◽  
Biological Rhythms ◽  
Physiological Factors ◽  
Sustained Activity ◽  
Recovery Sleep ◽  
Core Body ◽  
Elevated Body Temperature

Core body temperature (Tb) is influenced by many physiological factors, including behavioral state, locomotor activity, and biological rhythms. To determine the relative roles of these factors, we examined Tb in orexin knockout (KO) mice, which have a narcolepsy-like phenotype with severe sleep-wake fragmentation. Because orexin is released during wakefulness and is thought to promote heat production, we hypothesized that orexin KO mice would have lower Tb while awake. Surprisingly, Tb was the same in orexin KO mice and wild-type (WT) littermates during sustained wakefulness. Orexin KO mice had normal diurnal variations in Tb, but the ultradian rhythms of Tb, locomotor activity, and wakefulness were markedly reduced. During the first 15 min of spontaneous sleep, the Tb of WT mice decreased by 1.0°C, but Tb in orexin KO mice decreased only 0.4°C. Even during intense recovery sleep after 8 h of sleep deprivation, the Tb of orexin KO mice remained 0.7°C higher than in WT mice. This blunted fall in Tb during sleep may be due to inadequate activation of heat loss mechanisms or sustained activity in heat-generating systems. These observations reveal an unexpected role for orexin in thermoregulation. In addition, because heat loss is an essential aspect of sleep, the blunted fall in Tb of orexin KO mice may provide an explanation for the fragmented sleep of narcolepsy.

scholarly journals Cardiovascular Regulation and Body Temperature: Evidence From a Nap vs. Sleep Deprivation Randomized Controlled Trial

2018 ◽  
pp. 687-693 ◽  
Author(s):  
J. SŁOMKO ◽  
M. ZAWADKA-KUNIKOWSKA ◽  
J. J. KLAWE ◽  
M. TAFIL-KLAWE ◽  
J. NEWTON ◽  
...  
Keyword(s):  
Heart Rate ◽  
Body Temperature ◽  
Sleep Deprivation ◽  
Core Body Temperature ◽  
Controlled Trial ◽  
Cardiovascular Regulation ◽  
Sleep Fragmentation ◽  
Stroke Index ◽  
Healthy Men ◽  
Core Body

In this study we set out to understand is sleep fragmentation affects the cardiovascular regulation and circadian variability of core body temperature more or less than sleep deprivation. 50 healthy men (age 29.0±3.1 years; BMI 24.3±2.1 kg/m2) participated in a 3-day study that included one adaptative night and one experimental night involving randomization to: sleep deprivation (SD) and sleep fragmentation (SF). The evaluation included hemodynamic parameters, measures of the spectral analysis of heart rate and blood pressure variability, and the sensitivity of arterial baroreflex function. Core body temperature (CBT) was measured with a telemetric system. SF affects heart rate (61.9±5.6 vs. 56.2±7.6, p<0.01) and stroke index (52.7±11.1 vs. 59.8±12.2, p<0.05) with significant changes in the activity of the ANS (LF-sBP: 6.0±5.3 vs. 3.4±3.7, p<0.05; HF-sBP: 1.8±1.8 vs. 1.0±0.7, p<0.05; LF-dBP: 5.9±4.7 vs. 3.5±3.2, p<0.05) more than SD. Post hoc analysis revealed that after SD mean value of CBT from 21:30 to 06:30 was significantly higher compared to normal night’s sleep and SF. In healthy men SF affects the hemodynamic and autonomic changes more than SD. Sympathetic overactivity is the proposed underlying mechanism.

Natural hypothermia and sleep deprivation: common effects on recovery sleep in the Djungarian hamster

1996 ◽  
Vol 271 (5) ◽  
pp. R1364-R1371 ◽  
Author(s):  
T. Deboer ◽  
I. Tobler
Keyword(s):  
Sleep Deprivation ◽  
Brain Temperature ◽  
Alternative Hypothesis ◽  
Nrem Sleep ◽  
Wave Activity ◽  
Daily Torpor ◽  
Djungarian Hamster ◽  
Subsequent Increase ◽  
Recovery Sleep ◽  
Sleep Debt

Sleep, daily torpor, and hibernation have been considered to be homologous processes. However, in the Djungarian hamster, daily torpor is followed by an increase in slow-wave activity (SWA; electroencephalogram power density 0.75-4.0 Hz) that is similar to the increase observed after sleep deprivation. A positive correlation was found between torpor episode length and the subsequent increase in SWA, which was highest when SWA was assumed to increase with a saturating exponential function. Thus the increase in SWA propensity during daily torpor followed similar kinetics as during waking, supporting the hypothesis that when the animal is in torpor it is incurring a sleep debt. An alternative hypothesis, proposing that the mode of arousal causes the subsequent SWA increase, was tested by warming the animals during emergence from daily torpor. Irrespective of mode of arousal, more non-rapid eye movement (NREM) sleep and a similar SWA increase was found after torpor. The data are compatible with a putative neuronal restorative function for sleep associated with the expression of SWA in NREM sleep. During torpor, when brain temperature is low, this function is inhibited, whereas the need for restoration accumulates. Recovery takes place only after return to euthermia.

332 Non-REM EEG Spectral Power at Baseline and After Total Sleep Deprivation in Individuals with Sleep-Onset Insomnia

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A133-A133
Author(s):  
Myles Finlay ◽  
Devon Hansen ◽  
Lillian Skeiky ◽  
Hans Van Dongen
Keyword(s):  
Sleep Deprivation ◽  
Rem Sleep ◽  
Spectral Power ◽  
Sleep Onset ◽  
Sleep Eeg ◽  
Alpha Power ◽  
Healthy Controls ◽  
Total Sleep Deprivation ◽  
Delta Power ◽  
Sleep Homeostasis

Abstract Introduction The baseline non-REM sleep EEG of individuals with insomnia has been found to display increased spectral power at frequencies &gt;14Hz, which may reflect hyperarousal. There is some evidence in this population of reduced slow wave activity after total sleep deprivation (TSD), potentially indicating altered sleep homeostasis. We investigated non-REM sleep EEG spectra at baseline and after TSD in individuals with sleep-onset insomnia. Methods 10 individuals with sleep-onset insomnia and 5 healthy controls (ages 22-40y, 11 females) completed a 5-day laboratory study with an adaptation night, baseline night, assignment to 38h TSD (n=5 insomnia, n=5 control) or equivalent non-TSD control (n=5 insomnia), and recovery night. Sleep periods were 10h (22:00-08:00) with digital polysomnography (250Hz; Nihon Kohden). Following artifact rejection, 5s subepochs of the non-REM (stages N2, N3) sleep EEG (C3-M2 derivation) in baseline and recovery nights were subjected to spectral analysis. Spectra (0.2Hz bins) were averaged over subepochs in 30s epochs. Repeated-measures ANOVA compared baseline spectra between insomnia and controls, and baseline-recovery difference spectra between TSD insomnia, non-TSD insomnia, and TSD controls. Results Average non-REM sleep amount was 5.9 at baseline, increasing by 1.1h after TSD, with no differences between groups (p≥0.20). At baseline, the insomnia group showed increased power in theta/alpha (~4–12Hz), reaching significance in the lower spindle range, compared to controls (p&lt;0.05). As anticipated, no differences emerged between baseline and recovery nights in the non-TSD insomnia group. However, the TSD insomnia group showed increased delta (~1–3Hz) and theta/alpha (~6–10Hz) power (p&lt;0.05) during recovery. Healthy controls showed expected power increases in delta and lower spindle range, and decreases in upper spindle range (~14–15Hz), after TSD (p&lt;0.05). Conclusion Compared to healthy controls, individuals with sleep-onset insomnia showed increased non-REM sleep EEG power in the theta/alpha bands and low spindle frequency range, with further significant increases in theta/alpha in addition to delta power following TSD, despite small sample size. The increase in delta power following TSD was equivalent to that in healthy controls, suggesting no sleep homeostasis abnormality. Whether the elevated theta/alpha power may be related to hyperarousal is unclear. Support (if any) ONR grant N00014-13-C-0063

scholarly journals Sake yeast induces the sleep-promoting effects under the stress-induced acute insomnia in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shohei Nishimon ◽  
Noriaki Sakai ◽  
Seiji Nishino
Keyword(s):  
Locomotor Activity ◽  
Body Temperature ◽  
Adverse Effects ◽  
Oral Administration ◽  
Core Body Temperature ◽  
Nrem Sleep ◽  
Stressful Environment ◽  
And Performance ◽  
Core Body ◽  
Dose Dependent

AbstractSleep deprivation induces adverse effects on the health, productivity, and performance. The individuals who could not get enough sleep temporarily experience the symptoms of an induced acute insomnia. This study investigated the efficacy of sake yeast in treatment of acute insomnia in mice. The results of this study showed that sake yeast induced a significant dose-dependent wake reduction, a rapid eye movement (REM) and a non-REM (NREM) sleep enhancement during the first 6 h after the oral administration of sake yeast with locomotor activity and core body temperature decreases under the stressful environment in a new cage. In fact, the wake amounts at 3 h and 6 h were significantly reduced after the oral administration of sake yeast compared with the vehicle. The NREM sleep amounts at 3 h and 6 h significantly increased after the administration of sake yeast compared with the vehicle. The REM amount at 6 h significantly increased after the administration of sake yeast compared with the vehicle, but not at 3 h. The previous study suggested that the sleep-promoting effects of sake yeast could be referred from the activating effect of adenosine A2A receptor (A2AR). In summary, the sake yeast is an A2AR agonist and may induce sleep due to its stress-reducing and anti-anxiety properties. Further verification of the involvement of adenosine in the pathophysiology of insomnia is needed.

Sign in / Sign up

Export Citation Format

Share Document