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.

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

2021 ◽  
Author(s):  
Shohei Nishimon ◽  
Noriaki Sakai ◽  
Seiji Nishino
Keyword(s):  
Oral Administration ◽  
Core Body Temperature ◽  
Nrem Sleep ◽  
Stressful Environment ◽  
A2a Receptor ◽  
And Performance ◽  
Adenosine A2a ◽  
Core Body ◽  
Dose Dependent ◽  
A2ar Agonist

Abstract Sleep 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 conclusion, the sake yeast is a potential therapeutic agent for acute insomnia, being a A2AR agonist with stress-reducing and anti-anxiety properties, constituting a promising adjuvant treatment strategy for acute insomnia to traditional pharmacotherapy.

scholarly journals Temperature Monitoring and Perioperative Thermoregulation

2008 ◽  
Vol 109 (2) ◽  
pp. 318-338 ◽  
Author(s):  
Daniel I. Sessler ◽  
David S. Warner ◽  
Mark A. Warner
Keyword(s):  
Body Temperature ◽  
General Anesthesia ◽  
Core Temperature ◽  
Core Body Temperature ◽  
Neuraxial Anesthesia ◽  
General Anesthetics ◽  
The Core ◽  
Core Body ◽  
Dose Dependent ◽  
Body Heat

Most clinically available thermometers accurately report the temperature of whatever tissue is being measured. The difficulty is that no reliably core-temperature-measuring sites are completely noninvasive and easy to use-especially in patients not undergoing general anesthesia. Nonetheless, temperature can be reliably measured in most patients. Body temperature should be measured in patients undergoing general anesthesia exceeding 30 min in duration and in patients undergoing major operations during neuraxial anesthesia. Core body temperature is normally tightly regulated. All general anesthetics produce a profound dose-dependent reduction in the core temperature, triggering cold defenses, including arteriovenous shunt vasoconstriction and shivering. Anesthetic-induced impairment of normal thermoregulatory control, with the resulting core-to-peripheral redistribution of body heat, is the primary cause of hypothermia in most patients. Neuraxial anesthesia also impairs thermoregulatory control, although to a lesser extent than does general anesthesia. Prolonged epidural analgesia is associated with hyperthermia whose cause remains unknown.

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.

Decrease of Core Body Temperature in Mice by Dehydroepiandrosterone

2002 ◽  
Vol 227 (6) ◽  
pp. 382-388 ◽  
Author(s):  
Fernando Catalina ◽  
Leon Milewich ◽  
William Frawley ◽  
Vinay Kumar ◽  
Michael Bennett
Keyword(s):  
Body Temperature ◽  
Receptor Antagonist ◽  
Food Restriction ◽  
Serotonin Receptor ◽  
Biological Effects ◽  
Core Body Temperature ◽  
The Body ◽  
Serotonin Receptor Antagonist ◽  
Core Body ◽  
Dose Dependent

Dietary dehydroepiandrosterone (DHEA) reduces food intake in mice, and this response is under genetic control. Moreover, both food restriction and DHEA can prevent or ameliorate certain diseases and mediate other biological effects. Mice fed DHEA (0.45% w/w of food) and mice pair-fed to these mice (food restricted) for 8 weeks were tested for changes in body temperature. DHEA was more efficient than food restriction alone in causing hypothermia. DHEA injected intraperitoneally also induced hypothermia that reached a nadir at 1 to 2 hr, and slowly recovered by 20 to 24 hr. This effect was dose dependent (0.5–50 mg). Each mouse strain tested (four) was susceptible to this effect, suggesting that the genetics differ for induction of hypophagia and induction of hypothermia. Because serotonin and dopamine can regulate (decrease) body temperature, we treated mice with haloperidol (dopamine receptor antagonist), 5,7-dihydroxytryptamine (serotonin production inhibitor), or ritanserin (serotonin receptor antagonist) prior to injection of DHEA. All of these agents increased rather than decreased the hypothermic effects of DHEA. DHEA metabolites that are proximate (5-androstene-3β, 17β-diol and androstenedione) or further downstream (estradiol-17β) were much less effective than DHEA in inducing hypothermia. However, the DHEA analog, 16α-chloroepiandrosterone, was as active as DHEA. Thus, DHEA administered parentally seems to act directly on temperature-regulating sites in the body. These results suggest that DHEA induces hypothermia independent of its ability to cause food restriction, to affect serotonin or dopamine functions, or to act via its downstream steroid metabolites.

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 Contribution of serotonin and dopamine to changes in core body temperature and locomotor activity in rats following repeated administration of mephedrone

2015 ◽  
Vol 21 (6) ◽  
pp. 1127-1139 ◽  
Author(s):  
Sinead E. Shortall ◽  
Clare H. Spicer ◽  
Francis J. P. Ebling ◽  
A. Richard Green ◽  
Kevin C. F. Fone ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Body Temperature ◽  
Core Body Temperature ◽  
Repeated Administration ◽  
Core Body

Temporal phasing of locomotor activity, heart rate rhythmicity, and core body temperature is disrupted in VIP receptor 2-deficient mice

2011 ◽  
Vol 300 (3) ◽  
pp. R519-R530 ◽  
Author(s):  
Jens Hannibal ◽  
Hansen M. Hsiung ◽  
Jan Fahrenkrug
Keyword(s):  
Heart Rate ◽  
Locomotor Activity ◽  
Body Temperature ◽  
Circadian Rhythms ◽  
Wheel Running ◽  
Core Body Temperature ◽  
Running Activity ◽  
Wheel Running Activity ◽  
Core Body ◽  
Deficient Mice

Neurons of the brain's biological clock located in the hypothalamic suprachiasmatic nucleus (SCN) generate circadian rhythms of physiology (core body temperature, hormone secretion, locomotor activity, sleep/wake, and heart rate) with distinct temporal phasing when entrained by the light/dark (LD) cycle. The neuropeptide vasoactive intestinal polypetide (VIP) and its receptor (VPAC2) are highly expressed in the SCN. Recent studies indicate that VIPergic signaling plays an essential role in the maintenance of ongoing circadian rhythmicity by synchronizing SCN cells and by maintaining rhythmicity within individual neurons. To further increase the understanding of the role of VPAC2 signaling in circadian regulation, we implanted telemetric devices and simultaneously measured core body temperature, spontaneous activity, and heart rate in a strain of VPAC2-deficient mice and compared these observations with observations made from mice examined by wheel-running activity. The study demonstrates that VPAC2 signaling is necessary for a functional circadian clock driving locomotor activity, core body temperature, and heart rate rhythmicity, since VPAC2-deficient mice lose the rhythms in all three parameters when placed under constant conditions (of either light or darkness). Furthermore, although 24-h rhythms for three parameters are retained in VPAC2-deficient mice during the LD cycle, the temperature rhythm displays markedly altered time course and profile, rising earlier and peaking ∼4–6 h prior to that of wild-type mice. The use of telemetric devices to measure circadian locomotor activity, temperature, and heart rate, together with the classical determination of circadian rhythms of wheel-running activity, raises questions about how representative wheel-running activity may be of other behavioral parameters, especially when animals have altered circadian phenotype.

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