Showing papers on "Rapid eye movement sleep published in 1999"
TL;DR: It appears that earlySleep dominated by SWS facilitates consolidation of declarative memory whereas late sleep dominated by REM sleep facilitates consolidationof nondeclarativeMemory.
Abstract: A wordstem priming task (nondeclarative memory), and a mental spatial rotation task (declarative memory) were presented to subjects of an experimental "sleep" group (n = 11) and of a "wake" control group (n = 10). Repetition priming effects and recall of spatial memory were tested after 3-hr retention intervals, which followed learning and were placed either in the early or in the late half of the night. Sleep group subjects slept during the retention intervals while subjects of the wake group stayed awake. As expected, early retention sleep was dominated by slow wave sleep (SWS), whereas rapid eye movement (REM) sleep prevailed during late retention sleep. After early retention sleep, recall of spatial memory was superior to that after late retention sleep (p < 0.01), and also to that after retention intervals of wakefulness (p < 0.05). In contrast, priming was more effective after late than early retention sleep (p < 0.05). It appears that early sleep dominated by SWS facilitates consolidation of declarative memory whereas late sleep dominated by REM sleep facilitates consolidation of nondeclarative memory.
359 citations
TL;DR: Brain serotonergic neurons display a distinctive slow and regular discharge pattern in behaving animals and are activated in association with increased muscle tone/tonic motor activity, especially if the motor activity is in the repetitive or central pattern generator mode.
344 citations
TL;DR: It is concluded that sleep onset is associated with changes in levels of circulating catecholamine and interleukin-2, and loss of sleep and disordered sleep with decreases in slow wave sleep may serve to elevate nocturnal catechlamine levels and contribute to cardiovascular disease.
Abstract: The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on catecholamine and interleukin-2 (IL-2) levels in humans. Circulating levels of catecholamines and IL-2 were sampled every 30 min during 2 nights: undisturbed, baseline sleep and partial sleep deprivation-late night (PSD-L; awake from 0300-0600 h) in 17 healthy male volunteers. Sleep was monitored somnopolygraphically. Sleep onset was associated with a significant (P < 0.05) decline of circulating concentrations of norepinephrine and epinephrine, with a nocturnal nadir that occurred 1 h after nocturnal sleep. On the PSD-L night, levels of norepinephrine and epinephrine significantly (P < 0.05) increased in association with nocturnal awakening. During stage 3-4 sleep, levels of norepinephrine, but not epinephrine, were significantly lower (P < 0.05) compared to average levels during the awake period, stages 1-2 sleep, and rapid eye movement sleep. Nocturnal levels of circulating IL-2 did not change with sleep onset or in relation to PSD-L or the various sleep stages. We conclude that sleep onset is associated with changes in levels of circulating catecholamines. Loss of sleep and disordered sleep with decreases in slow wave sleep may serve to elevate nocturnal catecholamine levels and contribute to cardiovascular disease.
302 citations
TL;DR: The Bispectrals Index decreased during increasing depth of sleep in a fashion very similar to the decrease in Bispectral Index that occurs during general anesthesia.
Abstract: How does physiological sleep affect the Bispectral Index (BIS)? We collected electroencephalographic (EEG) data from five subjects during the early part of the night, comparing the changes in the BIS with the conventional EEG stages of sleep. We found that the BIS was a consistent marker of depth of sleep. Light sleep occurred at BIS values of 75‐90, slow-wave sleep occurred at BIS values of 20 ‐70, and rapid eye movement sleep occurred at BIS values of 75‐92. The effects of natural sleep on the BIS seem to be similar to the effects of general anesthesia on the BIS. The BIS may have a role in monitoring depth of sleep. Implications: Electroencephalographic data were collected from five subjects during sleep. We found that the Bispectral Index decreased during increasing depth of sleep in a fashion very similar to the decrease in Bispectral Index that occurs during general anesthesia. This study further highlights the electroencephalographic similarities of states of sleep and general anesthesia. (Anesth Analg 1999;88:659 ‐61)
238 citations
TL;DR: Exogenous melatonin administered to patients with internal desynchrony at the time of the maximal rise of melatonin secretion might increase the overall amplitude of the circadian pacemaker by reentraining the suprachiasmatic nucleus and thereby restore circadian driven rhythms, one of them being the circadian modulation of REM sleep.
Abstract: REM sleep behavior disorder (RBD) is clinically impressive by virtue of its vigorous sleep behaviors usually accompanying vivid, striking dreams. The main feature of the disorder, REM sleep without muscle atonia, has been shown in a variety of diseases; therefore, the disorder might possibly be underestimated. In an open-labeled trial, we treated six consecutive RBD patients over a 6-week period with 3 mg melatonin given within 30 minutes before bedtime. There was a dramatic clinical improvement in five of the six patients within a week which extended beyond the end of treatment for weeks or months. A second polysomnogram performed 6 weeks after the beginning of treatment showed a significant tendency toward normalization of the percentage of REM sleep, a significant reduction of 30-second epochs, scored as REM sleep without muscle atonia, a significant reduction of stage-shifts in REM, and a significant reduction in epochs considered as movement time in REM. All other sleep parameters were not changed consistently. We hypothesize that internal desynchrony might be a part of the underlying pathophysiology in RBD. Our data might give first evidence to the hypothesis that exogenous melatonin, administered to patients with internal desynchrony at the time of the maximal rise of melatonin secretion, might increase the overall amplitude of the circadian pacemaker by reentraining the suprachiasmatic nucleus and thereby restore circadian driven rhythms, one of them being the circadian modulation of REM sleep.
222 citations
TL;DR: The results are consistent with the hypothesis that locus coeruleus activity contributes to the maintenance of muscle tone in waking, and that reduction in locus coerceduleus discharge plays a role in the loss of muscletone in cataplexy and rapid-eye-movement sleep.
217 citations
TL;DR: Reexamination of published evidence relevant to "sleep intensity," including "negative rebounds," rebounds in other species, the effects of stress and fatigue, depth of sleep indicators, and extended sleep points out pitfalls in the designation of any specific pattern as intense sleep.
Abstract: Total sleep deprivation (TSD) of rats for 24 hours or less by continually enforced locomotion has consistently produced subsequent rebounds of slow-wave or high-amplitude EEG activity in NREM sleep, which has contributed to the widely held view that this EEG activity reflects particularly "intense" or restorative sleep. These rebounds usually have been accompanied by substantial rebounds of REM sleep. In contrast, chronic TSD (2 weeks or longer) by the disk-over-water (DOW) method has produced only huge, long-lasting rebounds of REM sleep with no rebound of high-amplitude NREM sleep. To evaluate whether the different rebounds result from different methods or from different lengths of deprivation, rats were subjected to 24-hour TSD by the DOW method. Rebounds included increases in high-amplitude and slow-wave activity; i.e., the methods produced similar rebound patterns following short-term TSD. (Chronic TSD by continually enforced locomotion would be strategically difficult and severely confounded with motor fatigue.) Rats subjected to DOW-TSD for 4 days, well before the development of severe TSD symptoms, showed primarily REM sleep rebounds. Rats subjected to 1 day of selective REM sleep deprivation, but not their closely yoked control rats, showed large, significant REM sleep rebounds, which evidently were not induced by the stress of the deprivation method per se. The combined findings prompted reexamination of published evidence relevant to "sleep intensity," including "negative rebounds," rebounds in other species, the effects of stress and fatigue, depth of sleep indicators, and extended sleep. The review points out pitfalls in the designation of any specific pattern as intense sleep.
204 citations
TL;DR: The data support previously reported findings that gamma activity has a significant relationship to the sleep-wake cycle and cognitive tasks and demonstrate that various components of the high-frequency spectrum behave differently in some situations.
159 citations
TL;DR: In this article, the authors explored the possibility that normal subjects carrying this HLA allele (25% of the general population) could display subclinical REM sleep abnormalities and increased daytime sleepiness.
Abstract: Narcolepsy, a neurological disorder characterized by excessive daytime sleepiness and abnormal REM sleep, is known to be tightly associated with the Human Leukocyte Antigen (HLA) DQ allele DQB1*0602. In this study, we have explored the possibility that normal subjects carrying this HLA allele (25% of the general population) could display subclinical REM sleep abnormalities and increased daytime sleepiness. Data from 525 middle-aged adults enrolled in the Wisconsin Sleep Cohort study were used for this analysis. Nocturnal polysomnography, sleep latency during the multiple sleep latency test (MSLT), and questionnaire items pertaining to excessive daytime sleepiness were compared between DQB1*0602 positive (n = 132) and negative (n = 393) participants. Results indicate shorter REM latency whether or not the latency was adjusted for wake after sleep onset (p = 0.003) and p = 0.02 respectively), increased sleep efficiency (p = 0.06) and decreased percent time spent in stage I sleep (p = 0.02) during nocturnal polysomnography in DQB1*0602 subjects. Data gathered using the Multiple Sleep Latency Test or the Epworth and Stanford sleepiness scales did not differentiate between DQB1*0602 positive and negative subjects. These results support the hypothesis that polymorphisms at the level of HLA DQ modulates sleep tendencies in humans.
148 citations
TL;DR: It is suggested that movement arousals may influence daytime sympathetic tone independently of RDI and nighttime saturation and respiratory disturbance index (RDI) and nighttime pulse oxyhemoglobin saturation.
139 citations
Book•
30 Oct 1999
TL;DR: Role of Peribrachial Area in Generation of Rapid Eye Movement Sleep and Pont-Geniculo-Occipital Wave and Sleep Factors and Endogenous Sleep Substances, S. Datta and M.M. Mirmiran.
Abstract: Eyelid Condition at Birth: Relationship to Adult Mammalian Sleep-waking Patterns, E Aserinsky Phylogeny and Evolution of Rapid Eye Movement (REM) Sleep, M G Frank Ontogenesis of REM Sleep, M Segawa Initiation of Rapid Eye Movement Sleep: Beyond the Brainstem, A R Morrison, L D Sanford, and R J Ross Muscle Atonia in REM Sleep, Y -Y Lai and J M Siegel PGO Wave Generation: Mechanism and Functional Significance, S Datta Norepinephrine and REM Sleep, P-H Luppi, D Gervasoni, C Peyron, C Rampon, B Barbagli, R Boissard, and P Fort New Directions for the Study of Cholinergic REM Sleep Generation: Specifying Pre- and Postsynaptic Mechanisms, M L Capece, H A Baghdoyan, and R Lydic Functional Role of Serotonin 5-HT1 and 5-HT2 Receptor in the Regulation of REM Sleep, J M Monti and D Monti Possible Role of GABA in the Regulation of REM Sleep with Special Reference to REM-OFF Neurons, B N Mallick, S Kaur, S K Jha, and J M Siegel Nitric Oxide: A Diffusible Modulator of Physiological Traits and Behavioral States, T O Leonard and R Lydic Neurotransmitters Changes and REM Sleep, T Kodama Spatio-Temporal Distribution of Neuronal Activities and REM Sleep, S Inoue, U K Saha, and T Musha Different Physiological Properties of Two Populations of PS-on Neurons in the Mesopontine Tegmentum, Y Koyama, Y Kayama, and K Sakai Hormones and REM Sleep, F Obal Jr and J M Krueger Endogenous Sleep Substances and REM Sleep, S Inoue, K Honda, M Kimura, and S-Q Zhang Brain Energy, Production, and Sleep Occurrence, R Cespuglio, H Faradji-Prevautel, and L Netchiporouk Rapid Eye Movement Sleep: From Cerebral Metabolism to Functional Brain Mapping, P Maquet and C Phillips REM Sleep and Apnea, D W Carley and M Radulovacki Thermoregulatory Control of the nonREM-REM Sleep Cycle, R Szymusiak, Md Noor Alam, and D McGinty REM Sleep Across Age and Sex, K Mishima, T Shimizu, and Y Hishikawa The Function of Fetal/Neonatal REM Sleep, M Mirmiran and Y G H Maas REM Sleep Deprivation Alters Factors Affecting Neuronal Excitability: Role of Norepinephrine and Its Possible Mechanism of Action, B N Mallick, H V A Adya, and s Thankachan REM Sleep Deprivation and Behavioral Changes, G W Vogel Cellular and Molecular Changes Occurring During REM Sleep, O Prospero-Garcia, L Navarro, E Murillo-Rodriguez, M Sanchez-Alavez, R Guzman-Marin, M Mendez-Diaz, M Gomez-Chavarin, A Jimenez-Anguiano, and R Drucker-Colin Intensity of REM Sleep, K Takahashi Why We Believe What We Believe About REM-Sleep Regulation, H Benington Hypothesis on REM Sleep from the Viewpoint of Neuronal Dynamics, M Nakao and M Yamamoto
TL;DR: Although various psychological measures correlate with sleep variables in sleep apnea subjects, many are explained by controlling age, body mass, and hypertension.
TL;DR: Earplugs worn during exposure to the noise produced a significant decrease in rapid eye movement latency and an increase in the percentage of rapid eye movements sleep, providing a reasonable basis for testing the effects of earplugs on the sleep of critically ill subjects.
Abstract: Background Sleep deprivation may contribute to impaired immune function, ventilatory compromise, disrupted thermoregulation, and delirium. Noise levels in intensive care units may be related to disturbed sleep patterns, but noise reduction has not been tested in this setting. Objective To measure the effect of a noise reduction intervention on the sleep of healthy subjects exposed to simulated intensive care unit noise. Methods After digital audiotape recording of noise and development of the noise reduction intervention, 5 nocturnal 8-hour periods of sleep were measured in 6 paid, healthy volunteers at 7-day intervals in a sleep disorders center. Polysomnographic data were collected by experienced sleep disorders technicians and scored by certified raters. After the first 3 quiet nights, earplugs were randomly assigned to be worn on the fourth and fifth nights during exposure to the recorded noise. Sound pressure levels were measured during all 5 nights. Results Sleep architecture and sound measurements on quiet nights did not differ significantly. Sound levels were significantly lower on quiet nights than on noise nights. Exposure to the noise increased the number of awakenings, percentage of stage 2 sleep, and rapid eye movement latency and decreased time asleep, sleep maintenance efficiency index, and percentage of rapid eye movement sleep. Earplugs worn during exposure to the noise produced a significant decrease in rapid eye movement latency and an increase in the percentage of rapid eye movement sleep. Conclusion The results provide a reasonable basis for testing the effects of earplugs on the sleep of critically ill subjects.
TL;DR: Prior food deprivation negated the effect of leptin on both REMS and SWS, a result that emphasizes the significance of the apparent coupling between sleep parameters and energy status.
Abstract: Leptin (ob protein) is an adipose tissue derived circulating hormone that acts at specific receptors in the hypothalamus to reduce food intake. The protein is also critically involved in energy balance and metabolic status. Here the effect of leptin on sleep architecture in rats was evaluated because food consumption and metabolic status are known to influence sleep. Sprague-Dawley rats were chronically implanted with electrodes for EEG and EMG recording and diurnal sleep parameters were quantified over 9-h periods following leptin administration. Murine recombinant leptin (rMuLep) was administered systemically to rats that either had undergone 18 h of prior food deprivation or had received food ad libitum. In the normally fed rats, leptin significantly decreased the duration of rapid eye movement sleep (REMS) by about 30% and increased the duration of slow wave sleep (SWS) by about 13%, the latter effect reflecting enhanced power in the delta frequency band. These results are consistent with studies that have linked changes in metabolic rate with effects on sleep. Leptin administration has previously been shown to alter neuroendocrine parameters that could have mediated these changes in sleep architecture. Unexpectedly, prior food deprivation negated the effect of leptin on both REMS and SWS, a result that emphasizes the significance of the apparent coupling between sleep parameters and energy status.
TL;DR: Dysmenorrheic pain is shown to be not only a disorder of menstruation but is manifest throughout the menstrual cycle, which disturbs sleep, which may exacerbate the effect of the pain on daytime functioning.
Abstract: Primary dysmenorrhea is characterized by painful uterine cramps, near and during menstruation, that have an impact on personal life and productivity. The effect on sleep of this recurring pain has not been established. We compared sleep, nocturnal body temperatures, and hormone profiles during the menstrual cycle of 10 young women who suffered from primary dysmenorrhea, without any menstrual-associated mood disturbances, and 8 women who had normal menstrual cycles. Dysmenorrheic pain significantly decreased subjective sleep quality, sleep efficiency, and rapid eye movement (REM) sleep but not slow wave sleep (SWS), compared with pain-free phases of the menstrual cycle and compared with the controls. Even before menstruation, in the absence of pain, the women with dysmenorrhea had different sleep patterns, nocturnal body temperatures, and hormone levels compared with the controls. In the mid-follicular, mid-luteal, and menstrual phases, the dysmenorrheics had elevated morning estrogen concentrations, higher mean in-bed temperatures, and less REM sleep compared with the controls, as well as higher luteal phase prolactin levels. Both groups of women had less REM sleep when their body temperatures were high during the luteal and menstrual phases, implying that REM sleep is sensitive to elevated body temperatures. We have shown that dysmenorrhea is not only a disorder of menstruation but is manifest throughout the menstrual cycle. Furthermore, dysmenorrheic pain disturbs sleep, which may exacerbate the effect of the pain on daytime functioning.
TL;DR: In this paper, a 1-mg oral dose of SR 46349B, a novel 5-HT2 antagonist, was administered three hours before bedtime to investigate the effect on the sleep EEG.
TL;DR: Findings highlight the role of subjective and REM sleep measures as correlates of short-term psychotherapy treatment response in major depressive disorder and suggest disturbed sleep may be a physiological indicator of increased limbic and brain stem arousal.
TL;DR: The findings indicate that rapid eye movement sleep may have been present in large amounts in the first mammals and suggest that it may have evolved in pre-mammalian reptiles.
TL;DR: The present study has demonstrated that the sleep‐promoting potency of 2‐[p‐(2‐carboxyethyl)phenethylamino]‐5′‐N‐ethylcarboxamido adenosine (CGS21680), a selective agonist for theAdenosine A2A receptor, varies depending on the location of the administration.
Abstract: The present study has demonstrated that the sleep-promoting potency of 2-[p-(2-carboxyethyl)phenethylamino]-5′-N-ethylcarboxamido adenosine (CGS21680), a selective agonist for the adenosine A2A receptor, varies depending on the location of the administration. CGS21680 was continuously administered to rats through a chronically implanted cannula for 6 h during their active phase. The tip of the cannula was located in the subarachnoid space or the brain ventricle neighbouring the established brain areas implicated in the regulation of sleep–wake phenomena, i.e. rostral basal forebrain, medial preoptic area, lateral preoptic area, posterior hypothalamus, and dorsal tegmentum of the pons and medulla. At an infusion rate of 2.0 pmol/min, the magnitude of increase in non-rapid eye movement sleep varied from 14 min (a 15% increase) to 96 min (a 103% increase), and those of rapid eye movement sleep varied from 6 min (a 40% increase) to 28 min (a 264% increase) from the respective baseline values. The largest increases in both types of sleep occurred when CGS21680 was administered to the subarachnoid space underlying the rostral basal forebrain. These findings were interpreted to mean that the major, if not the only, site responsible for the CGS21680-inducing sleep was located in or near the rostral basal forebrain. This interpretation was supported by the findings that the administration of CGS21680 to the rostral basal forebrain produced predominant expression of Fos within the shell of the nucleus accumbens and the medial portion of the olfactory tubercle, and that the microdialysis perfusion of CGS21680 into the shell of the nucleus accumbens also exhibited a sleep-promoting effect.
TL;DR: The apparent inhibition of the GG reflex during REM sleep may help explain why the upper airway is vulnerable to collapse during this state.
Abstract: 1. Genioglossus (GG) activation in response to upper airway negative pressure may be an important mechanism in the maintenance of airway patency. This reflex occurs during wakefulness but is diminished during stable non-rapid eye movement (NREM) sleep. Since obstructive events occur more commonly at wake-sleep transitions and during rapid eye movement (REM) sleep than during stable NREM sleep, we assessed the GG reflex during these two vulnerable states. 2. Seventeen healthy adults were studied throughout one evening and overnight. Electroencephalograms (EEGs), electro-oculograms (EOGs), submental electromyogram (EMG), GG EMG (intramuscular electrodes), and choanal plus epiglottic pressures were recorded. The GG reflex response to pulses of -8 cmH2O choanal pressure applied via nose mask during early inspiration was quantified repeatedly during relaxed wakefulness, within five breaths of wake-sleep transition (EEG alpha-theta transition) and during REM sleep. Only trials without EEG arousal were analysed, resulting in data from 14 subjects during sleep onset and 10 subjects during REM sleep (overall, 174-491 trials per state). 3. During wakefulness there was brisk GG reflex activation in response to negative pressure (amplitude: +78.5 +/- 28.3 % baseline (mean +/- s.e.m.); latency to maximal response: 177 +/- 16 ms). 4. At sleep onset, although there was marked variability among individuals, there was no significant reduction in the magnitude of the GG reflex for the group as a whole (amplitude: +33.2 +/- 8.2 % baseline; latency: 159 +/- 15 ms). 5. In contrast, during REM sleep there was a reduction of GG reflex (amplitude: -12.6 +/- 8.3 % baseline (P = 0.017 vs. awake); latency: 160 +/- 10 ms (n.s. vs. awake)) and greater airway collapsibility during the applied pressures (P = 0.043 vs. awake). 6. We conclude that there was no systematic reduction in the GG reflex to negative pressure at sleep onset. Nonetheless, it remains possible that sleep-deprived normal subjects and patients with sleep apnoea could react differently. 7. The apparent inhibition of the GG reflex during REM sleep may help explain why the upper airway is vulnerable to collapse during this state.
TL;DR: It is found that, during this state, a powerful glycinergic premotor inhibitory system acts to suppress hypoglossal motoneurons, which opens new avenues for the treatment of obstructive sleep apnea syndrome.
TL;DR: The results indicate that the preoptic area mediates the sleep-promoting activity of GHRH.
Abstract: Previous reports indicate that growth hormone-releasing hormone (GHRH) is involved in sleep regulation. The site of action mediating the nonrapid eye movement sleep (NREMS)-promoting effects of GHRH is not known, but it is independent from the pituitary. GHRH (0.001, 0. 01, and 0.1 nmol/kg) or a competitive antagonist of GHRH (0.003, 0.3, and 14 nmol/kg) was microinjected into the preoptic area, and the sleep-wake activity was recorded for 23 hr after injection in rats. GHRH elicited dose-dependent increases in the duration and in the intensity of NREMS compared with that in control records after intrapreoptic injection of physiological saline. The antagonist decreased the duration and intensity of NREMS and prolonged sleep latency. Consistent alterations in rapid eye movement sleep (REMS) and in brain temperature were not found. The GHRH antagonist also attenuated the enhancements in NREMS elicited by 3 hr of sleep deprivation. Histological verification of the injection sites showed that the majority of the effective injections were in the preoptic area and the diagonal band of Broca. The results indicate that the preoptic area mediates the sleep-promoting activity of GHRH.
TL;DR: A silent MR sequence that can record brain activation over many hours with simultaneous acquisition of an EEG is described, which shows activation of occipital cortex and deactivation of frontal cortex during REM sleep, in agreement with previous studies using other techniques.
Abstract: Functional imaging of human sleep has been performed with nuclear medicine methods, but MRI has been difficult to implement, in part because of the noise associated with echo-planar imaging as well as the difficulty in reading physiologic signals in the MRI environment. We describe a silent MR sequence that can record brain activation over many hours with simultaneous acquisition of an EEG. This shows activation of occipital cortex and deactivation of frontal cortex during REM sleep, in agreement with previous studies using other techniques. MRI-Sleep-REM sleep.
TL;DR: The natural inhibition of endogenous glucocorticoid secretion during early sleep seems to be essential for a sleep-related facilitation of declarative memory.
TL;DR: It is concluded that in young adult men, testosterone levels begin to rise on falling asleep, peak at about the time of first REM, and remain at the same levels until awakening.
Abstract: The relation between the pituitary-gonadal hormones' rhythm and sleep physiology in men is not fully elucidated. To examine whether the reproductive hormones are correlated with sleep architecture, we determined the nocturnal serum levels of testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) in six healthy young men. Serum hormone levels were obtained every 15 minutes from 1900 to 0700 hours with simultaneous polysomnographic sleep recordings. Hourly testosterone levels were lowest when subjects were awake (1900-2200 hours) than during sleep (2300-0700 hours). Testosterone nocturnal rise antedated the first REM by about 90 minutes. The rise in testosterone levels was slower when REM latency was longer. Mean nocturnal testosterone levels did not correlate with the number of rapid eye movement (REM) episodes. Also, pre-non-REM (NREM) testosterone levels were higher as compared with the pre-REM periods and lower during the first NREM period as compared with other nocturnal NREM periods. Serum LH levels disclosed a nocturnal rise that preceeded a similar rise in testosterone by about an hour. We conclude that in young adult men, testosterone levels begin to rise on falling asleep, peak at about the time of first REM, and remain at the same levels until awakening.
TL;DR: A significant decrease in the fronto-occipital as well as in the inter-frontal coherence values in the alpha range was observed with the falling of the vigilance level, which suggests that the brain mechanisms underlying these coherences are state dependent.
TL;DR: BDNF increased time spent in non-rapid eye movement sleep (NREMS) in rats and rabbits and REMS in rabbits and current results provide further evidence that various growth factors are involved in sleep regulation.
Abstract: Various growth factors are involved in sleep regulation. Brain-derived neurotrophic factor (BDNF) belongs to the neurotrophin family; it and its receptors are found in normal brain. Furthermore, ce...
TL;DR: The results indicate continued evaluation of auditory input salience during sleep, which diminishes during deep sleep, and is replaced by evaluation of stimulus context in a train of stimuli during REM sleep.
TL;DR: There were significant age-related reductions in high-voltage NREM sleep ("HS2"), the mean length of sleep bouts, and REM-onset duration in the 1-year-old rats, indicating that the changes seen in the older animals were evident by midlife.
Abstract: Human sleep in old age is characterized by a number of changes, including reductions in sleep efficiency, amounts of visually scored slow-wave and REM sleep, and amplitude of the diurnal sleep/wake rhythm. In older rats, some, but not all, of these traits have been reported, including a decrease in the mean duration of sleep bouts, an increase in the number of sleep bouts, and a modest reduction of REM sleep. Studies of the diurnal rhythm of total sleep have had varied results. There are, however, virtually no data indicating at what point across the rat's lifetime the changes seen in old age begin to occur. In order to more fully characterize sleep in older rats, and to develop data on when they first appear, we have examined sleep in young adult (3 months), middle-aged (12 months), and older (24 months) rats during 24 hours under constant dim light. Analyses of variance revealed no age-related changes in total sleep, NREM or REM sleep, wake time after sleep onset, or three different measures of the amplitude of the sleep/wake circadian rhythm. There were, however, significant age-related reductions in high-voltage NREM sleep ("HS2"), the mean length of sleep bouts, and REM-onset duration. These were seen in the 1-year-old rats, indicating that the changes seen in the older animals were evident by midlife.
TL;DR: It is concluded that mirtazapine, over a 50-fold dose range, significantly reduces central apnea expression during NREM and REM sleep in the rat and that the efficacy of this compound to suppress apnea in all sleep stages most probably arises from its mixed agonist/antagonist profile at serotonin receptors.
Abstract: Serotonin enhancing drugs, including L-tryptophan and, more recently, fluoxetine and paroxetine, have been tested as pharmacologic treatments for sleep apnea syndrome. Although some patients have demonstrated reduced apnea expression after treatment with these compounds, this improvement has been restricted to nonrapid eye movement (NREM) sleep, with some patients showing no improvement. This study reports the effects of mirtazapine, an antidepressant with 5-HT(1) agonist as well as 5-HT(2) and 5-HT(3) antagonist effects, on sleep and respiration in an established animal model of central apnea. We studied nine adult male Sprague-Dawley rats chronically instrumented for sleep staging. In random order on separate days, rats were recorded after intraperitoneal injection of: (1) saline, (2) 0.1 mg/kg +/- mirtazapine (labeled as Remeron), (3) 1 mg/kg mirtazapine, or (4) 5 mg/ kg mirtazapine. With respect to saline injections, mirtazapine at all three doses reduced apnea index during NREM sleep by more than 50% (p < 0.0001) and during REM sleep by 60% (p < 0.0001) for at least 6 h. In association with this apnea suppression normalized inspiratory minute ventilation increased during all wake/sleep states (p < 0.001 for each state). The duration of NREM sleep was unaffected by any dose of mirtazapine (p = 0.42), but NREM EEG delta power was increased by more than 30% at all doses (p = 0.04), indicating improved NREM sleep consolidation after mirtazapine injection. We conclude that mirtazapine, over a 50-fold dose range, significantly reduces central apnea expression during NREM and REM sleep in the rat. The efficacy of this compound to suppress apnea in all sleep stages most probably arises from its mixed agonist/antagonist profile at serotonin receptors. The implications of these findings for the management of sleep apnea syndrome must be verified by appropriate clinical trials.