Showing papers on "Rapid eye movement sleep published in 2001"

Emotional Memory Formation Is Enhanced across Sleep Intervals with High Amounts of Rapid Eye Movement Sleep

Abstract: Recent studies indicated a selective activation during rapid eye movement (REM) sleep of the amygdala known to play a decisive role in the processing of emotional stimuli. This study compared memory retention of emotional versus neutral text material over intervals covering either early sleep known to be dominated by nonREM slow wave sleep (SWS) or late sleep, in which REM sleep is dominant. Two groups of men were tested across 3-h periods of early and late sleep (sleep group) or corresponding retention intervals filled with wakefulness (wake group). Sleep was recorded polysomnographically. Cortisol concentrations in saliva were monitored at acquisition and retrieval testing. As expected, the amount of REM sleep was about three times greater during late than during early retention sleep, whereas a reversed pattern was observed for SWS distribution (P < 0.001). Sleep improved retention, compared with the effects of wake intervals (P < 0.02). However, this effect was substantial only in the late night (P < 0.005), during which retention was generally worse than during the early night (P < 0.02). Late sleep particularly enhanced memory for emotional texts. This effect was highly significant in comparison with memory for neutral texts (P < 0.01) and in comparison with memory after late and early wake intervals (P < 0.001). Cortisol concentration differed between early and late retention intervals but not between sleep and wake conditions. Results are consonant with a supportive function of REM sleep predominating late sleep for the formation of emotional memory in humans.

The REM Sleep-Memory Consolidation Hypothesis

Abstract: It has been hypothesized that REM (rapid eye movement) sleep has an important role in memory consolidation. The evidence for this hypothesis is reviewed and found to be weak and contradictory. Animal studies correlating changes in REM sleep parameters with learning have produced inconsistent results and are confounded by stress effects. Humans with pharmacological and brain lesion-induced suppression of REM sleep do not show memory deficits, and other human sleep-learning studies have not produced consistent results. The time spent in REM sleep is not correlated with learning ability across humans, nor is there a positive relation between REM sleep time or intensity and encephalization across species. Although sleep is clearly important for optimum acquisition and performance of learned tasks, a major role in memory consolidation is unproven.

Sleep, performance, circadian rhythms, and light-dark cycles during two space shuttle flights

Abstract: Sleep, circadian rhythm, and neurobehavioral performance measures were obtained in five astronauts before, during, and after 16-day or 10-day space missions. In space, scheduled rest-activity cycles were 20-35 min shorter than 24 h. Light-dark cycles were highly variable on the flight deck, and daytime illuminances in other compartments of the spacecraft were very low (5.0-79.4 lx). In space, the amplitude of the body temperature rhythm was reduced and the circadian rhythm of urinary cortisol appeared misaligned relative to the imposed non-24-h sleep-wake schedule. Neurobehavioral performance decrements were observed. Sleep duration, assessed by questionnaires and actigraphy, was only approximately 6.5 h/day. Subjective sleep quality diminished. Polysomnography revealed more wakefulness and less slow-wave sleep during the final third of sleep episodes. Administration of melatonin (0.3 mg) on alternate nights did not improve sleep. After return to earth, rapid eye movement (REM) sleep was markedly increased. Crewmembers on these flights experienced circadian rhythm disturbances, sleep loss, decrements in neurobehavioral performance, and postflight changes in REM sleep.

Disruption of the nocturnal testosterone rhythm by sleep fragmentation in normal men.

Abstract: Recently, we have demonstrated that in normal men the nocturnal testosterone rise antedated the first rapid eye movement (REM) sleep episode by about 90 min and was correlated with REM latency. To further elucidate whether the diurnal testosterone rhythm is a sleep-related phenomenon or controlled by the circadian clock, we determined serum testosterone levels in 10 men during the ultrashort 7/13 sleep-wake cycle paradigm. Using this schedule, subjects experienced partial sleep deprivation and fragmented sleep for a 24-h period. Serum testosterone levels were determined every 20 min between 1900–0700 h with simultaneous sleep recordings during the 7-min sleep attempts. The results were compared with those obtained in men during continuous sleep. Although mean levels and area under the curve of testosterone were similar in both groups, fragmented sleep resulted in a significant delay in testosterone rise (03:24 h ± 1:13 vs. 22:35 h ± 0:22). During fragmented sleep, nocturnal testosterone rise was observed ...

CO2 dialysis in the medullary raphe of the rat increases ventilation in sleep

Abstract: Central chemoreceptors are widespread within the brain stem. We hypothesize that function at different sites varies with arousal state. In unanesthetized rats, we produced focal acidification at single sites by means of microdialysis using artificial cerebrospinal fluid equilibrated with 25% CO2. Tissue acidosis, measured under anesthesia, is equivalent to that observed with 63 Torr end-tidal PCO2 and is limited to 600 microm. Focal acidification of the retrotrapezoid nucleus increased ventilation by 24% only in wakefulness via an increase in tidal volume (Li A, Randall M, and Nattie E. J Appl Physiol 87: 910-919, 1999). In this study of the medullary raphe, the effect of such focal acidification was in sleep (defined by electroencephalographic and electromyographic criteria): ventilation and frequency increased by 15-20% in non-rapid eye movement sleep, and frequency increased by 15% in rapid eye movement sleep. There was no effect in wakefulness. Chemoreception in the medullary raphe appears to be responsive in sleep. Central chemoreceptors at two different locations appear to vary in effectiveness with arousal state.

Microinjection of glutamate into the pedunculopontine tegmentum induces REM sleep and wakefulness in the rat

Abstract: The aim of this study was to test the hypothesis that the cells in the brain stem pedunculopontine tegmentum (PPT) are critically involved in the normal regulation of wakefulness and rapid eye movement (REM) sleep. To test this hypothesis, one of four different doses of the excitatory amino acid L-glutamate (15, 30, 60, and 90 ng) or saline (control vehicle) was microinjected unilaterally into the PPT while the effects on wakefulness and sleep were quantified in freely moving chronically instrumented rats. All microinjections were made during wakefulness and were followed by 6 h of polygraphic recording. Microinjection of 15- ng (0.08 nmol) and 30-ng (0.16 nmol) doses of L-glutamate into the PPT increased the total amount of REM sleep. Both doses of L-glutamate increased REM sleep at the expense of slow-wave sleep (SWS) but not wakefulness. Interestingly, the 60-ng (0.32 nmol) dose of L-glutamate increased both REM sleep and wakefulness. The total increase in REM sleep after the 60-ng dose of L-glutamate was significantly less than the increase from the 30-ng dose. The 90-ng (0.48 nmol) dose of L-glutamate kept animals awake for 2-3 h by eliminating both SWS and REM sleep. These results show that the L-glutamate microinjection into the PPT can increase wakefulness and/or REM sleep depending on the dosage. These findings support the hypothesis that excitation of the PPT cells is causal to the generation of wakefulness and REM sleep in the rat. In addition, the results of this study led to the identification of the PPT dosage of L-glutamate that optimally induces wakefulness and REM sleep. The knowledge of this optimal dose will be useful in future studies investigating the second messenger systems involved in the regulation of wakefulness and REM sleep.

Melatonin therapy for REM sleep behavior disorder

Abstract: Rapid eye movement sleep behavior disorder (RBD) is a parasomnia with clinical symptoms that include punching, kicking, yelling and leaping out of bed in sleep. Polysomnographic (PSG) finding showed REM sleep without muscle atonia. Clonazepam is generally used for treating RBD symptoms but melatonin was reported to be effective so we reconfirmed the effect of melatonin on RBD patients in the present study. We used melatonin (3–9 mg/day) which could ameliorate problem sleep behaviors remarkably, as well as %tonic activity in PSG variables. In the present study, melatonin was reconfirmed to be effective in RBD symptoms, especially for patients with low melatonin secretion, while its mechanism was not clearly known in the present study.

Basal forebrain acetylcholine release during REM sleep is significantly greater than during waking

Abstract: Cholinergic neurons of the basal forebrain supply the neocortex with ACh and play a major role in regulating behavioral arousal and cortical electroencephalographic activation. Cortical ACh release is greatest during waking and rapid eye movement (REM) sleep and reduced during non-REM (NREM) sleep. Loss of basal forebrain cholinergic neurons contributes to sleep disruption and to the cognitive deficits of many neurological disorders. ACh release within the basal forebrain previously has not been quantified during sleep. This study used in vivo microdialysis to test the hypothesis that basal forebrain ACh release varies as a function of sleep and waking. Cats were trained to sleep in a head-stable position, and dialysis samples were collected during polygraphically defined states of waking, NREM sleep, and REM sleep. Results from 22 experiments in four animals demonstrated that means ± SE ACh release (pmol/10 min) was greatest during REM sleep (0.77 ± 0.07), intermediate during waking (0.58 ± 0.03), and lowest during NREM sleep (0.34 ± 0.01). The finding that, during REM sleep, basal forebrain ACh release is significantly elevated over waking levels suggests a differential role for basal forebrain ACh during REM sleep and waking.

Sleep-disordered breathing in stable methadone programme patients: a pilot study.

Abstract: Aims. To explore the possibility that stable MMP patients have sleep-disordered breathing (SDB) and abnormal sleep architecture defined by nocturnal sleep stages and sleep efficiency. Design. Observational. Setting. Regional Methadone Service and sleep disorders laboratory in a university affiliated hospital. Participants and measurements. Ten stable MMP patients and nine normal subjects were assessed clinically and with overnight polysomnography. Findings. There were no differences in age, sex and body mass index between the groups. The methadone dose ranged between 50 and 120 mg/day. Six patients had central apnoea index (CAI) greater than 5, four had a CAI greater than 10 and three of these exhibited periodic breathing. No normal subject had central sleep apnoea. The patients had lower sleep efficiency ( p < 0.05), less slow wave sleep ( p < 0.01), less rapid eye movement sleep ( p < 0.05) and more Stage 2 sleep ( p < 0.05) than controls. Conclusions. Stable MMP patients have more sleep architecture abnormalities than controls and a higher prevalence of central sleep apnoea. Further studies are needed to confirm these findings, to delineate the mechanisms for the abnormalities and to assess whether the SDB is related to sudden death in stable MMP patients. We recommend that MMP patients have awake and sleep respiration assessed to identify those potentially at risk.

Brain-mind states: I. Longitudinal field study of sleep/wake factors influencing mentation report length.

Abstract: Study objectives To collect and analyze reports of mental activity across sleep/wake states. Design Mentation reports were collected in a longitudinal design by combining our Nightcap sleep monitor with daytime experience sampling techniques. Reports were collected over 14 days and nights from active and quiet wake, after instrumental awakenings at sleep onset, and after both spontaneous and instrumental awakenings from REM and NREM sleep. Setting All reports were collected in the normal home, work and school environments of the subjects. Participants Subjects included 8 male and 8 female undergraduate students (19-26 years of age). Interventions N/A. Measurements and results A total of 1,748 reports, averaging 109 per subject, were collected from active wake across the day (n=894), from quiet wake in the pre-sleep onset period (n=58), from sleep onset (n=280), and from later REM (n=269) and nonREM (n=247) awakenings. Median report lengths varied more than 2-fold, in the order REM > active wake > quiet wake > NREM = sleep onset. The extended protocol allowed many novel comparisons between conditions. In addition, while spontaneous REM reports were longer than those from forced awakenings, the difference was explained by the time within the REM period at which the awakenings occurred. Finally, intersubject differences in REM report lengths were correlated with similar differences in waking report lengths. Conclusions The use of the Nightcap sleep monitoring system along with waking experience sampling permits a more complete sampling and analysis of mental activity across the sleep/wake cycle than has been previously possible.

A model of sleep-disordered breathing in the C57BL/6J mouse.

Abstract: To investigate the pathophysiological sequelae of sleep-disordered breathing (SDB), we have developed a mouse model in which hypoxia was induced during periods of sleep and was removed in response ...

Conditions that affect sleep alter the expression of molecules associated with synaptic plasticity.

Abstract: Many theories propose that sleep serves a purpose in synaptic plasticity. We tested the hypothesis, therefore, that manipulation of sleep would affect the expression of molecules known to be involved in synaptic plasticity. mRNA expression of four molecules [brain-derived neurotrophic factor (BDNF), activity-regulated cytoskeleton-associated protein (Arc), matrix metalloproteinase-9 (MMP-9), and tissue plasminogen activator (tPA)] was determined after 8 h of sleep deprivation and after 6 h of a mild increase in ambient temperature, a condition that enhances sleep in rats. After sleep deprivation, BDNF, Arc, and tPA mRNAs in the cerebral cortex increased while MMP-9 mRNA levels decreased. Conversely, after enhanced ambient temperature, BDNF, Arc, and tPA mRNAs decreased while MMP-9 mRNA increased. In the hippocampus, sleep deprivation did not significantly affect BDNF and tPA expression, although Arc mRNA increased and MMP-9 mRNA decreased. Brain temperature enhancement decreased Arc mRNA levels in the hippocampus but did not affect BDNF, MMP-9, or tPA in this area. Results are consistent with the notion that sleep plays a role in synaptic plasticity.

Restraint increases prolactin and REM sleep in C57BL/6J mice but not in BALB/cJ mice.

Abstract: Sleep is generally considered to be a recovery from prior wakefulness. The architecture of sleep not only depends on the duration of wakefulness but also on its quality in terms of specific experiences. In the present experiment, we studied the effects of restraint stress on sleep architecture and sleep electroencephalography (EEG) in different strains of mice (C57BL/6J and BALB/cJ). One objective was to determine if the rapid eye movement (REM) sleep-promoting effects of restraint stress previously reported for rats would also occur in mice. In addition, we examined whether the effects of restraint stress on sleep are different from effects of social defeat stress, which was found to have a non-REM (NREM) sleep-promoting effect. We further measured corticosterone and prolactin levels as possible mediators of restraint stress-induced changes in sleep. Adult male C57BL/6J and BALB/cJ mice were subjected to 1 h of restraint stress in the middle of the light phase. To control for possible effects of sleep loss per se, the animals were also kept awake for 1 h by gentle handling. Restraint stress resulted in a mild increase in NREM sleep compared with baseline, but, overall, this effect was not significantly different from sleep deprivation by gentle handling. In contrast, restraint stress caused a significant increase in REM sleep compared with handling in the C57BL/6J mice but not in BALB/cJ mice. Corticosterone levels were significantly and similarly elevated after restraint in both strains, but prolactin was increased only in the C57BL/6J mice. In conclusion, this study shows that the restraint stress-induced increase in REM sleep in mice is strongly strain dependent. The concomitant increases in prolactin and REM sleep in the C57BL/6J mice, but not in BALB/cJ mice, suggest prolactin may be involved in the mechanism underlying restraint stress-induced REM sleep. Furthermore, this study confirms that different stressors differentially affect NREM and REM sleep. Whereas restraint stress promotes REM sleep in C57BL/6J mice, we previously found that in the same strain, social defeat stress promotes NREM sleep. As such, studying the consequences of specific stressful stimuli may be an important tool to unravel both the mechanism and function of different sleep stages.

Low-flow oxygen and bilevel ventilatory support: effects on ventilation during sleep in cystic fibrosis.

Abstract: We measured ventilation in all sleep stages in patients with cystic fibrosis (CF) and moderate to severe lung disease, and compared the effects of low-flow oxygen (LFO 2 ) and bilevel ventilatory support (BVS) on ventilation and gas exchange during sleep. Thirteen subjects, age 26 6 5.9 yr (mean 6 1 SD), body mass index (BMI) 20 6 3 kg/m 2 , FEV 1 32 6 11% predicted, underwent three sleep studies breathing, in random order, room air (RA), LFO 2 , and BVS 6 O 2 with recording of oxyhemoglobin saturation (Sp O2 ) (%) and transcutaneous carbon dioxide (TcCO 2 ) (mm Hg). During RA and LFO 2 studies, patients wore a nasal mask with a baseline continuous positive airway pressure (CPAP) of 4 to 5 cm H 2 O. Minute ventilation ( I ) was measured using a pneumotachograph in the circuit and was not different between wake and non‐rapid eye movement (NREM) sleep on any night. However, I was reduced on the RA and LFO 2 nights from awake to rapid eye movement (REM) (p , 0.01) and from NREM to REM (p , 0.01). On the BVS night there was no significant difference in I between NREM and REM sleep. Both BVS and LFO 2 improved nocturnal Sp O2 , especially during REM sleep (p , 0.05). The rise in TcCO 2 seen with REM sleep with both RA and LFO 2 was attenuated with BVS (p , 0.05). We conclude that BVS leads to improvements in alveolar ventilation during sleep in this patient group. It is well known that patients with cystic fibrosis (CF) and advanced lung disease develop hypoxemia and hypercapnia during sleep, particularly during rapid eye movement (REM) sleep (1‐3). Hypoventilation has been proposed as a major mechanism for these blood gas changes, although no direct measurements of ventilation have been made in REM sleep. Hypoxemia and hypercapnia are poor prognostic signs in patients with CF (4, 5). Therefore, it is possible that preventing the onset of respiratory failure during sleep in CF may prolong survival in patients. Studies of nocturnal oxygen therapy in CF have confirmed improved oxyhemoglobin saturation (Sp O2 ) during sleep (6, 7), but usually with accompanying increases in arterial Pa CO2 (7, 8). Moreover, long-term oxygen in patients with CF has failed to show improved survival (9). A number of descriptive noncontrolled retrospective studies have described noninvasive ventilation in patients with CF as being effective in improving or stabilizing arterial blood gas (ABG) tensions and as a bridge to transplantation (10‐16). Gozal (8) showed that noninvasive ventilation was more effective than oxygen therV ·

The Mind in REM Sleep: Reports of Emotional Experience

Abstract: Study Objectives: No consensus has been reached on the characteristics of emotional experience during rapid eye movement sleep (REM). Thus, the relationship between the emotional brain activation and mental activity in REM remains unclear. Our objective is to characterize emotional experience in REM in order to facilitate understanding of brain-mind correlations in this state. Design: We combined instrumental awakenings from REM with the subjects' own ratings of the occurrence and intensity of discrete emotion types for each line in their REM mentation reports. Setting: The study was performed in the subjects' own homes over three consecutive nights using ambulatory polysomnography. Participants: Nine normal healthy subjects, age 31-60 (mean=43.0). Interventions: Awakenings 5-15 minutes into REM periods across the night. Measurements and Results: Emotions were found in 74% of 88 mentation reports, with a balanced proportion of positive and negative emotions. Among the reports scored for emotions, 14% contained one emotion and 86% contained two or more different emotion types. Joy/elation was the most frequent emotion, found in 36% of the reports, followed by surprise (24%), anger (17%), anxiety/fear (11%), and sadness (10%). Anxiety/fear was significantly less intense than joy/elation, anger, and surprise. Except for surprise, no specific emotion type changed from the first to the second half of the night. Negative emotions and surprise but not positive emotions varied significantly across subjects. Conclusions: The analysis of subject reports of emotions following instrumental awakenings demonstrate a balanced and widespread occurrence of both positive and negative emotions in REM sleep dreams. Emotions in REM are likely to be powerfully modulated by the neurobiological processes which differentiate REM from waking.

Anandamide-induced sleep is blocked by SR141716A, a CB1 receptor antagonist and by U73122, a phospholipase C inhibitor.

Abstract: Anandamide (ANA) alters sleep by increasing the amount of time spent in slow wave sleep 2 (SWS2) and rapid eye movement sleep (REMS) at the expense of wakefulness (W) in rats. In this report, we describe a similar effect of ANA when injected itracerebroventricularly (i.c.v.) or into the peduriculopontine tegmental nucleus (PPTg) and the lack of an effect when ANA is administered into the medial preoptic area (MPOA). Furthermore, the i.c.v. or PPTg administration of SR141716A, a CB1 antagonist, or U73122, a PLC inhibitor, 15 min prior to ANA, readily prevents the ANA induced changes in sleep. The present results suggest that a cannabinoid system in the PPTg may be involved in sleep regulation and that the cannabinoid effect is mediated by the CB1 receptor coupled to a PLC second messenger system.

Influence of fear conditioning on elicited ponto-geniculo-occipital waves and rapid eye movement sleep.

Abstract: The amygdala plays a central role in fear conditioning, a model of anticipatory anxiety. It has massive projections to brainstem regions involved in rapid eye movement sleep (REM) and ponto-geniculo-occipital (PGO) wave generation. PGO waves occur spontaneously in REM or in response to stimuli. Electrical stimulation of the central nucleus of the amygdala enhances spontaneous PGO wave activity during REM and the amplitude of both the acoustic startle response and the elicited PGO wave (PGOE), a neural marker of alerting. This study examined the effects of fear conditioning on REM and on PGOE. On conditioning days, the number of REM episodes, the average REM duration and the REM percentage were decreased while REM latency was increased. The presentation of auditory stimuli in the presence of a light conditioned stimulus produced PGOE of greater amplitudes. The results suggest that fear, most likely involving the amygdala, can influence REM and brainstem alerting mechanisms.