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At least 19 recordsLinked to original sources
PubMed1992

Antiserum to prolactin decreases rapid eye movement sleep (REM sleep) in the male rat.

Previous reports suggest that blood-born prolactin (PRL) may selectively promote rapid eye movement sleep (REMS). To study the possible involvement of endogenous PRL in sleep regulation, rats were systemically injected with either antiserum to PRL or normal rabbit serum, and the sleep-wake activity was determined during the subsequent 12-h light cycle. The administration of normal rabbit serum in physiological saline did not alter sleep-wake activity compared to control recordings, whereas the PRL antiserum caused a modest and selective suppression in REMS. Immunoreactive PRL was eliminated from the serial plasma samples obtained between 6 to 11 h after the injection of the antiserum. Brain temperature was not affected by the antiserum. The results indicate that physiological pituitary PRL secretion has a slight REMS-promoting activity in the male rat. It is speculated that an increased release of pituitary PRL or the PRL-like substance previously demonstrated in the brain may significantly stimulate REMS.

Animals↗
PubMedDate not supplied

Changes in EEG activity and hypothalamic temperature as indices for non-REM sleep to REM sleep transitions.

A shift of physiological regulations from a homeostatic to a non-homeostatic modality characterizes the passage from non-NREM sleep (NREMS) to REM sleep (REMS). In the rat, an EEG index which allows the automatic scoring of transitions from NREMS to REMS has been proposed: the NREMS to REMS transition indicator value, NIV [J.H. Benington et al., Sleep 17 (1994) 28-36]. However, such transitions are not always followed by a REMS episode, but are often followed by an awakening. In the present study, the relationship between changes in EEG activity and hypothalamic temperature (Thy), taken as an index of autonomic activity, was studied within a window consisting of the 60s which precedes a state change from a consolidated NREMS episode. Furthermore, the probability that a transition would lead to REMS or wake was analysed. The results showed that, within this time window, both a modified NIV (NIV(60)) and the difference between Thy at the limits of the window (Thy(D)) were related to the probability of REMS onset. Both the relationship between the indices and the probability of REMS onset was sigmoid, the latter of which saturated at a probability level around 50-60%. The efficacy for the prediction of successful transitions from NREMS to REMS found using Thy(D) as an index supports the view that such a transition is a dynamic process where the physiological risk to enter REMS is weighted at a central level.

Activity Cycles↗
PubMed1993

Symposium: Normal and abnormal REM sleep regulation: REM sleep in depression-an overview.

Abnormalities of REM sleep, i.e. shortening of REM latency, lengthening of the duration of the first REM period and heightening of REM density, which are frequently observed in patients with a major depressive disorder (MDD), have attracted considerable interest. Initial hopes that these aberrant patterns of sleep constitute specific markers for the primary/endogenous sub-type of depression have not been fulfilled. The specificity of REM sleep disinhibition for depression in comparison with other psychopathological groups is challenged as well. Demographic variables like age and sex exert strong influences on sleep physiology and must be controlled when searching for specific markers of depressed sleep. It is still an open question whether abnormalities of sleep are state- or trait-markers of depression. Beyond baseline studies, the cholinergic REM induction test (CRIT) indicated a heightened responsitivity of the REM sleep system to cholinergic challenge in depression compared with healthy controls and other psychopathological groups, with the exception of schizophrenia. A special role for REM sleep in depression is supported by the well-known REM sleep suppressing effect of most antidepressants. The antidepressant effect of selective REM deprivation by awakenings stresses the importance of mechanisms involved in REM sleep regulation for the understanding of the pathophysiology of depressive disorders. The positive effect of total sleep deprivation on depressive mood which can be reversed by daytime naps, furthermore emphasizes relationships between sleep and depression. Experimental evidence as described above instigated several theories like the REM deprivation hypothesis, the 2-process model and the reciprocal interaction model of nonREM-REM sleep regulation to explain the deviant sleep pattern of depression. The different models will be discussed with reference to empirical data gathered in the field.

Journal Article↗
PubMed1993

Symposium: Normal and abnormal REM sleep regulation: REM sleep in successful, usual, and pathological aging: the Pittsburgh experience 1980-1993.

Successful psychological and physical adaptation in late life correlates with preservation of sleep quality and physiological integrity of nocturnal EEG sleep measures. Failure to adapt is associated with loss of sleep continuity, alterations in the temporal distribution of delta wave activity, and by either a relative increase in REM sleep (e.g. in mood disorders) or a decrease in REM sleep (e.g. neurodegenerative disorders). Maintenance of sleep (particularly REM sleep) into late life may not be just a correlate, but also possibly a mechanism, of successful aging and thus necessary to the long-term maintenance of vitality and engagement in life.

Journal Article↗
PubMed1993

Symposium: Normal and abnormal REM sleep regulation: REM sleep behaviour disorder: an update on a series of 96 patients and a review of the world literature.

REM sleep behaviour disorder (RBD) is an injurious clinical disorder of attempted dream-enactment ('oneirism') in humans which has a corresponding experimental animal model involving dorsolateral pontine tegmental lesions in cats. To date, our sleep disorders centre has collected data on 96 chronic RBD cases which can be compared with pooled data on 70 chronic RBD cases from other centres contained in 26 reports published in the world literature since 1985, when our initial cases were first reported. The data from our centre and from other centres demonstrate a male predominance in RBD (87.5% vs 63.5%); indicate a similar mean age of RBD onset (52.4 y vs 55.9 y); contain substantial numbers of diverse central nervous system disorders causally associated with RBD (47.9% vs 60.0%); and identify clonazepam treatment as being very effective in controlling both the (violent) dream and sleep behavioural disturbances of RBD. Our centre's data additionally reveal an 80% prevalence of elevated stage 3/4 (slow-wave) sleep% for age in RBD, and reveal a frequent presence of periodic and aperiodic limb movements during NREM sleep. Thus, RBD in humans is a complex syndrome in which there is generalized REM and NREM sleep motor dyscontrol, as was originally observed in the animal RBD model by Jouvet and Delorme in 1965.

Journal Article↗
PubMed1982

Quipazine has a biphasic effect on slow wave sleep and reduces REM sleep rebound in REM sleep deprived rats.

Rats implanted with electrodes for polygraphic recording were deprived of REM sleep for 24 hr. Following REM sleep deprivation animals were injected with quipazine maleate (7.5 mg/kg IP) and were polygraphically recorded for 48 hr. The results show that quipazine reduces REM sleep rebound and that it has a biphasic effect on slow-wave sleep: initial 6 hr suppression is followed by a delayed increase in the second 24 hr recording period. The initial suppression of slow-wave sleep we attribute to the stimulation of central serotonergic receptors while the effect on REM sleep rebound may result from quipazine's action on central catecholamines.

Animals↗
PubMed2000

Peculiar respiratory response observed during sleep-onset REM sleep of an infant with Ondine's curse.

We treated an infant with congenital central hypoventilation syndrome ("Ondine's curse"). She was cyanotic and given ventilatory support at the first hour after birth. An investigation of sleep state and respiration performed at the age of 3 months led to this diagnosis. Hypoventilation persisted in all sleep stages, with the most severely reduced tidal volumes occurring during delta-wave sleep (stages 3 and 4). In addition, severe secondary reduction in tidal volumes occurred in sleep-onset REM sleep. This phenomenon was absent in non sleep-onset REM sleep. At 4 months of age, her respiratory treatment was successfully converted to positive-pressure ventilation via a nasal mask, thus avoiding tracheotomy. This transition to noninvasive ventilatory support dramatically improved her quality of life during wakefulness. This report may be a clue to discuss the function of sleep-onset REM sleep seen in the early stage of life and suggests that nasal mask ventilation is a viable option in selected cases with congenital central hypoventilation syndrome (CCHS).

Female↗
PubMed2006

The effect of donepezil on sleep and REM sleep EEG in patients with Alzheimer disease: a double-blind placebo-controlled study.

STUDY OBJECTIVE: Examine the effects of donepezil on sleep and rapid eye movement (REM) sleep electroencephalogram (EEG) in patients with Alzheimer disease, using polysomnography, and the correlation between REM sleep EEG parameters and cognitive scores. DESIGN: Randomized, double-blind, placebo-controlled design. SETTINGS: Two sleep research centers, University Hospital. PARTICIPANTS: Thirty-five patients with mild to moderate Alzheimer disease, allocated to 2 groups: donepezil treated (n=17) and placebo treated (n=18). INTERVENTION: Patients were administered donepezil or placebo. OUTCOME MEASURES: Polysomnography with REM sleep EEG spectral analysis and cognitive evaluation using the Alzheimer Disease Assessment Scale, cognitive subscale, were performed at baseline and after 3 and 6 months. Slowing ratio was the ratio between slow and fast EEG frequency bands. Cognitive and sleep data were analyzed using analysis of variance. Correlations between cognitive improvement and REM sleep EEG were also calculated. RESULTS: REM sleep increased significantly after 3 and 6 months of donepezil treatment compared with baseline and placebo (p < .01). Overall theta (p = .04), frontal theta (p < .01) and frontal delta (p = .03) absolute power during REM sleep decreased after 6 months of donepezil treatment. The occipital slowing ratio decreased during treatment (p = .04). REM sleep overall and frontal and centroparietal alpha absolute power significantly correlated with the cognitive improvement rate on the Alzheimer Disease Assessment Scale, cognitive subscale (r = 0.75, r = 0.71, r = 0.78); p < .01). CONCLUSIONS: Donepezil treatment enhanced REM sleep and reduced slow frequencies of REM sleep EEG, suggesting a possible action upon REM sleep-related cholinergic neurons in patients with Alzheimer disease. Furthermore, REM sleep alpha power may predict the cognitive response to donepezil.

Aged↗
PubMed1996

Excitatory drive to the respiratory system in REM sleep.

REM sleep is sometimes divided into tonic and phasic stages. Tonic REM sleep processes are both excitatory and inhibitory to the respiratory system. Inhibitory effects arise from the atonic processes of the REM state and include atonia of thoracoabdominal and extrathoracic airway muscles. Excitatory effects include increases in respiratory rate, central respiratory drive and rate of rise of diaphragmatic activity. The combination of these varying antagonistic effects determines the level of ventilation.

Brain Stem↗
PubMed1983

The time course of slow wave sleep and REM sleep in habitual long and short sleepers: effect of prior wakefulness.

Three groups of young good sleepers were selected according to their habitual sleep length as short (SS), regular (RS), or long (LS) sleepers. Their sleep was recorded in three situations: reference nights, a recovery sleep night after 36 h of sleep deprivation, and a sleep night after a morning sleep recovery from sleep deprivation (12 h waking time). Total and cycle-by-cycle amounts of slow wave sleep (SWS) and REM sleep were studied both as a function of experimental conditions and of the group of subjects. In all three conditions, LS had less SWS than other sleepers while the differences in SWS amounts between groups were mainly due to different amounts in the second and third cycles, differences between conditions essentially due to variations of SWS within sleep cycle 1 (SWS1). SWS1 appeared to reflect some physiological process whose level increases during waking and declines during sleep. REM sleep proved to be proportional to sleep length.

Adult↗
PubMed2000

Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men.

CONTEXT: In young adults, sleep affects the regulation of growth hormone (GH) and cortisol. The relationship between decreased sleep quality in older adults and age-related changes in the regulation of GH and cortisol is unknown. OBJECTIVE: To determine the chronology of age-related changes in sleep duration and quality (sleep stages) in healthy men and whether concomitant alterations occur in GH and cortisol levels. DESIGN AND SETTING: Data combined from a series of studies conducted between 1985 and 1999 at 4 laboratories. SUBJECTS: A total of 149 healthy men, aged 16 to 83 years, with a mean (SD) body mass index of 24.1 (2.3) kg/m( 2), without sleep complaints or histories of endocrine, psychiatric, or sleep disorders. MAIN OUTCOME MEASURES: Twenty-four-hour profiles of plasma GH and cortisol levels and polygraphic sleep recordings. RESULTS: The mean (SEM) percentage of deep slow wave sleep decreased from 18.9% (1.3%) during early adulthood (age 16-25 years) to 3.4% (1.0%) during midlife (age 36-50 years) and was replaced by lighter sleep (stages 1 and 2) without significant increases in sleep fragmentation or decreases in rapid eye movement (REM) sleep. The transition from midlife to late life (age 71-83 years) involved no further significant decrease in slow wave sleep but an increase in time awake of 28 minutes per decade at the expense of decreases in both light non-REM sleep (-24 minutes per decade; P<.001) and REM sleep (-10 minutes per decade; P<.001). The decline in slow wave sleep from early adulthood to midlife was paralleled by a major decline in GH secretion (-372 microg per decade; P<.001). From midlife to late life, GH secretion further declined at a slower rate (-43 microg per decade; P<.02). Independently of age, the amount of GH secretion was significantly associated with slow wave sleep (P<.001). Increasing age was associated with an elevation of evening cortisol levels (+19. 3 nmol/L per decade; P<.001) that became significant only after age 50 years, when sleep became more fragmented and REM sleep declined. A trend for an association between lower amounts of REM sleep and higher evening cortisol concentrations independent of age was detected (P<.10). CONCLUSIONS: In men, age-related changes in slow wave sleep and REM sleep occur with markedly different chronologies and are each associated with specific hormonal alterations. Future studies should evaluate whether strategies to enhance sleep quality may have beneficial hormonal effects. JAMA. 2000;284:861-868

Adolescent↗
PubMed2001

Relationship between Delta, Sigma, Beta, and Gamma EEG bands at REM sleep onset and REM sleep end.

OBJECTIVE: The aim of the present study was to analyze in detail the relationship of two newly introduced measures, related to the Beta and Gamma EEG bands during REM sleep, with Delta and Sigma activity at REM sleep onset and REM sleep end, in order to understand their eventual role in the sleep modulation mechanism. METHODS: For this purpose, power spectra of 1 EEG channel (C4, referred to A1) were obtained by means of the fast Fourier transform and the power of the bands ranging 0.75-4.50 Hz (Delta), 4.75-7.75 (Theta), 8.00-12.25 (Alpha), 12.50-15.00 (Sigma), 15.25-24.75 (Beta), 25.00-34.75 (Gamma 1), and 35.00-44.75 (Gamma 2) was calculated for the whole period of analysis (7 h), in 10 healthy subjects. Additionally, two other time series were calculated: the ratio between Beta and Gamma2, and between Gamma1 and Gamma2 (Beta and Gamma ratios). For each subject, we extracted 3 epochs of 30 min corresponding to the 15 min preceding and the 15 min following the onset of the first 3 REM episodes. Data were then averaged in order to obtain group mean values and standard deviation. The same process was applied to the 30-min epochs around REM sleep end. RESULTS: The course of the Delta band around REM sleep onset was found to be characterized by a first phase of slow decline lasting from the beginning of our window up to a few seconds before REM onset; this phase was followed by a sudden, short decrease centered around REM onset, lasting for approximately 1.5-2 min. At the end of this phase, the Delta band reached its lowest values and remained stable up to the end of the time window. The Sigma band showed a similar course with stable values before and after REM sleep onset. The Beta and Gamma ratios also showed a 3-phase course; the first phase, in this case, was characterized by stable low values, from the beginning of our window up to approximately 5 min before REM onset. The following second phase was characterized by an increase which reached its maximum shortly after REM sleep onset (approximately 1 min). In the last phase, both Beta and Gamma ratios showed stable high values, up to the end of our time window. At REM sleep end, the Delta band only showed a very small gradual increase, the Sigma band presented a more evident gradual increase; on the contrary, both Beta and Gamma ratios showed a small gradual decrease. CONCLUSIONS: The results of the present study show a different time synchronization of the changes in the Delta band and in Beta and Gamma ratios, at around REM sleep onset, and seem to suggest that the oscillations of these parameters might be modulated by mechanisms more complex than a simple reciprocity. All these considerations point to the fact that REM sleep can be considered as a complex phenomenon and the analysis of high-frequency EEG bands and of our Beta and Gamma ratios represent an additional important element to include in the study of this sleep stage.

Adult↗
PubMed2001

Intrinsic dreams are not produced without REM sleep mechanisms: evidence through elicitation of sleep onset REM periods.

The hypothesis that there is a strict relationship between dreams and a specific rapid eye movement (REM) sleep mechanism is controversial. Many researchers have recently denied this relationship, yet none of their studies have simultaneously controlled both sleep length and depth prior to non-REM (NREM) and REM sleep awakenings, due to the natural rigid order of the NREM--REM sleep cycle. The failure to control sleep length and depth prior to arousal has confounded interpretations of the REM-dreams relationship. We have hypothesised that different physiological mechanisms underlie dreaming during REM and NREM sleep, based on recent findings concerning the specificity of REM sleep for cognitive function. Using the Sleep Interruption Technique, we elicited sleep onset REM periods (SOREMP) from 13 normal subjects to collect SOREMP and sleep onset NREM (NREMP) dreams without the confounds described above. Regression analyses showed that SOREMP dream occurrences were significantly related to the amount of REM sleep, while NREMP dream occurrences were related to arousals from NREM sleep. Dream properties evaluated using the Dream Property Scale showed qualitative differences between SOREMP and NREMP dream reports. These results support our hypothesis and we have concluded that although 'dreaming' may occur during both REM and NREM periods as previous researchers have suggested, the dreams obtained from these distinct periods differ significantly in their quantitative and qualitative aspects and are likely to be produced by different mechanisms.

Adolescent↗
PubMedDate not supplied

Posttraining increases in REM sleep intensity implicate REM sleep in memory processing and provide a biological marker of learning potential.

Posttraining rapid eye movement (REM) sleep has been reported to be important for efficient memory consolidation. The present results demonstrate increases in the intensity of REM sleep during the night of sleep following cognitive procedural/implicit task acquisition. These REM increases manifest as increases in total number of rapid eye movements (REMs) and REM densities, whereas the actual time spent in REM sleep did not change. Further, the participants with the higher intelligence (IQ) scores showed superior task acquisition scores as well as larger posttraining increases in number of REMs and REM density. No other sleep state changes were observed. None of the pretraining baseline measures of REM sleep were correlated with either measured IQ or task performance. Posttraining increases in REM sleep intensity implicate REM sleep mechanisms in further off-line memory processing, and provide a biological marker of learning potential.

Adult↗
PubMed1982

Thermoregulatory adjustments to thermal transients during slow wave sleep and REM sleep in man.

The present study was performed on five nude male subjects by increasing the ambient temperature during well-established slow wave sleep (SWS) and rapid eye movement (REM) sleep episodes. 1. Air temperature was raised from 25 to 41 degrees C at rates of + 0.8 degrees C.min-1 or + 1.6 degrees C min-1 and, afterwards, was maintained at 41 degrees C during 10 min before returning to the initial pre-heating condition. During these thermal transients, wall temperatures (Tw), dew-point temperature (Tdp) and air velocity (Va) were kept constant (Tw = 37.5 degrees C; Tdp = 10 degrees C; Va = 0.3 m.s.-1). Physiological data included 3 EEGs, 2 EOGs, 4 EMGs, heart rate, finger pulse amplitude, esophageal temperature and 10 local skin temperatures. Upper chest sweating rate was recorded by a 12 cm2-capsule using a dew-point hygrometer technique. 2. The results showed that during REM sleep sweat gland activity persists at a lower level than during SWS. The lower sensitivity of the thermoregulatory system described during the REM sleep episodes could be interpreted by an increase of the hypothalamic set-point temperature, or by an action of extra-hypothalamic thermosensitive neurons. However, a change at the sweat gland level cannot be ruled out.

Adult↗
PubMed1994

Does the function of REM sleep concern non-REM sleep or waking?

We have hypothesized that REM sleep is functionally and homeostatically related to NREM sleep rather than to waking. In other words, REM sleep rather than to waking. In other words, REM sleep occurs in response to NREM-sleep expression and compensates for some process that takes place during NREM sleep. Under normal conditions, the need for REM sleep does not accrue during waking. The primary basis for this hypothesis is the fact that REM-sleep expression is a function of prior NREM-sleep expression. That is, REM sleep follows NREM sleep within sleep periods, REM-sleep episodes occur at intervals determined by the amount of NREM-sleep time elapsed, and total time spent in REM sleep is consistently about 1/4 of prior NREM-sleep time, regardless of how much time is spent in NREM sleep. Our experimental tests of the hypothesis support it. (1) REM-sleep propensity accumulates quite rapidly during a 2-hr interval spent predominantly in NREM sleep. (2) The timing of individual REM-sleep episodes is controlled homeostatically, by accumulation within NREM sleep of a propensity for REM sleep. The NREM sleep-related model of REM-sleep regulation (Fig. 1) explains a number of phenomena of REM-sleep expression, including the frequent and periodic occurrence of REM-sleep episodes throughout sleep periods, that have been accommodated by the waking-related model but are not functionally accounted for by it. In our opinion, the NREM sleep-related model of REM-sleep regulation recommends itself partly by its simplicity. According to the waking-related model, two independent and competing sleep propensities accumulate during waking and are discharged in two distinct sleep states that perform different waking-related recovery processes. One behaviour, sleep, is thought to perform two independent and competing functions that alternate at regular intervals. In the NREM sleep-related model of REM-sleep regulation, sleep debt simply reflects a need for NREM sleep. That is, the cerebrally less activated state of NREM sleep enables some form of restoration made necessary by the cerebrally activated state of waking. Periodic occurrence of REM-sleep episodes is explained without postulating an oscillatory mechanism to gate expression of NREM sleep versus REM sleep. In assessing the comparative merits of the waking-related and NREM sleep-related models of REM-sleep regulation, one should consider the influence of time-worn habits of thought.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗