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Showing papers on "Rapid eye movement sleep published in 1996"


Journal ArticleDOI
12 Sep 1996-Nature
TL;DR: A group study of seven subjects who maintained steady REM sleep during brain scanning and recalled dreams upon awakening shows that regional cerebral blood flow is positively correlated with REM sleep in pontine tegmentum, left thalamus, both amygdaloid complexes, anterior cingulate cortex and right parietal operculum.
Abstract: RAPID-EYE-MOVEMENT (REM) sleep is associated with intense neuronal activity, ocular saccades, muscular atonia and dreaming1,2. The function of REM sleep remains elusive and its neural correlates have not been characterized precisely in man. Here we use positron emission tomography and statistical parametric mapping to study the brain state associated with REM sleep in humans. We report a group study of seven subjects who maintained steady REM sleep during brain scanning and recalled dreams upon awakening. The results show that regional cerebral blood flow is positively correlated with REM sleep in pontine tegmentum, left thalamus, both amygdaloid complexes, anterior cingulate cortex and right parietal operculum. Negative correlations between regional cerebral blood flow and REM sleep are observed bilaterally, in a vast area of dorsolateral prefrontal cortex, in parietal cortex (supramarginal gyrus) as well as in posterior cingulate cortex and precuneus. Given the role of the amygdaloid complexes in the acquisition of emotionally influenced memories, the pattern of activation in the amygdala and the cortical areas provides a biological basis for the processing of some types of memory during REM sleep.

1,080 citations


Journal ArticleDOI
16 May 1996-Nature
TL;DR: Administration of cortistatin depresses neuronal electrical activity but, unlike somatostatin, induces low-frequency waves in the cerebral cortex and antagonizes the effects of acetylcholine on hippocampal and cortical measures of excitability, which suggests a mechanism for cortical synchronization related to sleep.
Abstract: ACETYLCHOLINE (ACh) plays a key role in the transitions between the different phases of sleep1: Slow-wave sleep requires low ACh concentrations in the brain, whereas rapid-eye-movement (REM) sleep is associated with high levels of ACh. Also, these phases of sleep are differentially sensitive to a number of endogenous neuropeptides and cytokines, including somatostatin, which has been shown to increase REM sleep without significantly affecting other phases2. Here we report the cloning and initial characterization of cortistatin, a neuropeptide that exhibits strong structural similarity to somatostatin, although it is the product of a different gene. Administration of cortistatin depresses neuronal electrical activity but, unlike somatostatin, induces low-frequency waves in the cerebral cortex and antagonizes the effects of acetylcholine on hippocampal and cortical measures of excitability. This suggests a mechanism for cortical synchronization related to sleep.

400 citations


Journal ArticleDOI
TL;DR: The three states of mammalian being--wakefulness, REM sleep, and NREM sleep--are not mutually exclusive and may occur simultaneously, oscillate rapidly, or appear in dissociated or incomplete form to produce primary sleep parasomnias.

306 citations


Journal ArticleDOI
TL;DR: The data show that in healthy young women, sleep spindle frequency activity varies in parallel with core body temperature, whereas homeostatic sleep regulatory mechanisms, as indexed by the time course of EEG slow wave activity are not substantially affected by the menstrual cycle.
Abstract: Cyclic changes in hormones, body temperature, and metabolic rate characterize the menstrual cycle. To investigate whether these changes are associated with changes in sleep and the sleep electroencephalogram (EEG), a total of 138 sleep episodes from 9 women with no premenstrual syndrome symptoms were recorded every second night throughout one ovulatory menstrual cycle and analyzed in relation to menstrual phase. Ovulation and menstrual cycle stage were confirmed by measurements of temperature, urinary LH, and midluteal plasma levels of estrogen and progesterone. No significant variation across the menstrual cycle was observed for subjective ratings of sleep quality and mood as well as for objective measures of total sleep time, sleep efficiency, sleep latency, rapid eye movement sleep latency, and slow wave sleep. In nonrapid eye movement sleep, EEG power density in the 14.25-15.0 hertz band, which corresponds to the upper frequency range of the sleep spindles, exhibited a large variation across the menstrual cycle, with a maximum in the luteal phase. The data show that in healthy young women, sleep spindle frequency activity varies in parallel with core body temperature, whereas homeostatic sleep regulatory mechanisms, as indexed by the time course of EEG slow wave activity are not substantially affected by the menstrual cycle.

276 citations


Journal ArticleDOI
TL;DR: In this article, the influence of pulsed high-frequency electromagnetic fields of digital mobile radio telephones on sleep in healthy humans was investigated and a hypnotic effect with shortening of sleep onset latency, a REM suppressive effect with reduction of duration and percentage of REM sleep was found.
Abstract: In the present study we investigated the influence of pulsed high-frequency electromagnetic fields of digital mobile radio telephones on sleep in healthy humans. Besides a hypnotic effect with shortening of sleep onset latency, a REM suppressive effect with reduction of duration and percentage of REM sleep was found. Moreover, spectral analysis revealed qualitative alterations of the EEG signal during REM sleep with an increased spectral power density. Knowing the relevance of REM sleep for adequate information processing in the brain, especially concerning mnestic functions and learning processes, the results emphasize the necessity to carry out further investigations on the interaction of this type of electromagnetic fields and the human organism.

254 citations


Journal ArticleDOI
TL;DR: It is concluded that homeostatic mechanisms can largely account for the dynamics of the sleep EEG under conditions of reduced sleep pressure.
Abstract: Increasing sleep pressure is associated with highly predictable changes in the dynamics of the sleep electroencephalogram (EEG). To investigate whether the effects of reduced sleep pressure also can be accounted for by homeostatic mechanisms, nighttime sleep following an evening nap was recorded in healthy young men. In comparison with the baseline night, sleep latency in the postnap night was prolonged, rapid eye movement sleep (REMS) latency was reduced, and EEG power density in non-REMS was decreased in the delta and theta band. The buildup of both EEG slow-wave activity (SWA; power density in the 0.75-to 4.5-Hz range) and spindle frequency activity (SFA; power density in the 12.25-to 15.0-Hz range) in non-REMS episodes was diminished (SWA: episodes 1-3; SFA: episode 1). The typical declining trend of SWA over consecutive non-REM sleep episodes was attenuated. The time course of SWA could be closely simulated with a homeostatic model of sleep regulation, although some discrepancies in level and buildup of SWA were apparent. We conclude that homeostatic mechanisms can largely account for the dynamics of the sleep EEG under conditions of reduced sleep pressure.

224 citations


Journal ArticleDOI
TL;DR: Meta-analytical techniques used to re-examine the effects of exercise on sleep and examine possible moderators of these effects indicated that acute and chronic exercise increased slow wave sleep and total sleep time but decreased sleep onset latency and REM sleep.
Abstract: Studies attempting to ascertain the effects of acute and chronic exercise on measures of sleep have yielded conflicting results and interpretations. Methodological differences among studies may explain this lack of consensus; however, small sample sizes and subsequently low statistical power may also have contributed. In an attempt to resolve these issues, this review used meta-analytical techniques to: (a) re-examine the effects of exercise on sleep; and (b) examine possible moderators of these effects. Studies meeting the selection criteria were included in the analysis. Analyses of moderating factors were performed for stage 4 sleep and rapid eye movement (REM) sleep. The results indicated that acute and chronic exercise increased slow wave sleep (SWS) and total sleep time but decreased sleep onset latency and REM sleep. Moderating variables influencing the magnitude and direction of these effects were related to characteristics of the individual (e.g. sex, age, fitness level) and the exercise (e.g. time of day exercise was completed, type of exercise, exercise duration). Mechanisms which have been suggested to explain the relationship between exercise and sleep are discussed and directions for further research are provided.

222 citations


Journal ArticleDOI
Carlyle Smith1
TL;DR: It is proposed that accelerated neural plasticity takes place during elevated post-training PS and is especially vulnerable to disruption at specific post- training time periods called PS windows.

212 citations


Journal ArticleDOI
TL;DR: The data on REM sleep provide the first biochemically validated and direct evidence that suppression of DRN serotonergic activity increases REM sleep, and furnish a key complement to the laboratory's in vitro data indicating that mesopontine cholinergic neurons, a target ofDRN projections, are inhibited by 5-HT.
Abstract: In vivo microdialysis was used to analyze the role of dorsal raphe nucleus (DRN) neurons in regulating the sleep-waking cycle. Measurements of extracellular serotonin (5-HT) were made in the DRN of freely moving adult cats before and during microdialysis perfusion of 8- hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a selective 5-HT1A receptor agonist, in artificial CSF. Behavioral state alterations were measured by simultaneous polygraphic recordings. During waking and artificial CSF perfusion of probes histologically localized to the DRN, extracellular 5-HT was 4 fmol/7.5 micro L dialysate sample. With the addition of 8-OH-DPAT (10 microM in artificial CSF) to the perfusate, 5- HT levels in the same state decreased 50%, to 2 fmol/sample (p < 0.01), presumably through 5-HT1A autoreceptor-mediated inhibition of serotonergic neural activity. Concomitantly, this 8-OH-DPAT perfusion produced a short latency, threefold increase in rapid eye movement (REM) sleep, from 10 to 30% of the total recorded time (p < 0.05), whereas waking was not significantly affected. In contrast, and suggesting DRN specificity, 8-OH-DPAT delivery through a probe in the aqueduct did not increase REM sleep but rather tended to increase waking and decrease slow wave sleep. The data on REM sleep provide the first biochemically validated and direct evidence that suppression of DRN serotonergic activity increases REM sleep, and furnish a key complement to our laboratory's in vitro data indicating that mesopontine cholinergic neurons, a target of DRN projections, are inhibited by 5-HT. The 8-OH-DPAT-induced reduction of DRN 5-HT is consistent with the hypothesis that the concomitant REM sleep disinhibition is mediated by DRN serotonergic projections to mesopontine cholinergic neurons, which other data implicate in REM sleep production.

187 citations


Journal ArticleDOI
TL;DR: The results indicate that short sleepers live under a higher "non-REM sleep pressure" than long sleepers, however, the two groups do not differ with respect to the homeostatic sleep regulatory mechanisms.
Abstract: Homeostatic sleep regulation in habitual short sleepers (sleep episode 9 h, n = 7) was investigated by studying their sleep structure and sleep electroencephalogr...

184 citations


Journal ArticleDOI
TL;DR: The effects of progesterone on sleep closely resemble those of agonistic modulators of GABAA receptors such as benzodiazepines and correlate well with the increases in the levels of its GAB AA agonistic metabolites.
Abstract: There is much evidence that progesterone has hypnotic anesthetic properties. In this vehicle-controlled study, we examined the effects of three doses of progesterone (30, 90, and 180 mg/kg) administered intraperitoneally at light onset on sleep in rats. Progesterone dose dependently shortened non-rapid eye movement sleep (NREMS) latency, lengthened rapid eye movement sleep (REMS) latency, decreased the amount of wakefulness and REMS, and markedly increased pre-REMS, an intermediate state between NREMS and REMS. Progesterone also elicited dose-related changes in sleep state-specific electroencephalogram (EEG) power densities. Within NREMS, EEG activity was reduced in the lower frequencies (< or = 7 Hz) and was enhanced in the higher frequencies. Within REMS, EEG activity was markedly enhanced in the higher frequencies. The effects were maximal during the first postinjection hours. The concentrations of progesterone and the progesterone metabolites 3 alpha-hydroxy-5 alpha-pregnan-20-one and 3 alpha-hydroxy-5 beta-pregnan-20-one, both positive allosteric modulators of gamma-aminobutyric acid A (GABAA) receptors, were determined at different time intervals after vehicle and 30 or 90 mg/kg progesterone. Progesterone administration resulted in dose-dependent initially supraphysiological elevations of progesterone and its metabolites in the plasma and brain, which were most prominent during the first hour postinjection. The effects of progesterone on sleep closely resemble those of agonistic modulators of GABAA receptors such as benzodiazepines and correlate well with the increases in the levels of its GABAA agonistic metabolites. These observations suggest that the hypnotic effects of progesterone are mediated by the facilitating action of its neuroactive metabolites on GABAA receptor functioning.


Journal ArticleDOI
TL;DR: The present study suggests that an endogenous cannabinoid-like system is involved in the control of the sleep-waking cycle and demonstrates that the EEG effects of SR 141716A reflect arousal-enhancing properties.

Journal ArticleDOI
TL;DR: It was concluded that inactivation of ventrolateral periaqueductal gray neurons induces a very important increase in paradoxical sleep.

Journal ArticleDOI
TL;DR: Three patients are presented here whose RBD preceded the onset of PD by several years, and both the symptoms of PD and RBD improved with levodopa treatment, and it remains to be seen whetherlevodopa can be an alternative to clonazepam in idiopathic RBD without PD.
Abstract: Rapid eye movement (REM) sleep behavior disorder (RBD) involves complex behavior and a loss of muscle atonia occurring during REM sleep. Half of these patients with RBD have an underlying neurologic disorder including dementia, olivopontocerebellar atrophy, subarachnoid hemorrhage, and cerebrovascular disease. Clonazepam is the drug of choice for RBD. RBD has been rarely reported to precede the onset of Parkinson's disease (PD). Three patients are presented here whose RBD preceded the onset of PD by several years, and both the symptoms of PD and RBD improved with levodopa treatment. It is postulated that levodopa ameliorates RBD by suppressing REM sleep, and it remains to be seen whether levodopa can be an alternative to clonazepam in idiopathic RBD without PD.

Journal ArticleDOI
TL;DR: The chronic effects of antidepressant drugs (ADs) on circadian rhythms of behavior, physiology and endocrinology are reviewed and the effects of ADs on the coupling of the central circadian pacemaker to photic and nonphotic zeitgebers are discussed.

Journal ArticleDOI
TL;DR: The circadian distribution of ictal and interictal events and the means by which the neural generators of these seizure-prone vs. seizure-resistant sleep and arousal states modulate the timing of different seizure manifestations are described.
Abstract: This review article: (1) describes the circadian distribution of ictal and interictal events; (2) differentiates transitional arousal, non-rapid eye movement and rapid eye movement sleep components and their substrates; (3) suggests the means by which the neural generators of these seizure-prone vs. seizure-resistant sleep and arousal states modulate the timing of different seizure manifestations; (4) considers clinical and mechanistic findings for the reciprocal effects of seizures and antiepileptic drugs upon the sleep-wake cycle; and (5) assesses clinical and basic mechanisms of sleep deprivation effects upon seizures.

Journal ArticleDOI
TL;DR: The hypothesis that GABA release in the posterior hypothalamus mediates inhibition of posterior hypothalamic neurons, thereby facilitating slow-wave sleep (SWS) is supported.
Abstract: The activity of neurons in the posterior hypothalamus (PH) is thought to contribute to the production of wakefulness and electroencephalograph desynchronization. Inactivation of neuronal activity in this area is known to induce sleep. Most PH neurons decrease unit discharge during slow-wave sleep (SWS) relative to wake and rapid eye movement sleep. In the present study, we sought to examine potential sources of inhibition or disfacilitation underlying the reduction of PH unit activity during SWS in the cat. We employed the microdialysis technique in conjunction with high-performance liquid chromatography methods for the quantification of glutamate, glycine, and gamma-aminobutyric acid (GABA) release. We found a selective increase in GABA release during SWS in the PH. Glutamate and glycine levels were unchanged across the sleep-wake cycle. microinjection of the GABAA-receptor agonist muscimol, into the same areas from which microdialysis samples were collected, increased SWS time. Our studies support the hypothesis that GABA release in the posterior hypothalamus mediates inhibition of posterior hypothalamic neurons, thereby facilitating SWS.

Journal ArticleDOI
TL;DR: It is concluded that in contrast to typical SSRIs, nefazodone administration has little effect on sleep architecture in healthy volunteers.
Abstract: We studied the effect of acute (1 day) and subacute (16 days) administration of the new antidepressant, nefazodone (400 mg daily), and the selective serotonin re-uptake inhibitor (SSRI), paroxetine (30 mg daily), on the sleep polysomnogram of 37 healthy volunteers using a random allocation, double-blind, placebo-controlled design. Compared to placebo, paroxetine lowered rapid eye movement (REM) sleep and increased REM latency. In addition, paroxetine increased awakenings and reduced Actual Sleep Time and Sleep Efficiency. In contrast, nefazodone did not alter REM sleep and had little effect on measures of sleep continuity. We conclude that in contrast to typical SSRIs, nefazodone administration has little effect on sleep architecture in healthy volunteers.

Journal ArticleDOI
TL;DR: Forebrain structures may be functionally briefly disconnected from the brain-stem during this short-lasting stage of paradoxical sleep, which could possibly account for the mental content of a similar sleep period in humans.

Journal ArticleDOI
01 Jul 1996-Sleep
TL;DR: This study shows that only 36% of patients had normal results in all traditional autonomic tests during wakefulness, and RBD patients had a reduced tonic and phasic heart rate variability during sleep.
Abstract: In REM sleep behavior disorder (RBD) it has been reported that tachycardia may not accompany the impressive movements associated with dream mentation. Up to now there are no data concerning the cardiac autonomic activity during wakefulness as well as during sleep out of nocturnal dream-enacting behaviors, in RBD. We evaluated 14 RBD patients. Our study shows that only 36% of patients had normal results in all traditional autonomic tests during wakefulness. Moreover, RBD patients had a reduced tonic and phasic heart rate variability during sleep. Autonomic evaluation during sleep may show impairment earlier than the traditional tests during wakefulness. No difference was found between idiopathic RBD patients and symptomatic ones.

Journal ArticleDOI
01 Nov 1996-Sleep
TL;DR: Although it is possible that these findings are early signs of narcolepsy, subjects reported being free of any sleep-related complaints, further investigations into the determinants of multiple SOREMPs and their reliability among asymptomatic populations are warranted.
Abstract: The multiple sleep latency test (MSLT) is a valuable tool in the assessment of excessive daytime sleepiness (EDS). Additionally, multiple sleep onset rapid eye movement periods (SOREMPs) are a frequent occurrence in patients with narcolepsy. To date, however, few studies have evaluated the frequency of SOREMPs in a population of healthy control subjects. Subjects participating in a variety of sleep studies were screened with a nocturnal clinical polysomnogram, followed by the MSLT. Subjects were required to be drug free and have no sleep-related symptoms or medical or psychiatric conditions. Of the 139 subjects who were screened, 24 (17%) had two or more SOREMPs. These individuals were more likely to be male, younger, and sleepier than those with one or zero SOREMPs. The etiology of two or more SOREMPs in healthy controls was not apparent from the clinical or polysomnographic evaluation. Although it is possible that these findings are early signs of narcolepsy, subjects reported being free of any sleep-related complaints. Further investigations into the determinants of multiple SOREMPs and their reliability among asymptomatic populations are warranted.

Journal ArticleDOI
TL;DR: This study, the first to the authors' knowledge to use low-amplitude stimulation of LDT in freely moving cats, indicates the importance of mesopontine cholinergic neurons in REM sleep.

Journal ArticleDOI
TL;DR: The results of this study suggest that the stimulated area (LC) affects REMS, most likely by suppression of REMS generation process.

Journal ArticleDOI
TL;DR: It is suggested that the effects of BP 2.94 or carboperamide on sleep and waking could depend on changes in the availability of histamine at the postsynaptic H1 receptor, which would secondarily result in changes of sleep variables.

Journal ArticleDOI
TL;DR: It is concluded that cholinergic activation of the central amygdaloid nucleus produces a long-term facilitation of REM sleep occurrence.
Abstract: The effect on sleep organization of carbachol microinjected into different amygdaloid nuclei was analysed in 12 cats. Single carbachol doses of 8 micrograms in 0.50 microliter saline were delivered unilaterally or bilaterally into the central, basal, lateral or basolateral amygdaloid nucleus. Carbachol administration into the central nucleus induced a prolonged (5 days) enhancement of both REM sleep and its preceeding slow wave sleep episodes with PGO waves (sommeil phasique a ondes lentes, SPHOL), which was more pronounced following bilateral than unilateral carbachol administration. However, neither SPHOL nor REM sleep changes were produced by administration of carbachol into the other amygdaloid nuclei. We conclude that cholinergic activation of the central amygdaloid nucleus produces a long-term facilitation of REM sleep occurrence.

Journal ArticleDOI
01 Apr 1996-Sleep
TL;DR: It is proposed that serotonergic excitation can significantly attenuate the REM sleep-like suppression of XII nerve activity, and that this is achieved, in part, by substituting for the decreased endogenous 5HT in the XII nucleus.
Abstract: The facilitatory effect of serotonin (5HT) on hypoglossal (XII) motoneurons is likely to be reduced during rapid eye movement (REM) sleep, when the activity of the brainstem serotonergic system reaches its nadir. Therefore, we assessed the hypothesis that application of exogenous 5HT will attenuate the REM sleep-like suppression of XII motoneurons produced in decerebrate cats by pontine microinjections of a cholinergic agonist, carbachol. Microinjections of 5HT or 5-carboxamidotryptamine into the XII nucleus increased XII nerve activity to 182 +/- 53% (standard deviation; SD) of control. Subsequent pontine microinjections of carbachol reduced XII nerve activity by 55 +/- 21% of the pre-5HT level (n = 12). Microinjections of methysergide (a 5HT antagonist) into the XII nucleus reduced XII nerve activity to 54 +/- 17% of the pre-methysergide control (n = 6). Pontine carbachol injections after methysergide further reduced XII nerve activity by 49 +/- 20% of the pre-methysergide level. Treatments with both agonists and the antagonist attenuated the carbachol-induced decrease when compared to two previous studies using the same model: 1) In experiments with no injections of serotonergic agents, pontine carbachol injections decreased XII nerve activity by 90 +/- 6% of control. 2) After enhancement of XII nerve activity by inhibitory amino acid antagonists (to 135 +/- 60%), the subsequent carbachol-induced decrease was even larger, 112 +/- 62% of control. We propose that serotonergic excitation can significantly attenuate the REM sleep-like suppression of XII nerve activity, and that this is achieved, in part, by substituting for the decreased endogenous 5HT in the XII nucleus. The study also demonstrates that other, non-serotonergic, mechanisms also contribute to the carbachol-induced suppression.

Journal ArticleDOI
TL;DR: Another disorder of REM sleep dysregulation (besides narcolepsy) appears to be strongly associated with specific HLA class I1 genes.
Abstract: Twenty-five white men with rapid eye movement (REM) sleep behavior disorder, but without narcolepsy, underwent HLA class II antigen typing ; 84% (N = 21) were DQw1 (DQB1*05,06) positive (28% [N = 7] were DR2 positive) ; DQB1*0501 (N = 9) and DQB1*0602 (N = 7) were the most common phenotypes. The 84% DQw1 rate in men with REM sleep behavior disorder was significantly greater (p = 0.015) than the 56% DQw1 rate found in a local white comparison group (N = 66), and was greater than the 39 to 66% DQw1 rates published for 12 white groups (N = 40-418/group). Thus, another disorder of REM sleep dysregulation (besides narcolepsy) appears to be strongly associated with specific HLA class II genes.

Journal ArticleDOI
01 Oct 1996-Sleep
TL;DR: A participant gives his account of the history of electrophysiological dream research in the 40 years following the discovery of rapid eye movement sleep and of its relation to vivid dreaming in the adult human.
Abstract: A participant gives his account of the history of electrophysiological dream research in the 40 years following the discovery, reported by Aserinsky and Kleitman in 1953, of rapid eye movement sleep and of its relation to vivid dreaming in the adult human.

Journal ArticleDOI
TL;DR: Monitoring of Vietnam combat-related posttraumatic stress disorder inpatients found that SCID-diagnosed PTSD+MDD patients failed to exhibit the classic REM sleep architectural modifications associated with unipolar depression, despite the fact that several other psychophysiologic indices of dysphoria were detectable in their sleep.