Showing papers on "Rapid eye movement sleep published in 1993"
TL;DR: Activity in the upper delta band tended to gradually increase from night to night during the sleep restriction period, whereas after an initial increase, activity in the theta-alpha band changed in the opposite direction and progressive changes were also present in the EEG spectra of REM sleep and wakefulness.
Abstract: The effect of repeated partial sleep deprivation on sleep stages and electroencephalogram (EEG) power spectra during sleep and wakefulness was investigated in nine healthy young subjects. Three baseline nights of 8 hours (2300-0700 hours) were followed by four nights with 4 hours of sleep (2300-0300 hours) and three recovery nights of 8 hours (2300-0700 hours). Sleep restriction curtailed sleep stages 1 and 2 as well as rapid eye movement (REM) sleep, but left slow wave sleep largely unaffected. In the first two recovery nights, total sleep time and REM sleep were enhanced, and sleep latency was shortened. Slow wave sleep was increased only in the first recovery night. In accordance with the prediction of the two-process model of sleep regulation, slow wave activity (SWA; spectral power density in the 0.75-4.5-Hz range) in nonrapid eye movement (NREM) sleep increased by approximately 20% in the first night following sleep restriction, remained at this level in the subsequent 3 nights and decreased immediately after the first recovery night. In contrast to these immediate changes, progressive and more persistent changes were seen in the EEG activity of higher frequencies. Thus, activity in the upper delta band tended to gradually increase from night to night during the sleep restriction period, whereas after an initial increase, activity in the theta-alpha band changed in the opposite direction. The progressive changes were also present in the EEG spectra of REM sleep and wakefulness. Because the time course of these changes paralleled the cumulative deficit in REM sleep, they may represent a correlate of REM sleep pressure.
227 citations
TL;DR: Intracellular recordings under barbiturate anesthesia showed that, during spindle oscillations, the spike-bursts of intralaminar neurons are generated by brief low-threshold spikes with a much shorter refractory phase than in other thalamocortical cells.
216 citations
TL;DR: The results were consistent with the notion that delta activity is an indicator of depth within NREM sleep, and Epochs with high delta power had increased arousal threshold relative to epochs with low arousal threshold.
Abstract: This study was designed to functionally validate earlier described criteria for visual sleep scoring with respect to acoustical stimulus threshold for arousal. A further objective was to explore the relation between electroencephalographic (EEG) power spectrum and acoustical stimulus threshold for arousal. After habituation to an acoustical stimulus (a 1,000-Hz sine tone, increasing 1.5 dB per second for 45 seconds), values for latency to arousal after acoustical stimulus onset were analyzed. Arousal was determined based on EEG and electromyographic (EMG) criteria. There was a significant effect of sleep stage, with slow wave sleep 2 (SWS-2) having higher arousal threshold than slow wave sleep 1 (SWS-1), rapid eye movement (REM) sleep and transition type sleep. This indicates that the subdivision of nonrapid eye movement (NREM) sleep in the rat into SWS-1 and SWS-2 had functional validity in this paradigm. Time of day also had a significant effect, with lower arousal threshold in the last 2 hours (ninth and tenth hour of the light period) of the 8-hour registration period. Furthermore, there was a significant effect of EEG delta power density. Epochs with high delta power had increased arousal threshold relative to epochs with low arousal threshold. The results were consistent with the notion that delta activity is an indicator of depth within NREM sleep.
203 citations
TL;DR: GHRH has sleep-promoting effects in young adults, particularly when given at a time of decreased sleep propensity, as well as in the absence of sleep deprivation.
Abstract: Growth hormone-releasing hormone (GHRH) promotes rapid-eye-movement (REM) and non-REM sleep in animals, but there is little direct evidence for a hypnogenic action of GHRH in humans. In the present study, the possible somnogenic effects of intravenous bolus injections of a dose of GHRH eliciting physiological elevations of GH secretion in healthy young men were investigated. GHRH (0.3 micrograms/kg body wt) was given in early sleep [i.e., 1st slow-wave (SW) period], late sleep (i.e., 3rd REM period), and early sleep after sleep deprivation until 0400 h (i.e., 1st SW period). In the absence of sleep deprivation, injection of GHRH in early sleep did not modify SW sleep but increased REM sleep. GHRH administration in the third REM period was followed by a marked decrease of wake and an almost 10-fold increase in SW sleep. When GHRH was administered during the first SW period after sleep deprivation until 0400 h, the duration of wake decreased. Thus GHRH has sleep-promoting effects in young adults, particularly when given at a time of decreased sleep propensity.
147 citations
TL;DR: Sources of select aminergic and cholinergic inputs to this REM sleep induction zone were identified and quantitatively analyzed by using fluorescence retrograde tracing combined with immunofluorescence in the rat.
Abstract: Microinjection of cholinergic agonists in a dorsolateral part of the mesopontine tegmentum has been shown to induce a rapid eye movement (REM) sleep-like state. Physiological evidence indicates that not only acetylcholine but also various amine transmitters, including those implicated in behavioral state regulation, affect neuronal activity in this region of the pontine reticular formation. In the present study, sources of select aminergic and cholinergic inputs to this REM sleep induction zone were identified and quantitatively analyzed by using fluorescence retrograde tracing combined with immunofluorescence in the rat. In addition to previously demonstrated cholinergic projections from the pedunculopontine and laterodorsal tegmental nuclei, the REM sleep induction zone received various aminergic inputs that originated in widely distributed regions of the brainstem and hypothalamus. Serotoninergic afferents represented a mean of 44% of all aminergic/cholinergic source neurons projecting to the REM sleep induction zone, which was comparable to the mean percentage of 39% represented by cholinergic afferent neurons. The serotoninergic afferents originated from the raphe nuclei at all brainstem levels, with heavier projections from the pontine than from the medullary raphe nuclei. Unexpectedly, an additional major serotoninergic input was provided by serotoninergic neurons in the nucleus prosupralemniscus (B9). Noradrenergic afferent neurons represented a mean of 14% of all aminergic/cholinergic source neurons, which was only about one-third of the mean percentage of either cholinergic or serotoninergic source neurons. These noradrenergic projection neurons were located not only in the locus ceruleus (8%) but also in the lateral tegmentum, including the A5 (4%) and A7 (2%) cell groups. Histaminergic neurons in the tuberomammillary hypothalamic nucleus represented a minor group of afferent neurons (3%), and a still smaller input came from adrenergic C1 neurons. The pattern of these transmitter-specific afferent connections appeared to be similar regardless of the longitudinal level within the REM sleep induction zone. The present results are consistent with previous behavioral and physiological evidence for a role of the pontine REM sleep induction zone in triggering REM sleep. The regulation of REM sleep induction would be best understood in terms of a state-dependent interplay of cholinergic, serotoninergic, and other inputs all acting convergently upon neurons in the REM sleep-inducing region of the pontine reticular formation.
134 citations
TL;DR: In both groups of infants, prone body position was associated with a significant increase in sleep duration and in non-rapid eye movement sleep and a significant decrease in number of arousals and in their duration.
Abstract: Objective. To evaluate the potential relation between body position and sleep characteristics in normal infants. Patients. Two groups of 3-month-old healthy infants were evaluated: 40 infants who usually slept supine, and 40 who usually slept prone. The two groups were matched for gender, gestational age, postnatal age, birth weight, and total recording time. Recording techniques. The 80 infants were studied polygraphically during one night in the pediatric sleep laboratory. They were allowed to fall asleep in their usual sleep position, and every 3 hours were gently turned from prone to supine, or from supine to prone. Results. In each group, 6 infants were excluded from the analysis, because they woke up after having been turned over. In both groups, no significant difference was seen between the prone and the supine body positions for the following variables: number of sleep state changes; number of gross body movements; percent of rapid eye movement sleep; saturation with oxygen, arterial blood levels; number and duration of acid esophageal reflux; rectal temperature; mean respiratory rates; water evaporation rates from the forehead skin; and number or duration of central or of obstructive apneas. In both groups of infants, prone body position was associated with a significant increase in sleep duration (+ 6%) and in non-rapid eye movement sleep (+25%) and a significant decrease in number of arousals (–40%) and in their duration (–43%). Conclusions. No explanation has been found for the sleep-promoting effect of prone body positioning. The finding could be of interest to the study of infants9 sleep quality, as well as to the potential relation between body positions and sudden death during sleep.
133 citations
TL;DR: The findings in this blind man suggest that both his sleep structure and the severity of his daily sleep disruption are directly related to circadian phase and his circadian pacemaker cannot be entrained by periodic daily exposure to nonphotic time cues, including a very regular 24-hour sleep-wake schedule.
Abstract: Sleep disturbances and the failure to entrain circadian rhythms to the 24-hour day have been reported in the majority of totally blind subjects. The present case study of a totally blind man with a well-documented recurring sleep disturbance was designed to investigate the mutual relationship between sleep and the circadian timing system. The 63-year-old subject, a high school teacher with a regular work schedule, had suffered from cyclically recurring insomnia for the past 28 years. Analysis of a sleep log that he had kept for the past 15 years suggested that his circadian rhythms were not entrained to the 24-hour day. During a 3-month inpatient study, the period of the endogenous circadian pacemaker was assessed by analysis of ambulatory core body temperature, urinary excretion and a series of estimates of the phase of core body temperature cycles and plasma cortisol levels during constant routines. All circadian markers revealed periods in the range of 24.22-24.27 hours, with no evidence for a modulation of the observed periods by the sleep-wake cycle. During this 3-month inpatient study, a complete cycle of the subject's sleep disturbance and remission was polysomnographically documented while the subject lived on a regular 24-hour schedule. Because the subject's circadian rhythms were free-running and his sleep times were fixed, sleep occurred at virtually all circadian phases. Analysis of sleep latency, REM sleep latency, sleep duration, wake in sleep episode and REM sleep during sleep episode revealed a strong modulation by circadian phase. These findings in this blind man suggest that: 1) the period of his cyclically recurring sleep disturbance is directly related to the nonentrained period of an endogenous circadian pacemaker that drives circadian variation in core body temperature, urinary excretion, plasma cortisol and sleep propensity; 2) both his sleep structure and the severity of his daily sleep disruption are directly related to circadian phase and 3) his circadian pacemaker, which has an endogenous period that deviates only 0.2-0.3 hours from 24 hours, cannot be entrained by periodic daily exposure to nonphotic time cues, including a very regular 24-hour sleep-wake schedule.
126 citations
TL;DR: There is little, if any, contribution of these inhibitory amino acids to the depression of XII motoneurons during the carbachol-induced, REM sleep-like postural and respiratory depression; mechanisms other than fast synaptic inhibition must be involved.
124 citations
TL;DR: It is concluded that methamphetamine caused a dose-dependent decrease in daytime sleep tendency and improvement in performance in both narcoleptics and controls.
Abstract: Eight pairs of subjects (each consisting of a narcoleptic and a control matched on the basis of age, sex, educational background and job) were evaluated under the following double-blind, randomized treatment conditions: baseline, placebo, low dose and high dose methamphetamine. Subjects were drug-free for 2 weeks prior to beginning the protocol. Methamphetamine was the only drug taken during the protocol and was given in a single morning dose of 0, 20 or 40-60 mg to narcoleptics and 0, 5 or 10 mg to controls. The protocol was 28 days long, with each of the four treatment conditions lasting 4 days followed by 3 days of washout. Nighttime polysomnography and daytime testing were done during the last 24 hours of each treatment condition. Daytime sleep tendency was assessed with the multiple sleep latency test (MSLT). Daytime performance was assessed with performance tests including a simple, computer-based driving task. Narcoleptics' mean MSLT sleep latency increased from 4.3 minutes on placebo to 9.3 minutes on high dose, compared with an increase from 10.4 to 17.1 minutes for controls. Narcoleptics' error rate on the driving task decreased from 2.53% on placebo to 0.33% on high dose, compared with a decrease from 0.22% to 0.16% for controls. The effects of methamphetamine on nocturnal sleep were generally dose-dependent and affected sleep continuity and rapid eye movement (REM) sleep. Elimination half life was estimated to be between 15.9 and 22.0 hours. Mild side effects emerged in a dose-dependent fashion and most often involved the central nervous system and gastrointestinal tract. We concluded that methamphetamine caused a dose-dependent decrease in daytime sleep tendency and improvement in performance in both narcoleptics and controls. Methamphetamine at doses of 40-60 mg allowed narcoleptics to function at levels comparable to those of unmedicated controls.
111 citations
TL;DR: The data indicate that c- fos expression can be employed as a marker of state-dependent neuronal activity in cats injected with carbachol, and specific sites in which there were greater numbers of c-fos-expressing neurons during active sleep-carbachol are discussed.
Abstract: Microinjection of carbachol into the rostral pontine tegmentum of the cat induces a state that is comparable to naturally occurring active (REM, rapid eye movement) sleep. We sought to determine, during this pharmacologically induced behavioral state, which we refer to as active sleep-carbachol, the distribution of activated neuron within the pons and medulla using c-fos immunocytochemistry as a functional marker. Compared with control cats, which were injected with saline, active sleep-carbachol cats exhibited higher numbers of c-fos-expressing neurons in (1) the medial and portions of the lateral reticular formation of the pons and medulla, (2) nuclei in the dorsolateral rostral pons, (3) various raphe nuclei, including the dorsal, central superior, magnus, pallidus, and obscurus, (4) the medial and lateral vestibular, prepositus hypoglossi, and intercalatus nuclei, and (5) the abducens nuclei. On the other hand, the mean number of c-fos-expressing neurons found in the masseter, facial, and hypoglossal nuclei was lower in carbachol-injected than in control cats. The data indicate that c- fos expression can be employed as a marker of state-dependent neuronal activity. The specific sites in which there were greater numbers of c- fos-expressing neurons during active sleep-carbachol are discussed in relation to the state of active sleep, as well as the functional role that these sites play in generating the various physiological patterns of activity that occur during this state.
104 citations
TL;DR: During successful adaptation to the loss of a spouse, and in the absence of major depression, spousal bereavement is associated with elevation in the phasic measures of REM sleep but does not appear to be associated with other physiologic sleep changes typical of major depressed when studied at 3 to 23 months after the event.
TL;DR: The results show that cholinoceptive regions of the basal forebrain can increase wakefulness and reduce the ability of pontine carbachol to evoke the REM sleep-like state, and suggest that basal fore brain administration ofcarbachol activates an arousal-generating system that can successfully compete with the powerful cholinergicREM sleep- generating system of the pons.
Abstract: This study was performed to test the hypothesis that cholinoceptive basal forebrain systems can significantly influence cholinoceptive pontine mechanisms known to be important for generating rapid eye movement (REM) sleep. This hypothesis was examined by microinjecting the cholinergic agonist carbachol or saline (vehicle control) into the pons, the basal forebrain, or simultaneously into the pons and basal forebrain, while quantifying the effects on sleep and wakefulness in unanesthetized, chronically instrumented cats. All microinjections were made during wakefulness and were followed by 2 or 4 hr of recording. Polygraphic records were scored for wakefulness, non-REM sleep, REM sleep, and the REM sleep-like state evoked by pontine administration of carbachol (DCarb). Dependent variables quantified following each microinjection included the percentage of recording time spent in each state, the latency to onset of non-REM, REM, and DCarb, the number of episodes per hour of each state, and the duration of the longest episode of each state. A total of 149 microinjections were made into 15 forebrain and 11 pontine sites in eight cats. Basal forebrain administration of carbachol significantly increased wakefulness. Pontine microinjection of carbachol produced a state that polygraphically and behaviorally resembled REM sleep. This REM sleep- like state occurred in amounts significantly greater than natural REM sleep. Pontine carbachol also significantly decreased wakefulness and non-REM sleep. Simultaneous injection of carbachol into the pons and basal forebrain enhanced REM sleep, but the magnitude of this enhancement was significantly less than the increase in REM sleep evoked by carbachol injection into the pons alone. The results show that cholinoceptive regions of the basal forebrain can increase wakefulness and reduce the ability of pontine carbachol to evoke the REM sleep-like state. These findings suggest that basal forebrain administration of carbachol activates an arousal-generating system that can successfully compete with the powerful cholinergic REM sleep- generating system of the pons.
TL;DR: The evidence reviewed strongly implicates both GHRH and IL‐1 as key components in humoral sleep regulation.
Abstract: Growth hormone-releasing hormone (GHRH) and interleukin-1 (IL-1) are putative endogenous sleep-promoting substances. Evidence is reviewed showing that, 1) GHRH and IL-1 promote non-rapid eye movement sleep (NREMS); 2) if their production is enhanced, sleep is enhanced; and 3) if they are inhibited using either specific antibodies or peptide antagonists, sleep is reduced. Both are in the brain and both are also indirectly linked to sleep/wake cycles by various other evidence, e.g., growth hormone release and IL-1 plasma levels vary in phase with sleep/wake cycles. Finally, their actions are directly linked to each other; e.g., IL-1-induced growth hormone release is mediated via GHRH. The evidence reviewed strongly implicates both GHRH and IL-1 as key components in humoral sleep regulation. Humoral theories of sleep regulation are complementary to neural theories; both mechanisms affect each other and undoubtedly continuously interact to regulate sleep/wake cycles.
Journal Article•
TL;DR: Concomitant enhancement of both total sleep and REM appears to be a peculiar feature which clearly distinguishes DA D-1 antagonists from the other DA receptor blockers.
Abstract: A series of antipsychotics having different selectivity for dopamine (DA) D-1 and D-2 receptors were studied for their effects on sleep stages in the rat. Electroencephalographic activity was recorded and classified according to the stages of wakefulness, rapid eye movement (REM) sleep and non-REM sleep. Total sleep duration, non-REM and REM latencies, number and duration of REM episodes were calculated. The DA D-1 antagonists, SCH 23390 (0.001-0.1 mg/kg s.c.), SCH 39166 (0.01-0.3 mg/kg s.c.) and NNC-756 (0.003-0.1 mg/kg s.c.), enhanced markedly the time spent in sleep through a significant increase of both non-REM and REM. Enhancement of REM was due to an increase in the number of episodes. The selective DA D-2 antagonists, raclopride (0.03-1 mg/kg s.c.) and remoxipride (1-10 mg/kg s.c.), did not affect sleep stages. Haloperidol (0.1-3 mg/kg p.o.) increased the duration of total sleep through an increase of non-REM, leaving REM unmodified. The nonselective DA antagonists, chlorpromazine (0.3-3 mg/kg s.c.) and clozapine (0.3-3 mg/kg s.c.) produced either no effect or slightly increased non-REM, respectively. Both drugs reduced REM duration by lowering the number and duration of episodes. The data show that there are differences between DA D-1 and D-2 antagonists with regard to their effects on sleep and wakefulness. Concomitant enhancement of both total sleep and REM appears to be a peculiar feature which clearly distinguishes DA D-1 antagonists from the other DA receptor blockers.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: A broad range of REM sleep eye movement densities characterize both schizophrenics and depressives and substantially overlaps the normal range and should not be considered a biological marker for affective illness.
Abstract: Objective: To investigate the specificity of rapid eye movement (REM) sleep eye movement measures in schizophrenics, depressives, and nonpsychiatric controls. Design: Survey. Setting: Inpatient psychiatric hospital. Study Participants: Volunteer sample of male veterans who met Research Diagnostic Criteria (RDC) for schizophrenia (n=21) or major depressive disorder (n=24), or male veterans recruited from the community with no history of psychiatric illness (n=13). Patients with a concurrent RDC diagnosis of alcoholism were excluded. After data collection, three schizophrenics, two depressives, and one nonpsychiatric control were eliminated because of two or fewer REM periods on either of the two recording nights. Intervention: None. Main Outcome Measure: Computer-detected total night and within-night measures of REM sleep eye movement density, ie, the ratio of eye movement counts to stage REM minutes. Results: Using a 95% confidence interval, schizophrenics, depressives, and nonpsychiatric controls did not differ in total night or within-night measures of eye movement density. Within nights, eye movement density increased across REM periods in the schizophrenics and nonpsychiatric controls; the depressives showed a flatter withinnight distribution associated with their older age. Conclusions: A broad range of REM sleep eye movement densities characterize both schizophrenics and depressives and substantially overlaps the normal range. Adnormalities of REM sleep eye movement activity should not be considered a biological marker for affective illness.
TL;DR: The results demonstrate the importance of nap timing, suggesting a circadian variation of propensity to relapse into depression, and refute some of the current theories on the relationship between sleep and depressive symptomatology.
TL;DR: Rapid eye movement sleep, a stage of sleep that appears to be present in all marsupial and terrestrial placental mammals, was first identified in 1953 and suggests a role in memory processing.
TL;DR: The results support the view that D1 receptors may have a physiological function in producing arousal and the effects of the dopamine D1 receptor full agonist A68930 on sleep-wake patterns and grooming behaviour were studied in the rat.
TL;DR: A significant decrease of rapid eye movement sleep (REMS) and a significant lengthening of REMS latency were observed initially as well as at the end of treatment with citalopram, a highly specific serotonin uptake inhibitor.
Abstract: Drug-induced improvement of depression may be mediated by changes in sleep physiology. The aim of this study was to relate changes in sleep polygraphic variables to clinical state during treatment with citalopram, a highly specific serotonin uptake inhibitor. Sixteen patients took part. The study was single-blind and uncontrolled. A 1-week wash-out period was followed by 1 week of placebo administration, a medication period of 5 weeks, and a 1-week placebo period. For the entire group a significant decrease of rapid eye movement sleep (REMS) and a significant lengthening of REMS latency were observed initially as well as at the end of treatment. No changes in sleep continuity were found, but non-REMS stage 2 (percentage) was significantly increased. On the basis of clinical change, as expressed by the scores of the Hamilton Rating Scale for Depression, at the end of the citalopram treatment the patient group was split in two halves: eight less and eight more improved patients. The groups did not differ with respect to any sleep polygraphic varible.
TL;DR: Regional spectral analyses of the EEG during wakefulness and REM sleep was performed in patients with mild to moderate Alzheimer's disease and compared to that of healthy age-matched controls, finding regional differences in EEG slowing, relatively nonexistent in the awake EEG, were a prominent feature of the REM sleep EEG.
TL;DR: The results support the assumption of a "depressiogenic" effect of naps in patients with major depression after successful TSD.
Abstract: Total sleep deprivation (TSD) exerts beneficial but transient effects on mood in approximately 60% of patients with a major depressive disorder. The positive effects of a night of total sleep deprivation are generally reversed after the next night of sleep. Several anecdotal reports and a pilot study by our group indicated that even short naps during the period of sleep deprivation are capable of re-inducing depressive mood in responders to TSD. The present study explored whether the structure of naps at 9 a.m. was crucial for the "depressiogenic" impact of naps on mood. A negative effect on mood was replicated, but this effect was not related to any of the nap sleep variables. The effect of naps on mood was attenuated in the early afternoon. The results support the assumption of a "depressiogenic" effect of naps in patients with major depression after successful TSD.
TL;DR: There is a marked variability among individuals in the number of spindles and K-complexes and more so in older individuals than in younger, however, there is an overall decrease in these events with age.
TL;DR: The observation supported the hypothesis and showed primarily that the deprivation increased the enzyme activity in the rat brain, and showed also that the pons and the medulla were the first sites to be affected by deprivation.
Abstract: Since rapid eye movement (REM) sleep deprivation has been reported to affect the neuronal excitability in the brain, it was hypothesized that a change in the neuronal membrane-bound Na-K ATPase activity might be at least one of the factors inducing such a change. Therefore, in this study rats were deprived of REM sleep by using the platform technique and enzyme activity was estimated in the whole brain, in different regions of the brain and in microsomal preparations. Deprivation was carried out for varying periods and suitable control experiments were conducted to rule out the possibility of nonspecific effects. The observation supported our hypothesis and showed primarily that the deprivation increased the enzyme activity in the rat brain. It showed also that the pons and the medulla were the first sites to be affected by deprivation. The probable mechanism producing such a change is discussed.
TL;DR: Spontaneous rhythmic oscillations of cerebral blood flow velocity were found related to different stages of sleep, including rapid eye movement (REM) sleep and to a lesser degree during sleep stages 1, 2 and 3 and the waking state.
Abstract: In 10 normal young adults, middle cerebral artery blood flow velocity was measured continuously over one night by transcranial Doppler sonography. Polysomnography was used to assess the different sleep stages and waking state. During rapid eye movement (REM) sleep, middle cerebral artery blood flow velocity was higher than in any other sleep stage and wakefulness. During the waking state the velocity was higher than in sleep stage 2. Spontaneous rhythmic oscillations of cerebral blood flow velocity were found related to different stages of sleep. A fast Fourier's transformation of the Doppler wave forms revealed a periodicity of 20-75 seconds, which was most prominent during REM sleep and to a lesser degree during sleep stages 1, 2 and 3 and the waking state. These waves may correspond to intracranial pressure changes referred to as B-waves.
TL;DR: Sleep parameters of never-depressed borderline subjects and age- and sex-matched normal controls were compared by continuous 48-hr ambulatory electroencephalographic (EEG) monitoring to find reduced latency of rapid eye movement can be a trait indicator of liability to depression.
TL;DR: The present results are consistent with the hypothesis that diminished acetylcholine release in the pontine FTG comprises one mechanism by which morphine inhibits REM sleep.
Abstract: BACKGROUND: Systemically administered morphine inhibits rapid eye movement (REM) sleep; however, the neuronal mechanisms through which morphine disrupts REM sleep remain poorly understood. Recently, the authors have shown that morphine-mediated REM sleep inhibition is localized to a specific region of the pontine reticular formation: the gigantocellular tegmental field (FTG). Because cholinergic neurotransmission in the FTG is known to play a role in REM sleep generation, the present study examined the hypothesis that systemically administered morphine would cause decreased acetylcholine release in the FTG. METHODS: Microdialysis probes were stereotaxically positioned in the FTG of six barbiturate-anesthetized cats to measure acetylcholine release. Cholinergic input to the FTG arises from the laterodorsal (LDT) and pedunculopontine tegmental (PPT) brain stem nuclei. By electrically stimulating the LDT and PPT, it was possible to measure stimulation-evoked acetylcholine release in the FTG. Morphine sulfate (MSO4) was administered intravenously (500 micrograms.kg-1). High performance liquid chromatography with electrochemical detection was used to measure stimulation-evoked acetylcholine release in the FTG before and after the systemic administration of morphine sulfate. RESULTS: Acetylcholine release in the pontine FTG was depressed significantly (P < 0.01) by systemic morphine sulfate. Acetylcholine release without electrical stimulation of the LDT and PPT averaged 0.6 +/- 0.18 (mean +/- SD) pmol/10 min of dialysis. Before morphine sulfate was administered, electrical stimulation of cholinergic LDT and PPT neurons increased acetylcholine release within the FTG to 1.9 +/- 0.76 pmol/10 min. After morphine sulfate was administered, there was a 37% decrease in acetylcholine release within the FTG to average values of 1.2 +/- 0.63 pmol/10 min. There was no significant effect of morphine sulfate on spontaneous acetylcholine release in the absence of LDT and PPT stimulation. CONCLUSIONS: Because FTG levels of acetylcholine release increase during REM sleep, the present results are consistent with the hypothesis that diminished acetylcholine release in the pontine FTG comprises one mechanism by which morphine inhibits REM sleep.
TL;DR: Following heating, non-rapid eye movement sleep 2 (NREMS2 or deep NREMS) was significantly increased during the first 2 h of the recovery period compared with baseline and sleep-matched control conditions and During the first hour compared with the totally sleep-deprived condition.
TL;DR: The results show that despite relative clinical stability over time, the EEG sleep of schizophrenic patients continues to change following withdrawal of a neuroleptic and is dependent on the duration of the drug-free interval.
TL;DR: Control experiments suggest that the decrease in monoamine oxidase activity was primarily caused by the rapid eye movement sleep deprivation and was not due to nonspecific effects, which is consistent with past studies and may help to explain earlier observations.