Showing papers on "Slow-wave sleep published in 1977"
TL;DR: The results support the hypothesis that the suprachiasmatic nuclei may serve as a central neural pacemaker responsible for the generation and entrainment of a number of circadian rhythms in physiology and behavior, and that the regulation of rhythmic functions is mediated by neural efferents from the su PRS nuclei.
171 citations
TL;DR: The results are consistent with a hypothesis of pontine gigantocellular field unit involvement in the motor activation common to both waking and REM sleep, but are not consistent with an executive role for these neurons in the triggering of the REM sleep state.
155 citations
TL;DR: Differences between pre- and post-sleep SSS scores were correlated with the sleep states: increased sleepiness was correlated with SWS and decreased sleepiness with REM sleep and with post- sleep SSS ratings and REM sleep.
Abstract: The effects of REM and slow wave sleep (SWS) on subjective sleepiness were studied in 10 subjects placed on a 90-min sleep-wakefulness schedule for either 51/3 or 6 (24-hr) days. Subjects were permitted to sleep for 30-min periods separated by 60 min of enforced wakefulness. Sleep recordings showed that sleep onset REM periods occurred frequently; REM and SWS appeared during the same sleep period only 27 times; and REM sleep tended to occur on sleep periods that alternated with SWS periods. Sleepiness was measured using the Stanford Sleepiness Scale (SSS) given 15 min before (pre-sleep) and 15 min after (post-sleep) each sleep period. Average SSS ratings showed a 24-hr fluctuation in sleepiness. In addition, negative and positive SSS changes tended to alternate with each 90-min period. Significant correlations were found with post-sleep SSS ratings and SWS and with pre-sleep SSS ratings and REM sleep. Differences between pre- and post-sleep SSS scores were also correlated with the sleep states: increased sleepiness was correlated with SWS and decreased sleepiness with REM sleep.
119 citations
TL;DR: The finding that GHB is a natural constituent of mammalian brain and the previous observation that the GHB-induced hypersynchrony can be antagonized by anti-absence (anti-petit mal) drugs are discussed are discussed in view of the possibility thatGHB might play a role in the etiology of absence epilepsy in man.
115 citations
TL;DR: It is concluded that patients undergoing open heart surgery experience both acute and chronic disruptions of sleep that last well beyond the hospital period of convalescence and have considerable relevance for postoperative management.
Abstract: This study was designed to document quantitatively the sleep disturbances that occur after open heart surgery and to investigate a group of patients who underwent a thoracic surgical procedure not involving cardiopulmonary bypass. Nine patients were studied, six after open heart surgery and three after partial or complete pneumonectomy. In each patient, sleep patterns were recorded with use of all night polygraphy before and after operation and for up to 5 weeks on follow-up studies. After open heart surgery, patients manifested considerable suppression of electrophysiologic evidence of sleep as well as prolonged suppression of both rapid eye movement and slow wave sleep patterns. In the three patients subjected to thoracotomy these sleep indexes returned to preoperative levels much earlier. Evidence of stage 2 sleep was present in one of the three patients with thoracotomy on the first postoperative night, and in two of the three both rapid eye movement and slow wave sleep returned to preoperative levels by the time of hospital discharge. It is concluded that patients undergoing open heart surgery experience both acute and chronic disruptions of sleep that last well beyond the hospital period of convalescence. These sleep disturbances have considerable relevance for postoperative management.
114 citations
TL;DR: This work has recorded in the cat the first evidence of neurons whose rhythmic discharge is consistent with the hypothesis of a tonically active neural substrate for rapid eye movement (REM) sleep.
113 citations
TL;DR: It is suggested that the seizure of an E1 mouse may belong to a sensory precipitating epilepsy and might have a certain focus in some portion of the brain, which might be predisposed by some genetic factors and might be related to vestibular or some other sensory neural pathway and to the parietal cortex.
110 citations
TL;DR: Neither synthetic arginine vasopressin, nor synthetic oxytocin, injected intraventricularly in the amount of 10(-6) pg, was able to induce slow-wave sleep, and in the cats injected with synthetic or pineal AVT, the paradoxical sleep was completely suppressed.
108 citations
98 citations
TL;DR: A dose-dependent dissociation of effects on behaviour and motor control was revealed and the sleep-waking cycle was affected; the duration of REM sleep showed a consistent dose-related reduction although the total sleeping time was not considerably altered.
92 citations
TL;DR: In this article, 11 patients with upper airway apnoea during sleep (one with SHY-Drager syndrome) were monitored polygraphically for wakefulness, sleep, and cardiovascular variables.
Abstract: Eleven patients with upper airway apnoea during sleep (one with SHY-Drager syndrome) were monitored polygraphically for wakefulness, sleep, and cardiovascular variables. Systemic hypertension and most of the severe arrhythmias recorded during sleep were secondary to repetitive obstructive apnonea and were mediated through the autonomic nervous system. Sleep related elevations of pulmonary arterial pressure were not influenced by atropine or impaired autonomic functions. Upper airway sleep apnoea is sleep related; the type of sleep (REM or NREM) is critical in the appearance of abnormalities. The distinction between two patient subgroups (total sleep dependent and NREM sleep dependent) has haemodynamic, and possibly long-term, implications. Sleep apnoea syndrome should be looked for in pateints with the Shy-Drager syndrome.
TL;DR: Results indicated that narcoleptic dogs do not differ from normals with respect to percent of time spent in wakefulness and atonia with no theta, and normal dogs presented neither of these pathological states.
TL;DR: The administration of small doses of somatostatin into the neostriatal complex of unrestrained, freely moving rats induced general behavioral excitation associated with a variety of stereotyped movements, tremors, and a reduction of rapid eye movements (REM) and deep slow wave sleep (SWS).
Abstract: The administration of small doses of somatostatin (SRIF) (0.01 and 0.1 microgram) into the neostriatal complex of unrestrained, freely moving rats induced general behavioral excitation associated with a variety of stereotyped movements, tremors, and a reduction of rapid eye movements (REM) and deep slow wave sleep (SWS). In contrast, the higher doses of SRIF (1.0 and 10.0 microgram) caused movements to be uncoordinated and frequently induced more severe difficulties in motor control such as contralateral hemiplegia-in-extension which restricted or completely prevented the expression of normal behavioral patterns. As a result, the animals appeared drowsy and inhibited. Analysis of the sleep-waking cycle revealed prolonged periods of a shallow SWS while REM sleep and deep SWS were markedly reduced; electroencephalogram recordings revealed periods of dissociation from behavior. The administration of endocrinologically inactive as well as the active analogues of SRIF failed to induce effects comparable with those observed after the administration of the same dose of the native hormone (10.0 microgram).
TL;DR: EEG and behavioral effects confirmed that DSIP also induces, when intravenously injected, orthodox slow wave sleep.
TL;DR: Both the original and the synthetic nonapeptide Trp-Ala-Gly-Glys-Asp- ala-Ser-G ly-Glu enhance, in recipient rabbits, spindle and delta EEG activity as in orthodox slow wave sleep.
Abstract: Both the original and the synthetic nonapeptide Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu enhance, in recipient rabbits, spindle and delta EEG activity as in orthodox slow wave sleep.
TL;DR: The results demonstrate the value of direct quantification of delta-wave activity, the variable that underlies visual classification of slow-wave sleep into stages 2 to 4, and give rise to new hypotheses regarding the relative absence of side effects in spite of profound stage 4 suppression by flurazepam.
Abstract: Repeated administration of flurazepam reduced stage 4 sleep (high delta-wave concentration) but produced a greater increase in stage 2 duration so that total sleep time was increased. Computer analysis revealed that the increased amount of stage 2 (low delta-wave concentration) sleep provided a number and duration of delta waves sufficient to offset the loss of delta activity in stage 4. However, the amplitude of the average delta wave was reduced. These results demonstrate the value of direct quantification of delta-wave activity, the variable that underlies visual classification of slow-wave sleep into stages 2 to 4. They also give rise to new hypotheses regarding the relative absence of side effects in spite of profound stage 4 suppression by flurazepam and the mechanisms by which total sleep time is increased by this drug.
TL;DR: The most striking finding was that in mice with clearly entrained or free-running activity onsets, the circadian peak-through patterns in wakefulness, NREM, and REM sleep were not always distinct--they could be damped and/or polyphasic.
TL;DR: Clinical evidence suggested extension of the chronically "locked-in" patient's lesion dorsally into the pontine tegmentum correlates well with experimental evidence indicating that structures in the tegmental area are essential for normal sleep.
TL;DR: It was found that both high and low doses of anisomycin decreased rapid eye movement (REM) sleep, while only high doses of ChA and V produced such a decrease.
Abstract: The present investigation sought to determine the effects of Anisomycin (A), Chloramphenicol (ChA), Vincristine (V), and Penicilline G on the sleep-wake cycle of rats. It was found that both high and low doses of anisomycin decreased rapid eye movement (REM) sleep, while only high doses of ChA and V produced such a decrease. Slow wave sleep (SWS) was unaffected by these drugs. Penicilline G, on the other hand, had no effect on the sleep-wake cycle. It was further shown that the reduction of REM sleep was the result of a decrease in the number of REM periods rather than in the duration of each individual period. These results suggest that protein synthesis may participate in the mechanisms that trigger REM sleep.
TL;DR: Electrical stimulation of the baroceptive fibres of the vago-aortic trunks (VA St) reflexly induces a complete sleep cycle characterized by a progression of all stages of sleep previously described in chronic preparations, which is particularly noteworthy in REM-deprived cats.
TL;DR: In the present work, on the basis of an unselected collection of patients suspected of epilepsy, the diagnostic value of waking and sleep recordings each after 24 h sleep deprivation are compared with one another and the result is highly significant with a chi2 value of 13.01.
Abstract: In the present work, on the basis of an unselected collection of patients suspected of epilepsy, the diagnostic value of waking and sleep recordings each after 24 h sleep deprivation are compared with
TL;DR: Support is given for the view that the ascending 5-HT neurons are important for the maintenance of SWS 2 and paradoxial sleep (PS) and on the uptake of NA neurons showed that the NA neurons were also affected by the 5,7-HT treatment.
TL;DR: It is suggested that the differential development of the characteristics of sleep patterns reflects differential maturation of distinct nervous system elements.
Abstract: The sequence of developmental changes in sleep pattern organization was derived from 12-hr recordings in 10-, 20- and 40-day-old kittens. Each characteristic of sleep patterning exhibited a distinct maturational sequence. Earlier changes (10–20 days) included quiet sleep (QS) increments and somatic activity decrements; later changes (20–40 days) included emergence of EEG slow waves and spindles, decrements in active sleep (AS), and diminution of QS respiratory variability. Changes in the lengths of state epochs and the types of state transitions spanned the period studied. We suggest that the differential development of the characteristics of sleep patterns reflects differential maturation of distinct nervous system elements.
TL;DR: The 24-hr electrographic patterns (EEG, EOG, EMG) of normal pointer dogs were recorded in a laboratory setting and two states of sleep (slow-wave and rapid eye movement) and wakefulness (alert and drowsy) were identified.
TL;DR: The influence of afferent impulses of intestinal origin on the sleep stages was studied in fed and starved cats and low-frequency electrical stimulation of the mucosal surface in a small intestinal fistula reduced the latency of sleep onset.
TL;DR: Two to 4 different young adult males were studied while on five different regimens of sleep-wakefulness and REM sleep was responsive to sleep onset time.
Abstract: Two to 4 different young adult males were studied while on five different regimens of sleep-wakefulness. The regimens studied were: 3 hrs sleep, 6 hrs wakefulness; 4 hrs sleep, 8 hrs wakefulness; 6 hrs sleep, 12 hrs wakefulness; 10 hrs sleep, 20 hrs wakefulness; and, 12 hrs sleep, 24 hrs wakefulness. The EEG-EOG was recorded during the sleep period.
The largest change in sleep pattern occurred in the short regimens. In these regimens Stage 2 was reduced and Stages 3/4 increased. The amount of REM sleep was stable across all regimens. The temporal distribution of Stages REM and 4 was maintained within the modified regimens. Increases in amount of prior wakefulness acted predictably to increase the amount of Stage 4. REM sleep was responsive to sleep onset time.
TL;DR: It is suggested that TRH inhibits sleep and sleep-related GH release in normal subjects by rising to levels comparable to those on control nights during early sleep periods in all subjects examined.
Abstract: Effects of TRH on sleep and sleeprelated growth hormone (GH) release were examined in four normal volunteers. A bolus of 500 μg of synthetic TRH was injected iv at the onset of sleep, followed by continuous iv infusion of 1000 μg of TRH dissolved in saline for 3 h on two nights. Saline alone was infused on two control nights in each of these subjects. Polygraphic sleep records showed that TRH transiently interrupted sleep on both nights in all of the four subjects. The arousal phenomenon was observed from 80 to 151 min after the start of TRH administration until 20 to 212 min after the end of TRH infusion. The mean (±SE) percentage of awakening on the nights of TRH administration was significantly larger than on the control nights (36.4 ± 1.9% us. 1.3 ± 0.8%, P < 0.001). Plasma GH increased in close relationship to the initial appearance of slow wave sleep (SWS) within 40 min after sleep onset on both control nights in all four subjects. On nights of TRH administration, however, plasma GH levels during th...
TL;DR: The results indicate that chlordiazepoxide produces a marked synergism with alcohol withdrawal suppression of slow wave sleep, which needs to be reviewed for potentially prolonging tolerance ""carryover" and thereby being counterproductive for treatment outcome.
Abstract: Slow wave sleep abnormalities characterize the sleep of alcoholics. In this report, two questions are addressed: (1) Does the slow wave sleep loss in alcohol withdrawal relate to withdrawal treatment? (2) Do the slow wave sleep changes on and off alcohol relate to the clinical course of alcoholism? The first question was addressed by comparing recovery in sleep EEG and clinical measures following two types of alcohol withdrawal treatment. Eighteen subjects were randomly assigned to either a low dose ethanol or chlordiazepoxide treatment for alcohol withdrawal. The results indicate that chlordiazepoxide produces a marked synergism with alcohol withdrawal suppression of slow wave sleep. The second question was addressed by an experimental alcoholization study involving 9 subjects who drank for 5 consecutive days, with 18 ounces of 95 proof ethanol consumed daily. Changes in slow wave sleep from baseline (abstinent) values to those on alcohol showed faster rate of tolerance development for the low slow wave sleep subjects. The rate of tolerance development was significantly related to treatment outcome, with faster tolerance development associated with poorer treatment outcome. In this regard it is noted that the use of chlordiazepoxide in alcohol withdrawl needs to be reviewed for potentially prolonging tolerance ""carryover" and thereby being counterproductive for treatment outcome.
TL;DR: In this paper, a method was described for sleep deprivation of up to 12 rats at a time by placing them in two large rotating cylinders, and EEG data showed that total sleep time was significantly reduced from 47.0 percent to 3.8 percent of a 24-hour period.
Abstract: A method is described for sleep depriving up to 12 rats at a time by placing them in two large rotating cylinders. EEG data, previously unavailable for rats treated in this manner, show that total sleep time was significantly reduced from 47.0 percent to 3.8 percent of a 24-hr period. There was no selective reduction of REM or non-REM sleep.
TL;DR: The usually discarded ‘first laboratory night’ produces a mild situational insomnia in normal persons and thus can be useful in certain sleep studies.
Abstract: Forty-two normal human subjects were studied in the sleep laboratory for one night each. Fourteen were given placebo at bedtime, 14 took l-tryptophane 1 g, and 14 took l-tryptophane 3 g. Both tryptophane groups had significantly lower sleep latency than the placebo group. The usually discarded ‘first laboratory night’ produces a mild situational insomnia in normal persons and thus can be useful in certain sleep studies.