Showing papers on "Slow-wave sleep published in 1971"

Acetylcholine liberation from cerebral cortex during paradoxical (REM) sleep.

Abstract: The rate of liberation of free acetylcholine from the surface of prostigmin-treated cerebral cortex in the freely moving cat has been determined in states of slow wave sleep, paradoxical or activated sleep, and waking. The average rate during slow wave sleep (1.2 nanograms per minute per square centimeter of cortical surface) increased during paradoxical sleep (2.2 nanograms per minute) and during waking (2.1 nanograms per minute). The rate of acetylcholine release is thus related to the electroencephalogram pattern of desynchronized activatin of the cortex rahter than to the behavioral responsiveness of the animals.

Stage 4 Sleep: Influence of Time Course Variables

Abstract: Age, length of prior wakefulness, length of time asleep, and a circadian influence all affect stage 4 sleep. The amount of stage 4 sleep decreases as subject's age increases and as time asleep increases. Longer periods of wakefulness before sleep result in greater amounts of stage 4 sleep in the first 3 hours of sleep. Sleep periods that begin at times other than the regular onset time tend to produce less stage 4 sleep; this decrease suggests a circadian effect.

Neuronal discharges of the ventrolateral nucleus of the thalamus during sleep and wakefulness in the cat. I. Spontaneous activity.

Abstract: Neuronal discharges were recorded with extracellular microelectrodes in the ventrolateral nucleus (VL) of the thalamus in cats immobilized with gallamine. These animals had been previously implanted with a plastic cylinder under general anaesthesia a few days before chronic recording. The units recorded responded monosynaptically to brachium conjunctivum (BC) stimulation and were at times identified as true thalamo-cortical relay cells by antidromic activation from motor cortex stimulation. The responses obtained from these neurons to single shock stimuli applied to BC were examined during spontaneous episodes of waking (W), slow wave sleep (SWS) and fast wave sleep (FWS).

Total Prolonged Drug-Induced REM Sleep Suppression in Anxious-Depressed Patients

Abstract: Monoamine oxidase inhibitors (MAOI) are a class of drugs which are capable of totally suppressing REM sleep. The MAOI phenelzine was given to six anxious-depressed patients while daily behavioral and EEG sleep records were made. REM sleep was completely suppressed for from 14 to 40 nights. Upon discontinuation of MAOI REM sleep increased as much as 250% above normal levels. The bipolar EEG changes were paralleled by similar changes in depression and anxiety. The behavior of all six patients markedly improved at times when REM sleep was completely absent. Two of the four patients studied after MAOI discontinuation became profoundly anxious with REM compensation. The morning recall of dreams also closely paralleled the presence or absence of REM sleep. Evidence from this study and others indicate that suppression of REM sleep might help to alleviate depression.

Reported vs recorded sleep characteristics.

Abstract: Twenty-one carefully screened normal Ss used to the sleep laboratory filled out sleep and dream logs both at home and after one or more nights in the laboratory. Subjective descriptions of sleep ordinarily associated with reports of "poor" sleep were related to transient episodes of wakefulness. In general, subjective sleep parameters appeared related to episodes of wakefulness rather than to other sleep stages. Abrupt as opposed to gradual awakenings from sleep favored REM period dream recall. Terminal as opposed to earlier REM periods tended to be associated with detailed rather than vague or no-content dream recall. Presleep tension favored longer sleep latencies, while unusual fatigue promoted transient intercurrent wakefulness. By a number of criteria, Ss appeared to sleep better at home than in the lab.

Growth hormone levels during sleep in normal and growth hormone deficient children.

Abstract: Plasma growth hormone levels were determined from samples drawn at 15-minute intervals during the first 2 hours of spontaneous, nocturnal sleep in 16 normal children, one nongrowth hormone deficient dwarf, and three children with hypopituitarism. Depth of sleep was assessed by continuous EEC monitoring. Daytime growth hormone responses to insulin-induced hypoglycemia were also assessed in most of these children and in a larger group of normal and hypopituitary children. In the normal children and in the nongrowth hormone deficient dwarf, increases in plasma growth hormone after the onset of the slow wave pattern on EEG were equivalent to those seen after insulin-induced hypoglycemia. No significant changes in growth hormone levels were seen in the hypopituitary patients. Interpretation of growth hormone levels in blood specimens obtained by serial sampling after the onset of deep sleep appears to be as reliable a method of assessing pituitary function as the levels resulting from insulin-induced hypoglycemia. Although growth hormone analysis of a single sample taken about 1 hour after the onset of deep sleep should exclude the diagnosis of growth hormone deficiency in as many as 70% of the nongrowth hormone deficient individuals, a positive diagnosis of hyposomatotropism must be based on either serial sampling during deep sleep or challenge with insulin and/or arginine.

Reserpine and Sleep

Abstract: Recent studies of the effects of reserpine on human sleep have reported increased rapid eye movement (REM) sleep, and decreased slow-wave (SW) sleep. These results are relevant to theories linking serotonin and the catecholamines to the control of different stages of sleep. However, since reserpine causes release and subsequent depletion of both monoamines, it is difficult to relate changes in sleep profiles to specific alterations in one or the other amine system. The results to be reported here, when compared to those obtained with other treatments which affect the biogenic amines, encourage the view that level and turnover of serotonin are the primary mediators for reserpine-induced modifications of sleep. In two separate experiments, EEG sleep patterns from 20 male Ss were examined following single and repeated oral doses (1 mg) of reserpine. In the single-dose study, reserpine caused increased REM, and decreased SW sleep, effects which became statistically significant on the post-medication (P-M) recovery session. These changes were accompanied by reduced frequency per minute of sigma spindles (stage 2) decreased eye-movement density (stage REM) and a tendency toward increased brief arousals, especially during stage REM. Examination of parameters of the REM cycle revealed that the potentiation of REM sleep was due to its reduced latency of onset, and more frequent cyclic occurrence, not to increased duration of REM episodes. The results of the repeated-dose study replicated and amplified those of the first experiment, showing that medication caused a progressive increase in the amount of stage REM, accompanied by a simultaneous loss of SW sleep. The increase in REM was again due to acceleration of its cycle rather than lengthening of its episodes. During medication, epochs of stage REM were increasingly interrupted by brief arousals, with a simulteneous decline in the density of rapid eye movements. Most of these reserpine effects persisted into the P-M recovery session.

Absent Sleep Peak of Growth Hormone Release in Blind Subjects: Correlation with Sleep EEG Stages

Abstract: Absence of the peak of plasma growth hormone levels normally seen following the onset of sleep was observed in five blind subjects. These subjects also displayed a decreased amount of slow wave sleep (stages III and IV) and an increase in time spent in combined stages I, II and rapid eye movement sleep. Insulin hypoglycemia produced a normal rise in plasma growth hormone levels in three subjects so tested.

Differential Effect of Sleep Deprivation on the Two Slow Wave Sleep Stages in the Gat

Abstract: The effect of total sleep deprivation on the sleep stages and their interrelations was studied in 10 cats. EEG, EMG and eye movements were recorded for 24 h after 12 h and 24 h sleep deprivation and after no sleep deprivation. Sleep was divided into three stages: Light slow wave sleep (LSWS), deep slow wave sleep (DSWS) and rapid eye movement (REM) sleep. The total quantities of DSWS and REM sleep in the 24 h recordings increased with deprivation, as did the relative proportion (per cent of total sleep) of these sleep stages. The total quantity of LSWS did not change with sleep deprivation, and the LSWS per cent of total sleep decreased. The changes were most pronounced after 24 h deprivation and in the first hours of recovery sleep. Sleep deprivation reduced LSWS episode length and tended to increase DSWS and REM sleep episode length. The number of sleep cycles was increased, but the length of each cycle was not altered. The results support earlier findings of a functional dissociation between LSWS and DSWS and a functional relationship between DSWS and REM sleep.

The pharmacology of rapid eye movement sleep.

Abstract: Publisher Summary This chapter discusses the pharmacology of rapid eye movement sleep. Sleep is rest, quiescence, a time when bodily functions subside to a low point. Its purpose is surcease and restoration. Sleep can be defined as a rhythmical and temporary interruption of wakefulness, induced by internal, not external, factors, in which consciousness of environmental features subsides to a minimum; in which movement of the body is almost completely absent; in which there is an increase in the thresholds of reactivity and of reflex irritability; in which there occurs a continuum which leads from light sleep to deep sleep; in which there occurs, also, a rhythmical alternation of this light sleep-deep sleep cycle; in which at the peak of each of these cycles, certain functions become accelerated and, at least in the human, there occurs the phenomenon of dreaming; and in which there exists a built-in mechanism which after a time produces the phenomenon of arousal.

Diurnal and nocturnal sleep stage patterns following sleep deprivation

Abstract: The extent to which the propensities for Stage 4 and REM sleep are dependent upon amount of sleep loss, length of prior wakefulness, and circadian factors was examined. Diurnal and nocturnal sleep stage patterns in eight male and four female Ss were studied following 24 and 36 h of sleep deprivation, respectively. Stage 4 increased on day (p <.01) and night (p <.001) recovery but remained confined to the first third of sleep on both conditions. REM latency was reduced on day recovery (p <.05), but percentage REM did not change following sleep deprivation. The propensity for Stage 4 appears to be influenced by the amount of sleep loss and that for REM by circadian factors.

Electroencephalogram and Sensory Evoked Potentials: Findings in an Unresponsive Patient With Pontine Infarct

Abstract: The unusual finding of clinical unresponsiveness in association with an electroencephalogram resembling wakefulness has been related to lesions of the human neuraxis extending up to the photomesencephalic junction. In such a patient in whom an extensive infarct of the pons induced a state of clinical unresponsiveness, we were able to demonstrate the presence of a nearly normal EEG which included a driving response to intermittent photic stimulation, summated photic evoked responses within the range of normal variability, and slow wave sleep patterns. Evoked responses to clicks and the rapid eye movement phase of sleep were absent. Although alert behavior was never observed, it is felt that caution should be exercised in interpreting the significance of this finding in any mute paralyzed patient who exhibits an EEG pattern resembling wakefulness.

Effect of carbon monoxide exposure on human sleep and psychomotor performance.

Abstract: Four volunteers exposed for 9 hr (11 p.m. to 8 a.m.) to 75 or 150 ppM CO had COHb concentrations of 5.9 and 12.7%, respectively. Sleep habits and subsequent performance were measured. CO induced slight changes in sleeping habits including more deep sleep at expense of light sleep (especially at beginning of exposure) and a reduction in number of sleep stage changes. However, REM sleep was not affected. No effect of CO on complex cognitive or psychromotor activity measured by mental arithmetic, time estimation, tracking and monitoring under moderate or heavy stress, tone-time difference estimation, and critical flicker fusion tests.

Longitudinal Sleep Study in Hypomania

Abstract: The sleep pattern of a hypomanic patient, was studied for 17 of 25 consecutive nights during which time he received no drug therapy. There was a marked reduction in actual sleep time and in slow-wave sleep and a modest reduction in stage 1 rapid eye movement (REM) sleep. There was increase in time awake and drowsy, and there was an abnormal mixture of wave forms. There is a striking similarity between the sleep pattern of this patient and that recorded from psychotic depressives. This may be of importance in furthering our understanding of the relationship between mania and depression.

Effects of fenfluramine on sleep-wakefulness in cats

Abstract: Five cats were prepared with chronically implanted electrodes for recording sleep-wakefulness patterns. Four of these animals received fenfluramine at each of three dose levels and data was recorded for the following 12 hours. Percent of time in paradoxical sleep was significantly reduced by 2.5 and 7.5 mg/kg, but not by 0.5 mg/kg, of fenfluramine. The higher doses also increased slow-wave sleep and, at 7.5 mg/kg (an anorexigenic dose), total sleep time was significantly increased. Under similar conditions amphetamine, at an anorexigenic dose of 1 mg/kg, significantly suppressed both paradoxical sleep and slow-wave sleep in three cats.

Growth hormone secretion during sleep: impairment in glucose tolerance and nonsuppressibility by hyperglycemia.

Abstract: Intravenous and oral glucose tolerance tests were done and EEG were monitored on healthy subjects following nights of normal sleep, following nights during which deep sleep and concomitant GH release were delayed until early in the morning, and following nights in which deep sleep and GH elevation were deprived. Glucose tolerance tests were also done at 1:00 am while awake and while sleeping, 90 min following the GH-release deep sleep period. Glucose tolerance was unchanged following the night of deep sleep deprivation, during which time no GH peaks were found. However, following deep sleep during which GH release occurred, significant glucose intolerance was seen. Glucose intolerance was demonstrated both in the sleeping subject at 1:00 am and in the awake subject on the morning following deep sleep and concomitant GH release delay. Serum immunoreactive insulin concentrations during the glucose tolerance tests following GH release were unchanged as compared to control. Sustained hyperglycemia pr...

Chlorpromazine and human sleep

Abstract: The aim of this study was to examine human physiological sleep profiles, including the amount and distribution of electroenoephalographic (EEG) stages of sleep, variations in specific frequency bands in the EEG spectrum and certain phasic phenomena such as movement arousals, sigma spindles and rapid eye movements, following oral administration of a moderate dose (150 mg) of chlorpromazine (CPZ) to 12 young male volunteers. At this dose level the drug had few systematic effects on sleep, although it did reduce the latency of onset of stage REM and the number of movement arousals, while increasing the amount of slow-wave (SW) sleep. These effects persisted during the post-medication recovery night, but at no time was there any systematic change in the total amount or percent of REM sleep, the duration of the REM-to-REM cycle, the average length of REM episodes or the density of rapid eye movements during stage REM. Frequency analysis of EEG revealed that CPZ produced a trend toward increased fast (beta) activity recorded from pre-central placements during stage REM, and reduced density of sigma spindles in stage 2 sleep. Thus, for the most part, a single moderate dose of CPZ left the tonic, phasic and sequential properties of the sleep cycle unaltered. These results confirm previous investigations showing that for small to moderate clinical doses, CPZ invariably enhances SW sleep and reduces the frequency of movement arousals. On the other hand, the effect of the drug on stage REM apparently depends on dose. Small doses potentiate REM sleep or accelerate its onset, whereas larger doses either reduce stage REM or leave it unaffected. Several authors have pointed out that most hypnotic agents cause substantial alterations of the sleep profile, and that their withdrawal can cause profound disruption of sleep and marked clinical disturbance. It also has been suggested that there exists a relation between drug dependency and the degree of initial REM suppression caused by a drug. The finding confirmed by the present study that clinical doses of CPZ cause mild sedation, and enhanced SW sleep without any significant modification of REM, sleep, indicates that CPZ has features which may recommend it as a standard hypnotic.

Anemia in sleep-deprived rats receiving anticoagulants.

Abstract: Independent groups of rats were deprived of sleep and treated with the anticoagulant drugs phenylindanedione or dicoumarol for 1 to 8 days. These animals developed an extremely severe anemia which was accelerated by p-chlorophenylalanine. The red cell count and amount of hemoglobin decreased to half of normal values. No decrease occurred in animals subjected to any one single treatment. Histological examination indicated hemolysis, hypoplasia of hemopoietic organs, slight hemorrhage, but no evidence of stress. The severity of the anemia was inversely related to the amount of sleep permitted during sleep deprivation. This new syndrome demonstrates marked effects of sleep deprivation on both maturation and destruction of red blood cells. Depletion of serotonin by injection of parachlorophenylalanine blocked the increase in amount of brain waves of the type commonly seen in slow wave sleep but did not eliminate the production of these waves. This result is at variance with the theory that serotonin is the neurochemical responsible for the "priming" of slow wave sleep.

“Sleep Apnoea” and Sleep Regulating Mechanism –A case effectively treated with monochlorimipramine–

Abstract: The patient was a 69-year old male, with apnoea-tonic convulsion in sleep as the chief complaint. Over the period of 17 years prior to his admission to our clinic he had been treated as a case of night epilepsy, without improvement but aggravation. Satisfactory results of our treatment are briefly summarized as follows. 1) Anticonvulsants including diphenyl-hydantoin proved ineffective, and phenobar-bital aggravated seizures markedly. 2) Methyl phenidate and imipramine or monochlorimipramine proved to be effective, and the last drug was completely suppressed the sleep apnoea. During 15 months after discharge the continuous use of this drug has effectively inhibited the seizures up to date. 3) EEG of our case shows abnormal sleep pattern which has no deep sleep pattern. And no remarkable EEG changes were observed before and after administration of monochlorimipramine, but body movements during sleep were more frequent after the administration. 4) By recording EEG at the onset of this seizure there was recognized flat EEG suggesting that the tonic convulsion occurring after apnoea is an anoxic convulsion. 5) As for the action mechanism of monochlorimipramine, on the basis of our findings that this sleep apnoea is closely associated with a certain depth of sleep, which resembles sleep paralysis of narcolepsy, and it has been concluded that the action mechanism of imipramine and monochlorimipramine is directed to the disturbance of sleep regulating mechanism. 6) It is assumed that the mechanism of the present case consists of visceral crisis of tabes dorsalis, resultant hypoexcitability of the brain stem reticular activating system and disturbance of sleep regulating mechanism.