Biomedical subjects

D J Dijk

Publications and source records attributed to D J Dijk.

90 records · Page 5Linked to original sources

PubMed1990

A quantitative analysis of phasic and tonic submental EMG activity in human sleep.

Submental muscle activity and slow-wave activity in the EEG (mean power density in the 0.75-4.5-Hz band) were determined for consecutive 20-sec epochs in 34 all-night recordings of human sleep. Muscle activity was quantified by calculating the statistical variance of the digitized electromyogram (EMG). The tonic level of muscle activity was lower in REM sleep (REMS) than in nonREMS, and higher in the first nonREMS episode but an increasing trend within all subsequent nonREMS episodes. EEG slow-wave activity increased in the first part of all nonREMS episodes and decreased in the first part of all REMS episodes. The absolute or relative difference in muscle activity between two consecutive 20-sec intervals was used for defining EMG arousals. The density of arousals did not differ significantly among nonREMS episodes. Weak and moderate arousals showed an increasing density over consecutive REMS episodes. While arousals were uniformly distributed within REMS episodes, they were concentrated at the beginning and the end of nonREMS episodes.

Adult↗

PubMed1990

Electroencephalogram power density and slow wave sleep as a function of prior waking and circadian phase.

Human sleep electroencephalograms, recorded in four experiments, were subjected to spectral analysis. Waking prior to sleep varied from 12 to 36 h and sleep was initiated at different circadian phases. Power density of delta and theta frequencies in rapid-eye-movement (REM) sleep and non-REM (NREM) sleep increased monotonically as a function of prior waking. The increase of power density in the theta frequencies contrasts with the reported decrease of theta activity as detected by period-amplitude analysis. Slow wave activity (power density, 0.25-4.0 Hz) in NREM sleep during the first 3 h of sleep did not deviate significantly from the homeostatic process S of the two-process model of sleep regulation. In contrast, visually scored slow wave sleep, stages 3 and 4, deviated from this prediction at some circadian phases. It is concluded that, in accordance with the two-process model of sleep regulation, slow wave activity in NREM sleep depends on prior waking and is not significantly influenced by circadian phase.

Adult↗

PubMed1990

Time course of EEG power density during long sleep in humans.

In nine subjects sleep was recorded under base-line conditions with a habitual bedtime (prior wakefulness 16 h; lights off at 2300 h) and during recovery from sleep deprivation with a phase-advanced bedtime (prior wakefulness 36 h; lights off at 1900 h). The duration of phase-advanced recovery sleep was greater than 12 h in all subjects. Spectral analysis of the sleep electroencephalogram (EEG) revealed that slow-wave activity (SWA; 0.75-4.5 Hz) in non-rapid-eye-movement (NREM) sleep was significantly enhanced during the first two NREM-REM sleep cycles of displaced recovery sleep. The sleep stages 3 and 4 (slow-wave sleep) and SWA decreased monotonically over the first three and four NREM-REM cycles of, respectively, base-line and recovery sleep. The time course of SWA in base-line and recovery sleep could be adequately described by an exponentially declining function with a horizontal asymptote. The results are in accordance with the two-process model of sleep regulation in which it is assumed that SWA rises as a function of the duration of prior wakefulness and decreases exponentially as a function of prior sleep. We conclude that the present data do not provide evidence for a 12.5-h sleep-dependent rhythm of deep NREM sleep.

Adult↗

PubMed1990

Effect of zopiclone and midazolam on sleep and EEG spectra in a phase-advanced sleep schedule.

Midazolam (15 mg), a benzodiazepine (BDZ) hypnotic, and zopiclone (7.5 mg), a non-BDZ hypnotic, were administered to young, healthy subjects prior to bedtime. They went to bed at 2300 hours after taking placebo (PL-23), and then on three occasions at 1900 hour after taking placebo (PL-19) or one of the hypnotics. Advancing bedtime by 4 hour increased the combined value of waking, stage 1, and movement time. Compared to PL-19, both drugs reduced sleep latency and stage 3, and increased stage 2. Spectral analysis of the EEG in non-rapid-eye-movement sleep revealed a declining trend of power density in the low-frequency range in the course of the night. Activity in the 1 to 10 Hz range was markedly depressed by the two hypnotics, whereas activity in the spindle range (11 to 14 Hz) was augmented. The former changes persisted throughout the 12-hour recording period. The fact that both hypnotics bind to BDZ receptors could be responsible for the similar effects on the EEG spectra.

Adult↗

PubMed1989

Effects of seganserin, a 5-HT2 antagonist, and temazepam on human sleep stages and EEG power spectra.

The effects of seganserin, a specific 5HT2 antagonist, on human sleep were assessed in two experiments and compared to the effects of temazepam and sleep deprivation. During daytime recovery sleep after sleep deprivation, seganserin did not significantly enhance visually scored slow wave sleep (SWS, stages 3 + 4) or the EEG power density in the delta frequencies. Under these conditions temazepam reduced the power density in the delta and theta frequencies. During nighttime sleep after a nap in the evening, seganserin caused an increase in SWS, a reduction in intermittent wakefulness, and an enhancement of the power density in the delta and theta frequencies during non-rapid eye movement (NREM) sleep. Temazepam induced a reduction in the power density in the delta and theta frequencies. It is concluded that the 5HT2 antagonist, seganserin, can induce SWS. However, since the spectral results showed that the changes in the sleep EEG were not identical to those induced by sleep deprivation it seems premature to conclude that 5HT2 receptors are primarily involved in NREM sleep regulation.

Adult↗

PubMed1989

Sleep EEG spectral analysis in a diurnal rodent: Eutamias sibiricus.

1. Sleep was studied in the diurnal rodent Eutamias sibiricus, chronically implanted with EEG and EMG electrodes. Analysis of the distribution of wakefulness, nonrapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep over the 24 h period (LD 12:12) showed that total sleep time was 27.5% of recording time during the 12 h light period and 74.4% during the 12 h dark period. Spectral analysis of the sleep EEG revealed a progressive decay in delta power density in NREM sleep during darkness. Power density of the higher frequencies increased at the end of darkness. Power density of the higher frequencies decreased and that of the lower frequencies increased during light. 2. Analysis of the distribution of vigilance states under three different photoperiods (LD 18:6; 12:12; 6:18) revealed that changes in daylength mainly resulted in a redistribution of sleep and wakefulness over light and darkness. Under long days the percentage of sleep during light was enhanced. The time course of delta power density in NREM sleep was characterized by a long rising part and a short falling part under long days, while a reversed picture emerged under short days. As a consequence, the power density during days. As a consequence, the power density during light was relatively high under long days. 3. After 24 h sleep deprivation by forced activity, no significant changes in the percentages of wakefulness and NREM were observed, whereas REM sleep was slightly enhanced. EEG power density, however, was significantly increased by ca. 50% in the 1.25-10.0 Hz range in the first 3 h of recovery sleep. This increase gradually decayed over the recovery night. 4. The same 24 h sleep deprivation technique led to a ca. 25% increase in oxygen consumption during recovery nights. While the results of the EEG spectral analysis are compatible with the hypothesis that delta power density reflects the 'intensity' of NREM sleep as enhanced by prior wakefulness and reduced by prior sleep, such enhanced sleep depth after sleep deprivation is not associated with reduced energy expenditure as might be anticipated by some energy conservation hypotheses on sleep function.

Animals↗

PubMed1989

Effects of SWS deprivation on subsequent EEG power density and spontaneous sleep duration.

In order to test predictions of the 2-process model of sleep regulation, the effects of slow wave sleep (SWS) deprivation by acoustic stimulation during the first part of the sleep period on EEG power density and sleep duration were investigated in 2 experiments. In the first experiment, 8 subjects were deprived of SWS during the first 5 h of a baseline nocturnal sleep period without awakening. Compared to the same interval of undisturbed sleep, power densities in the delta frequencies were attenuated. In the hour following SWS deprivation, power densities in the delta and theta frequencies were considerably enhanced in comparison with the same interval of undisturbed sleep. No change in sleep duration was observed. In the second experiment, 8 subjects were sleep deprived for 1 night and recovery sleep was initiated at 11 a.m. on 2 occasions. In 1 condition subjects were deprived of SWS during the first 3 h of recovery sleep. In the other condition recovery sleep was not experimentally disturbed. During undisturbed recovery sleep, power densities in the delta and theta frequencies were higher than during baseline sleep. During SWS deprivation, power densities in this frequency range were lower than during undisturbed recovery sleep. In the hour following SWS deprivation, power densities were enhanced relative to the same interval of undisturbed recovery sleep. Again, SWS deprivation did not cause an increase of sleep duration. The observed changes in EEG power density support the hypothesis that this EEG parameter reflects the homeostatic process S.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Sex differences in the sleep EEG of young adults: visual scoring and spectral analysis.

Baseline sleep of 13 men (mean age of 23.5 years) and 15 women (21.9 years) was analyzed. Visual scoring of the electroencephalograms (EEGs) revealed no significant differences between the sexes in the amounts of slow-wave sleep and rapid-eye-movement (REM) sleep. Spectral analysis, however, detected significantly higher power densities during non-REM sleep over a wide frequency range (0.25-11.0 Hz) in the female versus male subjects. Also, during REM sleep, power densities were higher in the females. Analysis of the time course of EEG power density during sleep revealed that the differences between males and females persisted throughout the sleep episode. Comparison of these differences with published data on the effects of sleep deprivation on EEG power spectra did not suggest a common mechanism underlying sleep deprivation effects and the sex difference in sleep EEGs. It is concluded that sex differences in EEG power spectra are not likely to be caused by sex differences in sleep regulatory mechanisms but may, for instance, be caused by sex differences in skull characteristics.

Adult↗

PubMed1989

Bright morning light advances the human circadian system without affecting NREM sleep homeostasis.

Eight male subjects were exposed to either bright light or dim light between 0600 and 0900 h for 3 consecutive days each. Relative to the dim light condition, the bright light treatment advanced the evening rise in plasma melatonin and the time of sleep termination (sleep onset was held constant) for an average approximately 1 h. The magnitude of the advance of the plasma melatonin rise was dependent on its phase in dim light. The reduction in sleep duration was at the expense of rapid-eye-movement (REM) sleep. Spectral analysis of the sleep electroencephalogram (EEG) revealed that the advance of the circadian pacemaker did not affect EEG power densities between 0.25 and 15.0 Hz during either non-REM or REM sleep. The data show that shifting the human circadian pacemaker by 1 h does not affect non-REM sleep homeostasis. These findings are in accordance with the predictions of the two-process model of sleep regulation.

Adult↗

PubMed1987

Reduction of human sleep duration after bright light exposure in the morning.

In 8 subjects the spontaneous termination of sleep was determined after repetitive exposure to either bright or dim light, between 6.00 and 9.00 h, on 3 days preceding sleep assessment. Sleep duration was significantly shorter following bright light than following dim light. During sleep the time course of EEG energy was not affected by the light treatment. Analysis of the time course of body temperature during sleep indicated an earlier rise of body temperature following the bright light treatment. In terms of the two-process model of sleep regulation this can be interpreted as a direct effect of light on the circadian phase of the wake up threshold.

Adult↗

PubMed1987

Quantitative analysis of the effects of slow wave sleep deprivation during the first 3 h of sleep on subsequent EEG power density.

The relation between EEG power density during slow wave sleep (SWS) deprivation and power density during subsequent sleep was investigated. Nine young male adults slept in the laboratory for 3 consecutive nights. Spectral analysis of the EEG on the 2nd (baseline) night revealed an exponential decline in mean EEG power density (0.25-15.0 Hz) over successive nonrapid eye movement--rapid eye movement sleep cycles. During the first 3 h of the 3rd night the subjects were deprived of SWS by means of acoustic stimuli, which did not induce wakefulness. During SWS deprivation an attenuation of EEG power densities was observed in the delta frequencies, as well as in the theta band. In the hours of sleep following SWS deprivation both the power densities in the frequency range from 1 to 7 Hz and the amount of SWS were enhanced, relative to the same period of the baseline night. Both the amount of EEG energy accumulating subsequent to SWS deprivation and its time course could be predicted accurately from the EEG energy deficit caused by SWS deprivation. The data show that the level of integral EEG power density during a certain period after sleep onset depends on the amount of EEG energy accumulated during the preceding sleep rather than on the time elapsed since sleep onset. In terms of the two-process model of sleep regulation (Borbély 1982; Daan et al. 1984) this finding indicates that EEG power density reflects the rate of decay of the regulating variable, S, rather than S itself, as was originally postulated.

Acoustic Stimulation↗

PubMed1987

Studies in wild house mice. II. Testosterone and aggression.

The relationship between testosterone level and attack latency was studied in genetically different wild house mice by means of castration and subsequent testosterone therapy. This was done to provide adequate physiological knowledge for further research on the genetic basis of individual differences in these mice. The findings show that individual variation in attack latency is related not only to variation in baseline plasma testosterone level (via a dose-response relation), but also to variation in responsiveness to testosterone that is induced before puberty. In addition it is shown that in fast-attacking mice the maintenance of the attack latency level reached by maturation is independent of testosterone, whereas this is not the case in mice that are reluctant to attack.

Aggression↗

PubMed1987

EEG power density during nap sleep: reflection of an hourglass measuring the duration of prior wakefulness.

The relation between the duration of prior wakefulness and EEG power density during sleep in humans was assessed by means of a study of naps. The duration of prior wakefulness was varied from 2 to 20 hr by scheduling naps at 1000 hr, 1200 hr, 1400 hr, 1600 hr, 1800 hr, 2000 hr, and 0400 hr. In contrast to sleep latencies, which exhibited a minimum in the afternoon, EEG power densities in the delta and theta frequencies were a monotonic function of the duration of prior wakefulness. The data support the hypothesis that EEG power density during non-rapid eye movement sleep is only determined by the prior history of sleep and wakefulness and is not determined by clock-like mechanisms.

Adult↗

PubMed1986

Sleep disorders in depression.

Recently some hypotheses explaining sleep disturbances in depression have been proposed. One hypothesis assumes an advanced phase position of the circadian pacemaker controlling a.o. REM sleep (REMS) production. In another a deficiency of process S is proposed. In this paper the sleep of depressed patients and healthy subjects is compared with respect to REMS production and EEG power density (a possible reflection of process S). Data were derived from the literature and from own experiments. The results provide support only for the S deficiency hypothesis.

Adult↗

PubMed1984

The corticomedial amygdala and learning in an agonistic situation in the rat.

Social agonistic behaviour of intact male rats is strongly reduced by the experience of defeat by a dominant male conspecific. Small electrolytic lesions in the corticomedial amygdala strongly affected this behavioural change due to defeat. No effects of the lesions were observed before and during the defeat. Some learning is still possible in corticomedial amygdala lesioned animals. A comparison of the effects of lesions made before the defeat with lesions made after the defeat revealed that the lesions primarily produce a retention deficit in social learning.

Aggression↗

PubMedDate not supplied

EEG slow waves and sleep spindles: windows on the sleeping brain.

Slow waves and sleep spindles are prominent features of the EEG in non-REM sleep and some of the neurophysiological mechanisms underlying their genesis have been elucidated. In humans, slow-wave activity in non-REM sleep increases and EEG activity in the frequency range of sleep spindles decreases when wakefulness prior to sleep is varied from 2 to 40 h. The opposite changes are observed in the course of sleep, even when sleep is scheduled out of phase with the circadian rhythm of sleep propensity. Within non-REM sleep episodes the association between slow waves and sleep spindles is bi-phasic: both activities are correlated positively at the beginning and end of non-REM sleep episodes whereas in the middle part of non-REM sleep episodes high values of slow-wave activity coincide with low levels of spindle activity. An extension of wakefulness enhances the rise rate of slow-wave and spindle activity at the onset of sleep. Since macroscopic slow waves and sleep spindles both are dependent on hyperpolarization and synchronization of neurons in thalamo-cortical and cortical circuits, the sleep deprivation induced changes in these EEG activities may be related to reduced activating input to thalamo-cortical and cortical neurons, local facilitation of their hyperpolarization or facilitation of their synchronization. The precise regulation of slow-wave and spindle activity as a function of the duration and intensity of prior sleep and wakefulness demonstrates that these EEG oscillations are accurate indicators of non-REM-sleep homeostasis and suggests that they are fundamental to the sleeping brain.

Animals↗

PubMedDate not supplied

All night spectral analysis of EEG sleep in young adult and middle-aged male subjects.

The sleep EEGs of 9 young adult males (age 20-28 years) and 8 middle-aged males (42-56 years) were analyzed by visual scoring and spectral analysis. In the middle-aged subjects power density in the delta, theta and sigma frequencies were attenuated as compared to the young subjects. In both age groups power density in the delta and theta frequencies declined from NREM period 1 to 3. In the sigma frequencies, however, no systematic changes in power density were observed over the sleep episode. In both age groups the decay of EEG power (0.75-7.0 Hz) over successive NREM-REM cycles and the time course of EEG power during NREM sleep was analyzed. The decay rate of both EEG power density over successive NREM-REM cycles and EEG power density during NREM sleep was smaller in the middle-aged subjects than in the young subjects. It is concluded that the age-related differences in human sleep EEG power spectra are not identical to the changes in EEG power spectra observed in the course of the sleep episode. Therefore age-related differences in EEG power spectra cannot be completely explained by assuming a reduced need for sleep in older subjects. The smaller decay rate of EEG power during NREM sleep in the middle-aged subjects is interpreted as a reduced sleep efficiency. The results are discussed in the frame work of the two-process model of sleep regulation.

Adult↗

PubMedDate not supplied

The significance of sleep physiological disturbances in depression.

Since the discovery of the antidepressant effects of interventions in the sleep-wake cycle, a number of hypotheses have emerged according to which disturbances in sleep physiology are not merely expressions but essential components of the pathophysiology of depression. Three hypotheses are presented, the "Phase-advance", the "S-deficiency" and the "ACh-hypersensitivity" hypotheses. They explain the therapeutic effects of total, partial and selective sleep deprivation as consequences of the normalization of disturbed sleep regulation. The question is dealt with whether there are indications that the hypothesized sleep regulatory disturbances exist and whether there is a relationship between the effects of sleep deprivation on sleep regulation and clinical state. None of the hypotheses is totally supported, none can be fully rejected.

Circadian Rhythm↗