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PubMed1989

The phosphorylated analogue of DSIP enhances slow wave sleep and paradoxical sleep in unrestrained rats.

Continued 10-h nocturnal intracerebroventricular infusion of 0.5 nmol P-DSIP, the phosphorylated analogue of delta-sleep-inducing peptide (DSIP), significantly increased slow wave sleep (22%) and paradoxical sleep (81%) in unrestrained rats. The increase in the amount of sleep was largely due to an increase in the number of sleep episodes. Larger and smaller doses were ineffective in doses ranging from 0.025 to 25 nmol. The sleep-promoting potency of P-DSIP was 5 times greater than that of DSIP compared by the same assay.

Animals↗
PubMed1989

Effects of sleep interruption on REM-NREM cycle in nocturnal human sleep.

Forty-four normal male students, aged 18-23 years were studied. After adaptation and baseline night (BN), 3 or 4 consecutive nights were interrupted by a forced awakening (10-90 min) once a night (ENs). Subjects (Ss) were awakened after they had slept for the first sleep cycle plus 20 min of NREM sleep in the 2nd cycle. The REM latencies following return to sleep showed a bimodal distribution separated by 25-30 min. The ENs were divided into 2 clusters: SOREMP (sleep onset REM period) and non-SOREMP nights. After interruption, the 2nd and the 3rd REM durations increased on non-SOREMP nights compared to SOREMP nights. We plotted, separately for SOREMP and non-SOREMP nights, the fluctuation of REM episode probability (FRP) at successive points in time. We examined the correspondence of FRPs derived from the sleep-independent, the sleep-dependent, and the reset hypotheses, with FRP of intact BN. On both SOREMP and non-SOREMP nights, none of the 3 models corresponded with BN. Thus, we suggest that, for both SOREMP and non-SOREMP nights, intervening wakefulness cancels the pre-awakening REM rhythm, and a new REM rhythm starts with or without SOREMP. We discuss factors influencing the rate of SOREMP occurrence (SOREMP %), such as circadian effect, individual differences, length of interruption, and pre-awakening NREM duration.

Adult↗
PubMed1976

Neurohumoral correlates of sleep: further biochemical and physiological characterization of sleep perfusates.

Twenty cats were prepared surgically with electrodes for recording the EEG, Eye Movements and EMG and a push-pull cannula system in the midbrain reticular formation (MRF) allowing the extraction of perfusates during wakefulness or REM sleep. Proteins in the perfusates were analyzed by Isoelectric Focusing (IEF) polyacrylamide gels and Sodium Dodesyl Sulphate (SDS) slab gels. In addition analysis of glycoproteins was done by gas chromatography. In some cats the contribution of cerebrospinal fluid (CSF) proteins to perfusate proteins from brain tissue was studied by intraventricular injections of labelled leucine. The effect of sleep alterations on the protein cycle during sleep and wakefulness was also studied. The results of these experiments showed that most of the proteins in the perfusates are acidic, and that REM sleep perfusates contain 2 proteins M.W. 73.000 and 45.000 not present in awake perfusates, CSF or serum. It was also shown that CSF proteins do not appear to contribute to the proteins in perfusates, and that altering the sleep wake cycle, induces changes in the rhythm of protein release in perfusates. It is suggested that some relatively large polypeptides may participate in the regulation of REM sleep.

Animals↗
PubMed1988

Sleep-promoting effect following intracerebroventricular injection of a phosphorylated analogue of delta sleep-inducing peptide (DSIP-P) in rats.

The effect of phosphorylated delta sleep-inducing peptide (DSIP-P) on sleep of rats was studied. DSIP-P (20 or 200 pmol/kg) was injected into the third cerebroventricle of male rats immediately before the onset of the dark period of a 12:12 h light-dark cycle. DSIP-P resulted in increases of slow-wave sleep (SWS) (17.3%, P less than 0.01) and paradoxical sleep (PS) (32.3%, P less than 0.05) during the subsequent dark period without shortening sleep latency in the dose of 200 pmol/kg. The SWS-promoting effect was carried over to the next light period. These changes returned to control levels on the second day. These results indicate that DSIP-P is a long-lasting sleep-promoting substance in rats.

Animals↗
PubMedDate not supplied

High doses of systemic DHEA-sulfate do not affect sleep structure and elicit moderate changes in non-REM sleep EEG in rats.

The hormone dehydroepiandrosterone (DHEA) and its metabolite DHEA-sulfate (DHEAS) occur in huge quantities in the plasma as well as in the brain of vertebrates. To investigate whether DHEAS modulates sleep-wake behavior, we assessed the sleep response to three doses (25, 50, and 100 mg/kg) of intraperitoneally administered DHEAS, mixed with oil, in 8 rats. DHEAS injections produced dose-dependent and long-lasting elevations in the plasma levels of both DHEAS and DHEA. DHEAS administration did not affect sleep time and architecture but exerted persistent effects on the electroencephalogram (EEG) within non-rapid eye movement sleep: 50 mg/kg DHEAS significantly augmented EEG power in the frequency range of sleep spindles, and 100 mg/kg DHEAS depressed EEG power in the slow-wave frequency bands. The findings indicate that DHEAS changes the sleep EEG in a dose-dependent way, possibly through a modulation of GABA- and glutamate-induced currents.

Analysis of Variance↗
PubMed2002

Non-rapid-eye-movement sleep propensity after sleep deprivation in human subjects.

The circadian modulation of occurrence of non-rapid-eye-movement sleep (NREM) was investigated in 37 volunteers under dim-light conditions after 24-h total sleep deprivation using a 26-h 10/20-min ultra-short sleep-wake schedule. The propensity of NREM showed rapid increase followed by gradual decrease during the subjective day and nocturnal bouts during the subjective night coinciding with melatonin production. The mean propensity of NREM during the subjective day was smaller than that during the subjective night, even though the sleep debt due to the 24-h sleep deprivation would have enhanced NREM more strongly during the subjective day than that during the subjective night. These results suggest that the occurrence of NREM sleep is modulated by a circadian pacemaker.

Adult↗
PubMed2004

Midlife women's responses to a hospital sleep challenge: aging and menopause effects on sleep architecture.

OBJECTIVE: To distinguish aging from menopause effects on sleep architecture, we studied an episode of disturbed hospital sleep in asymptomatic midlife women during the follicular phase of an ovulatory cycle and three control groups differing by age or menopause status. METHODS: Fifty-one studies were conducted in four groups of volunteers: young cycling (YC, 20-30 years, n = 14), older cycling (OC, 40-50 years, n = 15), ovariectomized receiving estrogen therapy (OVX, 40-50 years, n = 12), and spontaneously postmenopausal (PM, 40-50 years, n = 10). Subjects were admitted to the University Hospital General Clinical Research Center (GCRC) for a first-night sleep study conducted during a 24-hour, frequent blood sampling protocol. RESULTS: Despite similar estrogen concentrations in the YC (28 +/- 4 pg/ml) and OC (34 +/- 6 pg/ml) groups, OC women had reduced sleep efficiency (79% +/- 2%) vs. YC (87% +/- 3%; p = 0.009). In the OVX and PM groups where estrogen concentrations were markedly different, sleep efficiency was also reduced vs. the YC group (OVX vs. YC, 79% +/- 3% vs. 87% +/- 3%, p = 0.05; PM vs. YC, 75% +/- 3% vs. 87% +/- 3%, p = 0.007). Wake time was longer in the three older groups (103 +/- 10 minutes, 101 +/- 12 minutes, 123 +/- 12 minutes for OC, OVX, PM, respectively) vs. YC (63 +/- 13 minutes, p < 0.05). The number of stage shifts was positively associated with advancing age (rho = 0.3, p < 0.03) but not with estrogen concentration. CONCLUSIONS: Aging-related sleep deficits in response to an experimental stressor occur in midlife women prior to menopause.

Adult↗
PubMed1988

Stability of EEG sleep and sleep quality in healthy seniors.

When the electroencephalogram-recorded (EEG) sleep of 19 healthy seniors (9 men, 10 women) aged 60-82 years was restudied after an average interval of 2.2 years, most measures of EEG sleep and sleep quality were stable over time. Both elderly men and women showed more awakenings during the second recording series, but no change in visual or computer-scored delta activity. Furthermore, gender-dependent sleep changes were noted only in phasic rapid eye movement (REM) measures (increasing in men, decreasing in women). Reports of sleep quality were also stable over time despite the increase in awakenings, with women reporting a lower sleep quality than men.

Aged↗
PubMed1991

Acute deprivation of the terminal 3.5 hours of sleep does not increase delta (0-3-Hz) electroencephalograms in recovery sleep.

Sleep electroencephalograms (EEG) and electrooculograms were recorded in nine young adult males on a baseline night, a night in which they were deprived of an average of 3 hr 27 min of sleep by early awakening, and on a recovery night. Records were analyzed by visual sleep stage scoring and period-amplitude analysis; the results of both were tabulated by successive nonrapid eye movement periods (NREMPs) and rapid eye movement (REM) periods. Neither visually scored delta nor REM measures were affected by this substitution of waking for sleep. Although there was a significant increase in the 0-3-Hz time/epoch on the recovery night, this finding was not confirmed in the accompanying report. These results, taken in association with data from previous studies, are consistent with the hypothesis that, in an acute experiment, visually scored delta and computer-measured 0-3-Hz EEGs increase above the baseline levels only if there has been loss of stage 3/4 EEG (or of sleep) from the first two NREMPs. The findings here are inconsistent with older reports and indicate that further parametric data are required to construct a quantitative model of the relation of sleep EEG waveforms to the duration of prior waking.

Adult↗
PubMed2004

Clonidine effects on all-night human sleep: opposite action of low- and medium-dose clonidine on human NREM-REM sleep proportion.

Norepinephrine (NE) is considered to play a permissive role in the occurrence of rapid eye movement (REM) sleep. Clonidine is an NE alpha-2-receptor agonist, which has been considered to act mainly on the autoreceptors of presynaptic noradrenergic neurons to reduce their release of NE. However, previous studies of clonidine effects on REM sleep have produced controversial results and the effects of clonidine remain uncertain. To clarify the pharmacological effects of clonidine on human sleep, the sleep electroencephalograms (EEG) recorded from 15 young normal subjects after a single administration of either a low (25 micro g) or medium (150 micro g) dose of clonidine were examined, and fast Fourier transformation (FFT) spectral analyses of the C3-A2 EEG were performed. Low-dose clonidine significantly increased the amount of REM sleep and decreased the amount of non-REM (NREM) sleep during the second one-third of the drug nights compared to the corresponding hours of baseline night recordings. In contrast, medium-dose clonidine significantly decreased REM and increased NREM on drug nights compared to baseline nights in the entire night. The opposite actions of low and medium doses of clonidine on NREM-REM proportion may indicate that low-dose clonidine mainly affects the alpha-2-receptors on locus coeruleus-NE neurons presynaptically, reducing the release of NE, whereas medium-dose clonidine acts more post-synaptically.

Adrenergic alpha-2 Receptor Agonists↗
PubMedDate not supplied

Sleep studies in benign epilepsy of childhood with rolandic spikes. II. Analysis of discharge frequency and its relation to sleep dynamics.

Polygraphic all-night sleep recordings of 11 children with benign epilepsy of childhood with rolandic spikes (BERS) were investigated from the viewpoint of spike distribution. Spike/min ratios were calculated with regard to different sleep stages and waking, identical stages of the consecutive cycles, and stages 1-2 taking place on the descending versus the ascending slopes of sleep cycles. Maximum spike/min ratios were related to slow sleep stages, especially delta sleep, and in general to the first cycle. Stages 1-2 on the descending (DESC) slopes of consecutive cycles showed a decrease in spike density during the night, as opposed to the increasing rate of activation of the same stages on the ascending (ASC) slopes. Based on our results, we suggest that the actual drive of spiking as well as seizures in BERS is the functional overweight of sleep-inducing mechanisms.

Brain↗
PubMed1981

Effects of sleep-promoting factor from human urine on sleep cycle of cats.

Slow-wave sleep (SWS) and rapid-eye-movement sleep (REM) were recorded in cats for 32 h a) under control conditions, b) following intraventricular infusions of artificial cerebrospinal fluid (CSF), and c) following infusions of sleep-promoting factor S prepared from human urine (SPU). During the first 12 h after receiving artificial CSF, the cats slept 4.9 +/- 0.2 h in slow-wave sleep (SWS) and 1.4 +/- 0.1 h in REM. Similar values were obtained from the same cats under control conditions. After infusions of SPU, the duration of SWS in the same cats increased to an average of 6.9 +/- 0.5 h with no significant change in REM averaged over 12 h; a transient decrease of REM in the first 4 h was fully compensated in subsequent hours. The increased SWS induced by the sleep-promoting factor from human urine subsided after 12 h, and there was no compensatory increase in wakefulness during the subsequent 20 h. The normal sleep cycle was not affected. In cats, therefore, the primary effect of SPU is to increase normal SWS, with little effect on REM.

Animals↗
PubMed1986

Brain temperature changes coupled to sleep states persist during interleukin 1-enhanced sleep.

The effects of human interleukin 1 (IL 1) on the architecture of rabbit sleep-wake cycles and brain temperature (Tbr) changes coupled to states of vigilance were examined. Cerebral intraventricular infusion of IL 1 induced increased slow-wave sleep (SWS), increased electroencephalographic slow-wave (0.5-4 Hz) amplitudes, and fever. Heat-inactivated IL 1 failed to elicit these responses. IL 1 also significantly inhibited rapid-eye-movement (REM) sleep; however, inactivated IL 1 also reduced REM sleep; thus some of the IL 1-induced REM reduction may be related to the infusion process. The duration and number of sleep cycles (REM-to-REM interval) were unaffected by IL 1. Similarly, Tbr changes that normally occur during the transition from one arousal state to another remained unchanged after IL 1 infusion, even though rabbits were simultaneously febrile. We conclude that IL 1 selectively enhances SWS while leaving sleep cycles and Tbr changes coupled to states of vigilance undisturbed.

Animals↗
PubMed1994

Constant light suppresses sleep and circadian rhythms in pigeons without consequent sleep rebound in darkness.

Sleep patterns and circadian rhythms of body temperature, activity, body weight, and electroencephalographic (EEG) power spectra of pigeons were compared among three photic conditions: a 12:12-h light-dark cycle (LD), followed successively by constant bright (LL) and dim light (DD) periods. LL suppressed non-rapid-eye-movement and rapid eye movement sleep and circadian rhythms of the measured variables without producing increased drowsiness or other physiological or behavioral changes. Sleep patterns after LL-DD transitions also showed no evidence of prior sleep deprivation during LL. Sleep latency after LL-DD transitions was 93 min longer than after L-D transitions in LD. Total sleep and EEG slow wave activity during the first 24 h in DD did not differ from D in LD. Free-running circadian rhythms subsequently reappeared in DD after LL.

Animals↗
PubMed1995

Noradrenergic activity in rat brain during rapid eye movement sleep deprivation and rebound sleep.

Noradrenergic locus ceruleus neurons are most active during waking and least active during rapid eye movement (REM) sleep. We expected REM sleep deprivation (REMSD) to increase norepinephrine utilization and activate the tyrosine hydroxylase (TH) gene critical for norepinephrine production. Male Wistar rats were deprived of REM sleep with the platform method. Rats were decapitated after 8, 24, or 72 h on small (REMSD) or large (control) platforms or after 8 or 24 h of rebound sleep after 72 h of the platform treatment. During the first 24 h, norepinephrine concentration, measured by high-performance liquid chromatography/electrochemical detection, was lower in the neocortex, hippocampus, and posterior hypothalamus in REMSD rats than in large-platform controls. After 72 h of REMSD, TH mRNA, measured by in situ hybridization, was increased in the locus ceruleus and norepinephrine concentrations were increased. Polygraphy showed that small-platform treatment caused effective and selective REMSD. Serum corticosterone measurement by radioimmunoassay indicated that the differences found in norepinephrine and TH mRNA were not due to differences in stress between the treatments. The novel finding of sleep deprivation-specific increase in TH gene expression indicates an important mechanism of adjusting to sleep deprivation.

Animals↗
PubMed1996

Natural hypothermia and sleep deprivation: common effects on recovery sleep in the Djungarian hamster.

Sleep, daily torpor, and hibernation have been considered to be homologous processes. However, in the Djungarian hamster, daily torpor is followed by an increase in slow-wave activity (SWA; electroencephalogram power density 0.75-4.0 Hz) that is similar to the increase observed after sleep deprivation. A positive correlation was found between torpor episode length and the subsequent increase in SWA, which was highest when SWA was assumed to increase with a saturating exponential function. Thus the increase in SWA propensity during daily torpor followed similar kinetics as during waking, supporting the hypothesis that when the animal is in torpor it is incurring a sleep debt. An alternative hypothesis, proposing that the mode of arousal causes the subsequent SWA increase, was tested by warming the animals during emergence from daily torpor. Irrespective of mode of arousal, more non-rapid eye movement (NREM) sleep and a similar SWA increase was found after torpor. The data are compatible with a putative neuronal restorative function for sleep associated with the expression of SWA in NREM sleep. During torpor, when brain temperature is low, this function is inhibited, whereas the need for restoration accumulates. Recovery takes place only after return to euthermia.

Animals↗
PubMed2000

Systemic injection of a nitric oxide synthase inhibitor suppresses sleep responses to sleep deprivation in rats.

We hypothesized that nitric oxide (NO) may play a role in homeostatic sleep regulation. To test this hypothesis, we studied the sleep deprivation (SD)-induced homeostatic sleep responses after intraperitoneal administration of an NO synthase inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME, a cumulative dose of 100 mg/kg). Amounts and intensity of sleep were increased in response to 8 h of SD in control rats (n = 8). Sleep amounts remained above baseline for 16 h after SD followed by a negative rebound. Rapid eye movement sleep (REMS) and non-REMS (NREMS) intensities were elevated for 16 and 4 h, respectively. L-NAME treatment (n = 8) suppressed the rebound increases in NREMS amount and intensity. REMS rebound was attenuated by L-NAME in the first dark period after SD; however, a second rebound appeared in the subsequent dark period. REMS intensity did not increase after SD in L-NAME-injected rats. The finding that the NO synthase inhibitor suppressed rebound increases in NREMS suggests that NO may play a role as a signaling molecule in homeostatic regulation of NREMS.

Animals↗
PubMed1987

Effects of delta-sleep-inducing peptide on 24-hour sleep-wake behaviour in severe chronic insomnia.

Impaired daytime functions are a significant part of chronic insomnia besides sleep disturbance. Therefore, the effects of intermediate-term delta-sleep-inducing peptide (DSIP) administration on sleep and daytime performance were investigated in 14 middle-aged chronic insomniacs. DSIP was administered under placebo-controlled, double-blind conditions for 7 successive nights. Polysomnograms were obtained for placebo baseline, beginning and end of DSIP treatment, and one placebo posttreatment night; daytime psychological state and mental performance were extensively tested before and after 6 DSIP injections. The treatment substantially improved night sleep with the first and additionally with repeated doses. These effects were maintained for the first posttreatment (placebo) night. Efficiency of night sleep and daytime rest reached the levels of normal controls. Alertness and performance at daytime increased significantly. The study demonstrates the efficacy of DSIP for the treatment of impaired sleep and daytime functions as well.

Adult↗