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PubMed2000

Granulocyte-macrophage colony-stimulating factor modulates rapid eye movement (REM) sleep and non-REM sleep in rats.

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a hematopoietic cytokine that may affect various functions of the CNS because the molecule and its receptors are expressed in the brain. The present study examines the effects of GM-CSF on sleep using rats and the secretion of three neurotransmitters/hormones that are involved in sleep regulation. When infused intracerebroventricularly at doses as low as 10 pmol for 10 hr during the dark period, GM-CSF promoted predominantly rapid eye movement (REM) sleep and moderate amounts of non-REM sleep without eliciting fever. An injection of GM-CSF (3.0 pmol) into the arcuate nucleus increased the release of nitric oxide (NO) from the hypothalamus but did not alter plasma levels of growth hormone. The release of somatostatin (SRIF) from the medial basal hypothalamus was stimulated by 1 x 10(-)(11) M GM-CSF. These findings indicated that centrally administered GM-CSF stimulates SRIF release through activation of the NO system in the hypothalamus. Because SRIF promotes REM sleep, it may also mediate the effects of GM-CSF on REM sleep. The present study indicates a novel central effect of GM-CSF that modulates sleep, supporting the notion that hematopoietic cytokines also play roles in the CNS.

Animals↗
PubMed1993

Arousal responses to added inspiratory resistance during REM and non-REM sleep in normal subjects.

BACKGROUND: Arousal in response to increased airflow resistance during sleep, especially rapid eye movement sleep (REM), could be an important protective mechanism against asphyxia. METHODS: The arousal response to the application of an external inspiratory resistance of 25 cm H2O/l/s was determined during REM and non-REM sleep in ten healthy men. RESULTS: The number of arousals occurring within two minutes of the load application was significantly higher during REM sleep than during either of the non-REM sleep stages 2 and 3/4, and was similar to that during stage 1. The proportion of arousals to non-arousals decreased significantly from stage 1 to stage 4. The mean time to arousal in REM was significantly shorter than in non-REM stages 1, 2 or 3/4 and increased significantly from stage 1 to stage 3/4. The duration of sleep (comparing the results of the first with the second half of the sleep period time) did not modify the arousal response in stages 2 and 3/4. CONCLUSIONS: The results show a significantly increased arousal response to an added inspiratory resistive load in REM sleep compared with non-REM sleep stages 2, 3 or 4 in normal men. In the context of previous studies these data could add support to the hypothesis that the decreased arousal response during REM sleep in patients with sleep apnoea might be due to an impairment of the normal "central processing" of this stimulus.

Adult↗
PubMed1993

Symposium: Normal and abnormal REM sleep regulation: Dreaming and REM sleep.

The discovery, 40 years ago, of REM sleep and of its putative association with dreaming in the adult human raised the possibility that neuroscientific investigations of REM-sleep physiology would someday 'explain' the distinctive features of dream experience. I argue here against the possibility, since replicated psychological data demonstrate that REM sleep is neither a necessary nor a sufficient condition for dreaming to occur. Dreaming depends, rather, upon the possession of conscious representational intelligence in conjunction with any psychophysiological state in which ideation is being driven neither volitionally nor by external stimulation.

Journal Article↗
PubMedDate not supplied

Increased voluntary alcohol drinking concurrent with REM-sleep deprivation.

The alcohol intake of twenty adult Long-Evans male rats was recorded before, during and after rapid eye movement sleep (REM) deprivation produced with the flowerpot technique modified by using a cuff pedestal and an electrified grid floor instead of water. The alcohol intake reached a steady level of 2.8 g/kg/day in the 3 weeks before REM deprivation. During seven REM-sleep deprivation days the alcohol intake was significantly elevated, finally increasing to 3.7 g/kg/day. A rebound decrease in alcohol drinking was then observed during the "REM-rebound" phase immediately after the termination of REM-sleep deprivation. The results suggest a possible vicious circle of REM-sleep deprivation increasing alcohol drinking and alcohol intake causing REM-sleep deprivation.

Alcohol Drinking↗
PubMed1983

REM sleep burst neurons, PGO waves, and eye movement information.

Pontogeniculooccipital (PGO) waves appeared almost simultaneously in both lateral geniculate nuclei (LGB), but in each case on had a larger amplitude and preceded the other by a few milliseconds. The larger, earlier wave is called the primary wave. Primary waves were found to appear with equal frequency in each LGB. During rapid eye movement sleep (REM sleep), LGB primary waves were ipsilateral to the direction of rapid eye movements. During REM sleep a group of cat midbrain neurons, which we call PGO burst cells, fired in stereotyped bursts at fixed latencies before ipsilateral primary waves, but they almost never fired bursts when the primary waves were contralateral. PGO burst neuron discharge also correlated with the direction of rapid eye movements during REM sleep. In wakefulness, PGO burst cells fired single spikes, not bursts, which had some correlation with LGB waves when averaged by computer. The results suggest that PGO burst cells are output elements in the PGO wave-generation system ad that PGO waves convey eye movement information to the sensory visual system in REM sleep. They also may have a role in the production of saccade-related waves in the visual system during wakefulness.

Action Potentials↗
PubMed1986

An analgesic effect of enkephalinase inhibition is modulated by monoamine oxidase-B and REM sleep deprivations.

Both the MAO-B inhibitor deprenyl (2.5-10 mg/kg, ip, 60 min prior) and the MAO-B substrate beta-phenylethylamine (PEA, 40 micrograms, icv) potentiated the analgesic action of the enkephalinase inhibitor phosphoramidon (250 micrograms, icv) in animals allowed normal sleep. The enhancing effect of PEA on phosphoramidon analgesia was further potentiated by deprenyl (5 mg/kg, ip) pretreatment. Deprenyl (5 mg/kg, ip) or PEA (40 micrograms, iv) given alone did not induce analgesia in animals allowed undisturbed sleep. REM sleep deprivation (REMSD) decreased the basal pain threshold and abolished the analgesic effect of phosphoramidon. The administration of deprenyl and/or PEA failed to restore the analgesic effect of phosphoramidon in REM sleep deprived animals. The results indicate that excess PEA has a stimulatory effect on the analgesic activity of endogenously released enkephalins in rats allowed undisturbed sleep but not in REM sleep deprived animals. It is suggested that the failure of phosphoramidon to induce analgesia after REMSD, is probably due to a functional insufficiency of an enkephalinergic system.

Animals↗
PubMed1990

REM sleep deprivation during 5 hours leads to an immediate REM sleep rebound and to suppression of non-REM sleep intensity.

Nine healthy male subjects were deprived of REM sleep during the first 5 h after sleep onset. Afterwards recovery sleep was undisturbed. During the deprivation period the non-REM EEG power spectrum was reduced when compared to baseline for the frequencies up to 7 Hz, despite the fact that non-REM sleep was not experimentally disturbed. During the recovery interval a significant rebound of REM sleep was observed, which was only accompanied by a very slight increase of power in the lower non-REM EEG frequencies. In order to control for intermittent wakefulness, the same subjects were subjected to non-REM sleep interruption during the first 5 h after sleep onset 2 weeks later. Again subsequent recovery sleep was undisturbed. The interventions resulted in a similar amount of wakefulness in both conditions. During the intervention period, the non-REM EEG power spectrum was only marginally reduced in the delta frequency range. REM sleep duration was only slightly reduced. During the recovery interval, however, a substantial increase in EEG power in the delta frequency range was noted, without notable changes in REM time. It is concluded that an increased pressure for REM sleep results in longer REM episodes and a reduced intensity of non-REM sleep.

Adult↗
PubMed2000

Circadian and homeostatic control of rapid eye movement (REM) sleep: promotion of REM tendency by the suprachiasmatic nucleus.

The daily timing of rapid eye movement (REM) sleep reflects an interaction between the circadian pacemaker located in the suprachiasmatic nucleus of the hypothalamus (SCN) and a homeostatic process that induces compensatory REM sleep in response to REM sleep loss. Whether the circadian variation in REM sleep propensity is caused by active promotion, inhibition, or passive gating of REM sleep homeostasis by the SCN is unknown. To investigate these possibilities, compensatory responses to 24 hr REM sleep deprivation (RSD) were compared between SCN-lesioned (SCNx) and sham-lesioned rats at different times of day in constant dark. The attempts to enter REM sleep (REM tendency) increased during RSD in all rats and were modulated by circadian phase in sham-lesioned, but not SCNx rats. REM sleep homeostasis interacted with circadian time, such that REM tendency doubled during the rest phase in sham-lesioned rats relative to SCNx rats (F((6,93)) = 17.9; p = 0.0001). However, REM tendency was indistinguishable between SCNx and sham-lesioned rats during the activity phase, suggesting the SCN does not inhibit REM tendency at this time. By contrast, the amount of compensatory REM sleep examined 2, 6, 12, or 24 hr after RSD did not depend on circadian phase. Thus, transitions into REM sleep are facilitated by the SCN during the rest phase, but the amount of REM sleep, once initiated, is determined primarily by homeostatic mechanisms. This work supports a role for the SCN in the active promotion of REM sleep at specific times of day.

Animals↗
PubMed2001

Extracellular serotonin levels in the medullary reticular formation during normal sleep and after REM sleep deprivation.

Rapid eye movement (REM) sleep is hypothesized to result from the activity of REM sleep-generating and REM sleep-inhibiting neurons. The serotoninergic (5-HT) neurons of the dorsal raphe nucleus (DRN) represents one such population of REM-sleep inhibiting neurons since they are silent during REM sleep. Consistent with the decrease in activity of 5-HT neurons, the brain extracellular levels of 5-HT are lower during REM sleep compared to wakefulness. It is not known whether serotonin release is also reduced as a consequence of REM sleep rebound. Using microdialysis sampling coupled to HPLC-ECD, we measured the extracellular levels of 5-HT and its metabolite (5-HIAA) in the medial medullary reticular formation (mMRF) of freely behaving rats during normal sleep, REM sleep deprivation as well as during REM sleep rebound. We found that the levels 5-HT and 5-HIAA were significantly decreased by REM sleep deprivation. The reduction of 5-HT release was maintained during REM sleep rebound but the extracellular level of its main metabolite was increased. In addition, even during REM sleep rebound, 5-HT release during sleep was low compared to wakefulness. Taken together these data support the permissive role of 5-HT neurotransmission for REM sleep expression.

Animals↗
PubMed1993

Symposium: Normal and abnormal REM sleep regulation: The importance of REM sleep for brain maturation.

A number of studies, some done by us, are reviewed concerning the function of foetal/neonatal REM sleep. The hypothesis is put forward that REM sleep in early life serves as an indicator for: (1) the degree of brain maturation, and (2) the promotion of further brain development. This hypothesis, although not exclusive, differs from: the original theory of Roffwarg et al. (1966) that REM sleep serves as "wakefulness" during the period in which wakefulness is limited; and also from the theory of Crick and Mitchson (1983-the "unlearning" hypothesis of REM sleep). As the functions of sleep in general, and REM sleep in particular, are still unclear, we hope this review will suggest new possibilities for future research.

Journal Article↗
PubMed1992

Biperiden administration during REM sleep deprivation diminished the frequency of REM sleep attempts.

Sixteen subjects were assigned to a group using either placebo or biperiden, with eight subjects in each group. Both groups were studied for one acclimatization night, one baseline night, four nights of rapid eye movement (REM) sleep deprivation and two recovery nights. All the subjects received either placebo or 4 mg biperiden 1 hour before sleep during the four nights of REM sleep deprivation. During the baseline and the recovery nights both groups received placebo capsules. The results showed that REM sleep time during the REM sleep deprivation was reduced by 70-75% below the baseline night in both groups. The number of attempts to enter REM sleep was significantly reduced by biperiden as compared to placebo for each of the four REM sleep deprivation nights. Because the total sleep time in the biperiden group was reduced, the number of REM sleep attempts was corrected by the total sleep time. The adjusted number of REM sleep attempts was also significantly reduced in the biperiden group. REM sleep latency showed a reduction in the placebo group, whereas in the biperiden group REM sleep latency was unchanged throughout the deprivation nights. In the recovery night REM sleep time was increased in both groups, with no differences between the groups. The REM sleep latency showed a reduction in the first recovery night in both groups that persisted through the second recovery night. The above findings support the role of biperiden as a REM sleep suppressive drug.

Adult↗
PubMed1998

Nefazodone and REM sleep: how do antidepressant drugs decrease REM sleep?

In previous uncontrolled studies, nefazodone, a new antidepressant drug, increased REM sleep or had no effect on REM sleep. We report a double-blind, placebo-controlled, parallel group study on effects of nefazodone (N) on polysomnographic sleep variables in healthy human volunteers. Nefazodone was administered for 16 consecutive days, and nocturnal sleep, as well as multiple sleep latency test (MSLT), was monitored before, during, and after N administration. We found that N had no effect on any measured REM sleep variable including REM sleep duration, REM density, and nocturnal REM sleep distribution. Nefazodone also had no significant effect on nocturnal total sleep time or NREM variables, but increased daytime alertness measured by the MSLT. Since N is a potent serotonin reuptake blocker, the present findings that N had no effect on REM sleep cast doubt on the hypothesis that antidepressant drugs decrease REM sleep by increasing serotonergic neurotransmission. A review of other relevant work also casts doubt on this hypothesis.

Adolescent↗
PubMed1999

Alpha activity in the human REM sleep EEG: topography and effect of REM sleep deprivation.

The topographical distribution of alpha activity (8.125-11.125 Hz) in the REM sleep EEG, its time course within and across REM sleep episodes, and the effects of selective REM sleep deprivation were investigated in 8 young males. Power spectra of bipolar derivations along the antero-posterior axis in the left (F3C3, C3P3, P301) and right (F4C4, C4P4, P402) hemisphere were calculated. Alpha activity increased along the antero-posterior axis in both hemispheres, and was dominant in the right hemisphere. It decreased within and across REM sleep episodes. Selective REM sleep deprivation resulted in a reduction of alpha activity in the REM sleep EEG. However, the topographical distribution and the time course were not affected. It is suggested that alpha activity in the REM sleep EEG is a marker of REM sleep homeostasis.

Brain↗
PubMed1975

Differential effects of chlorpromazine, imipramine, nitrazepam and amobarbital on REM sleep and REM density in man.

The effect of chlorpromazine (CPZ), imipramine (IMP), nitrazepam (NZP) and amobarbital sodium (AMOB) on the REM period of sleep (REMP) was investigated on four subjects by means of all-night sleep polygraphy with the schedule PPPDDDPP where P is placebo and D active drug. CPZ 25 mg resulted in a slight increase in %REMP, and no significant change in REM density (1 second fraction method) and total REM activity during the drug and withdrawal nights. IMP 25 mg produced moderate decrease in %REMP in the three drug nights, whereas REM density decreased only in the first drug night. NZP 5 mg resulted in a slight parallel suppression of %REMP, REM density and total REM activity during the drug nights. AMOB 200 mg produced a slight decrease in %REMP and marked decrease in REM density during the drug nights. Rebound increase of %REMP and a tendency of carry over decrease of REM density were observed in the withdrawal nights. Decrease in the REM density was more marked in AMOB than in NZP drug night. The importance of the simultaneous analysis of %REMP and REM density for the study of effects of psychotrophic drugs on sleep was emphasized.

Adult↗
PubMed1984

Theta rhythm during REM sleep and waking: correlations between power, phase and frequency.

Short segments of hippocampal EEG in the rat were recorded during rapid-eye-movement sleep (REM) and active waking behaviors. Fourier analysis was used to reveal the time-varying changes of theta power, frequency, coherence and phase in stratum radiatum (apical dendritic layer) of CA1 region. In all cases studied during REM sleep or active waking, a significant, positive correlation of radiatum theta phase and peak theta frequency was found. The radiatum phase was found to range from 100 to 170 degrees and increased towards 180 degrees at high (7.8-8.6 c/sec) theta frequency. Electrodes at sites other than stratum radiatum did not show this phase-frequency relation. By selectively averaging across spectra of EEG with the same selected peak theta frequency, it was found that the power at the first or second theta harmonic, the integrated power of fast EEG (30-100 c/sec) and the radiatum theta phase all generally increased with increasing theta frequency. The results indicate that the radiatum theta phase (and frequency) is dynamically varying during normal behaviors. Together with previous findings on the pharmacology of theta phase, the results suggest that both atropine-sensitive and atropine-resistant inputs are present during normal behaviors.

Animals↗