Rapid eye movement sleep

About: Rapid eye movement sleep is a research topic. Over the lifetime, 3740 publications have been published within this topic receiving 183415 citations. The topic is also known as: REM sleep & REMS.

The dose effects of zolpidem on the sleep of healthy normals.

Abstract: This study determined the dose effects of zolpidem in 12 healthy males with normal sleep patterns. Subjects spent 7 weeks, 3 consecutive nights per week, in the laboratory and had a 4-night washout between treatments. The first week was a screening and adaptation week. Then subjects received zolpidem (2.5, 5.0, 7.5, 10.0, or 20.0 mg) or placebo on the first two nights for each of the next 6 consecutive weeks. Treatments were organized in a Latin square design and administered in a double-blind fashion. On the third night of each treatment, subjects always received placebo. The 5.0 mg and larger doses of zolpidem significantly decreased latency to persistent sleep and wake before sleep. Sleep maintenance measures were not affected by zolpidem. The 7.5 mg and higher doses of zolpidem significantly increased total sleep time. The only significant sleep stage effect was a decrease in percent of rapid eye movement sleep at only the 20 mg dose. No consistent discontinuation effects were found. Zolpidem was hypnotically active at doses as low as 5.0 and 7.5 mg, and sleep stage effects occurred only at the 20 mg dose, thus separating the dose range of hypnotic and sleep stage effects.

Effect of caffeine on sleep: eeg study in late middle age people

Abstract: 1 The effect of caffeine alkaloid base (300 mg) on whole night sleep was investigated by electrophysiological techniques in six late middle age subjects (mean age 56 years), comparison being made with decaffeinated coffee and with no drink prior to sleep, using each condition five times in a balanced order on non-consecutive nights. 2 After caffeine the mean total sleep time decreased on average by 2 h, the mean sleep latency increased to 66 minutes. The number of awakenings increased and the mean total intervening wakefulness was more than doubled after caffeine. 3 In the first 3 h of sleep a decreased amount of stage 3 + 4 was observed, accompanied by an increased amount of stage 2 and of intervening wakefulness, without a significant change in the amount of rapid eye movement sleep. 4 The change in sleep pattern observed suggests an increased capability for arousal and decreased ability to develop or sustain deeper stages of non-rapid eye movement sleep after caffeine.

Serotonergic dorsal raphe neurons cease firing by disfacilitation during paradoxical sleep

Abstract: Using in vivo extracellular unit recordings combined with microdialysis infusion in the cat, we found that the cessation of discharge of presumed serotonergic dorsal raphe neurons during paradoxical sleep (PS) was completely blocked by either histamine or phenylephrine, an alpha1 adrenoceptor agonist, but not by bicuculline, a GABA receptor antagonist. In addition, application of mepyramine, a specific H1 histamine receptor antagonist, or prazosin, a specific alpha1 adrenoceptor antagonist, suppressed the spontaneous discharge of raphe neurons during both quiet waking and sleep. The present data suggest that this cessation of dorsal raphe unit activity is caused by the mechanism of disfacilitation resulting from the cessation of discharge of norepinephrine- or histamine-containing neurons during PS.

Sleep and sleep electroencephalogram in depressed patients treated with phenelzine.

Abstract: Background: The beneficial effect of antidepressant interventions has been proposed to depend on suppression of rapid eye movement (REM) sleep or inhibition of electroencephalographic (EEG) slow-wave activity (SWA) in non-REM sleep. Use of the monoamine oxidase inhibitor phenelzine sulfate can eliminate REM sleep. We studied the relation between REM sleep suppression and antidepressant response and the effect of phenelzine therapy on sleep EEG power spectra. Methods: Open-labeled prescriptions of 30 to 90 mg of phenelzine were given to 11 patients with major depressive disorder (6 men and 5 women; mean age, 41.4 years); all were physically healthy. Mood, dream recall, sleep, sleep EEG, and ocular and muscular activity during sleep were studied before treatment and during the third and fifth weeks of pharmacotherapy. Results: Sixpatientsremittedfromdepression,2responded partially, and 3 showed no antidepressant response. Independent from clinical response, REM sleep was dramatically suppressed. On average, only 4.9 minutes of REM sleep was observed in treatment week 5, and it was completely absent in 6 patients. This effect was compensated for by increased stage 2 sleep. In non-REM sleep, EEG power was higher than at baseline between 16.25 and 25 Hz. Slow-wave activity (power within 0.75-4.5 Hz) and the exponential decline of SWA during sleep were not affected. Conclusions: Antidepressant response to phenelzine treatment does not depend on elimination of REM sleep or inhibition of SWA in non-REM sleep. In depressed patients, REM sleep is regulated independently from nonREM sleep and can be manipulated without altering the dynamics of SWA. Arch Gen Psychiatry. 2001;58:268-276