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.

Fluoxetine in major depression: efficacy, safety and effects on sleep polygraphic variables.

Abstract: Fluoxetine (60 mg), a selective inhibitor of the reuptake of 5-HT, was compared in a double-blind trial to amitriptyline (150 mg) in a sample of 34 patients fitting the Research Diagnostic Criteria for a major depressive disorder. Patients were studied after a drug washout period of 10 days and an active treatment period of 42 days. Sleep polygraphic recordings were performed before and at the end of the study. As indicated by the significant decrease in the Hamilton Depression scale and the Montgomery Asberg Depression scale, fluoxetine showed similar antidepressant effects to amitriptyline with significantly fewer adverse effects. Fluoxetine and amitriptyline decreased the amount of REM sleep, a well known effect of classical antidepressants. Fluoxetine showed some specific effects on sleep continuity (potentially dose related) as indicated by the significant increase in the number of awakenings and in stage shifts, without interfering with the therapeutic response.

The effect of venlafaxine on behaviour, body weight and striatal monoamine levels on sleep-deprived female rats.

Abstract: Partial sleep deprivation is clinically associated with fatigue, depressive symptoms and reduced memory. Previously, it has been demonstrated that venlafaxine, an atypical antidepressant, increases the levels of noradrenaline and serotonin in rat hippocampus. The aim of this study was to evaluate the effects of venlafaxine on depression, anxiety, locomotor activity and memory in a model of REM sleep (REMs) deprivation in rats. We have also studied the influence of venlafaxine on monoamine levels in the striatum. Six groups of animals (N=20 each) were treated with saline or venlafaxine (1 or 10 mg/kg) during 10 days, submitted or not to REMs deprivation and studied with the forced swimming test of Porsolt (STP), plus-maze, passive avoidance and open-field tests right after sleep deprivation. Animals were also studied for passive avoidance 24 h later (rebound period). Brain samples for monoamine measurements were collected either immediately after REMs deprivation or after 24 h. Both REMs deprivation and venlafaxine showed an antidepressant effect. An anxiolytic effect was also observed after REMs deprivation. Previous treatment with venlafaxine blocked the antidepressant and anxiolytic effects of REMs deprivation. REMs deprivation alone and treatment with venlafaxine 10 mg/kg increased locomotor activity, and this effect was inhibited by venlafaxine in REMs deprived rats. Both venlafaxine treatment and REMs deprivation induced weight loss. Venlafaxine treatment, but not REMs deprivation, induced an increase in striatal dopamine (DA) levels. The combination of REMs deprivation and venlafaxine treatment was associated with an increase in serotonin turnover 24 h after rebound sleep. In this study, venlafaxine treatment hindered most behavioral effects of REMs deprivation and was associated with an interference on dopamine and serotonin systems in the striatum.

Circadian and arousal state influences on thermoregulation in the pigeon.

Abstract: We report here the characteristics of spinal thermosensitivity in pigeons as a function of arousal state and time of day. At any time in the light-dark (LD) cycle, the thresholds for shivering and panting were lower during non-rapid-eye-movement (NREM) sleep than during wakefulness. These thresholds in both awake and sleeping animals were lower during D than during L. The gain of the metabolic response to spinal cooling was nearly the same in wakefulness and NREM sleep. Shivering and panting responses to spinal thermal stimulations were impaired during REM sleep compared with wakefulness and NREM sleep. The results support the idea that central nervous system mechanisms controlling arousal states and circadian rhythmicity have separate and additive influences on temperature regulation in the pigeon.

Estradiol and Progesterone Modulate Spontaneous Sleep Patterns and Recovery from Sleep Deprivation in Ovariectomized Rats

Abstract: NATURAL CHANGES IN ESTRADIOL AND PROGESTERONE LEVELS ACROSS THE MENSTRUAL CYCLE, AND ESPECIALLY DURING PREGNANCY AND MENOPAUSE, have been associated with sleep disturbances and changes in sleep EEG in women.1,2 Hormone replacement therapy (estradiol, progesterone, or both) can improve sleep quality in postmenopausal women under baseline conditions.3–8 It is unclear, however, whether hormone replacement therapy can reduce cognitive performance deficits resulting from sleep deprivation9,10 or facilitate sleep recovery after sleep deprivation.11 Given the prevalence of chronic, partial sleep deprivation12 and the frequency with which women are given hormone treatments,13–15 it is important to determine whether and how such treatments may influence the ability to recover lost sleep. Rodents have been used frequently as models to examine the effects of ovarian hormones on sleep. Changes in hormonal levels during the estrous cycle were associated with changes in sleep patterns,16–20 whereas in ovariectomized rats, estradiol treatment reduced sleep, especially rapid eye movement sleep (REMS), under baseline conditions.21–27 The effects of hormonal changes associated with estrous cycles on recovery sleep after sleep deprivation may not, however, parallel those on baseline sleep. Despite baseline differences in sleep, intact rats did not show estrous cycle-related differences in amounts of non-REMS (NREMS) and REMS during recovery, nor in NREMS EEG delta activity (an index of NREMS intensity and drive), after 6 h of sleep deprivation.28 In mice, neither ovariectomy29 nor lack of aromatase (an enzyme that converts testosterone into estradiol)30 affected recovery REMS or NREMS delta activity after 6 h of sleep deprivation. Although these studies suggest that endogenous sex hormones do not influence recovery sleep after 6 h of sleep deprivation in rodents, the stage of the estrous cycle at the beginning of 4 days of REMS deprivation has been reported to affect the pattern of recovery sleep.31 Nonetheless, the clinically more relevant question of whether hormone replacement after loss of ovarian hormones affects the ability to compensate for lost sleep has not been addressed directly using rodent models. To examine whether and how replacement of estradiol and/or progesterone after ovariectomy modulates the pattern of baseline sleep and recovery sleep after 6 h of sleep deprivation, we implanted estradiol- and/or progesterone-containing capsules subcutaneously in ovariectomized adult rats. These capsules produced relatively stable physiological levels of circulating hormones. The analytic advantage of this approach is that it allows comparisons between baseline sleep and recovery sleep after sleep deprivation under identical hormonal conditions. This is not possible using intact females, because estrous cycles do not include intervals with stable hormonal levels that are long enough to accommodate lengthy baseline and recovery periods, particularly during proestrus and estrus when estradiol and progesterone levels change rapidly.32,33 Gonadally intact and hormonally untreated male rats were studied for comparison.