REM sleep deprivation diminishes fear in rats.

To test the hypothesis that REM sleep deprivation decreases fear, the behavior of 44 rats was measured in an open-field test. Prior to this test, the animals were exposed to 4 days to one of four treatments, i.e., either a dry environment control, a wet environment control, a 2-day REM deprivation period, or a 4-day REM deprivation period. During the test both exploration and three parameters of emotionality were recorded. The results offered convincing evidence in support of the hypothesis.     

REM sleep deprivation increases aggressiveness in male rats.

As a test of the hypothesis that REM deprivation increases aggressiveness in rats, the effects of two and four days of REM deprivation were measured on the frequency and latency with which male rats attack mice. The results showed that REM deprivation increased the frequency of attacks, the muricide rate, and the latency to first attack in a “dose-related” fashion. To a degree these behaviors persisted through a 21-day recovery period.     

REM sleep deprivation and food competition in male rats

As a test of the hypothesis that REM deprivation lowers the threshold for “motivational” behaviors, 17 male rats that had been REM deprived were tested against 17 non-deprived male rats in three series of food competition tests, i.e., an immediate, a 3 hr, and a 48 hr series of posttreatment tests. The results provide support for the hypothesis that REM deprivation generally activates “motivational” behaviors, in that the REM deprived animals won more frequently as had been predicted. However, the response gradients of the two groups over the course of the postteatment test series did not conform to prediction. These data are discussed together with the results of other studies which suggest that perhaps the list of behaviors which have been subsumed under the category—“motivational behaviors” is too broad to be of real scientific value.     

The effect of a REM sleep deprivation procedure on different aspects of memory function in humans

Previous studies have suggested that memory is dependent on the occurrence of REM sleep. Research has mainly focused on two distinct types of memory function, declarative and procedural, and it seems that the latter may more directly depend on REM sleep. Memory consolidation has been more investigated than acquisition, maintenance, and recall, despite the fact that sleep may affect flow of information into/from storage. Moreover, tests have often been limited to stimuli within only one modality (usually visual or verbal). This study aimed to clarify the role of REM sleep in memory by investigating aspects of memory function, processing, and modality in the same experimental setting. Tests of acquisition and consolidation of multiple aspects of memory function within the visual and verbal modalities were administrated to subjects before and after REM sleep deprivation. Results show that test performance was not affected by REM sleep deprivation.     

Non-REM sleep as a source of learning deficits induced by REM sleep deprivation.

Procedures that deprive animal subjects of rapid eye movement sleep have often been associated with learning impairments. Previously, the conclusion has been drawn that these learning impairments are due to the absence of some positive function of rapid eye movement sleep. The present research indicates more precisely that typical impairments associated with the deprivation procedures may be due to isolated periods of non-REM sleep, rather than due to the simple absence of rapid eye movement sleep. Mice were tested for acquistion of a complex maze task, and subjected to post-trial rapid eye movement sleep deprivation by the pedestal method. Only animals demonstrating (non-REM) sleep behaviors during deprivation gave evidence of learning deficits.     

REM sleep deprivation affects extinction of cued but not contextual fear conditioning

Previous research has demonstrated that rapid eye movement (REM), or paradoxical, sleep deprivation can interfere with the retention of certain types of learning tasks, particularly spatial learning. The present study investigated the effects of 6 h of REM sleep deprivation on the retention and extinction of both cued and contextual conditioning tasks in rats. Sleep-deprived animals showed normal retention of both types of conditioning tasks but retarded extinction of the cued task and a trend toward attenuated spontaneous recovery of the contextual task. The results provide further evidence for the involvement of REM sleep in learning and memory processes.     

Short-term homeostasis of REM sleep assessed in an intermittent REM sleep deprivation protocol in the rat

An intermittent rapid eye movement (REM) sleep deprivation protocol was applied to determine whether an increase in REM sleep propensity occurs throughout an interval without REM sleep comparable with the spontaneous sleep cycle of the rat. Seven chronically implanted rats under a 12 : 12 light-dark schedule were subjected to an intermittent REM sleep deprivation protocol that started at hour 6 after lights-on and lasted for 3 h. It consisted of six instances of a 10-min REM sleep permission window alternating with a 20-min REM sleep deprivation window. REM sleep increased throughout the protocol, so that total REM sleep in the two REM sleep permission windows of the third hour became comparable with that expected in the corresponding baseline hour. Attempted REM sleep transitions were already increased in the second deprivation window. Attempted transitions to REM sleep were more frequent in the second than in the first half of any 20-min deprivation window. From one deprivation window to the next, transitions to REM sleep changed in correspondence to the amount of REM sleep in the permission window in-between. Our results suggest that: (i) REM sleep pressure increases throughout a time segment similar in duration to a spontaneous interval without REM sleep; (ii) it diminishes during REM sleep occurrence; and (iii) that drop is proportional to the intervening amount of REM sleep. These results are consistent with a homeostatic REM sleep regulatory mechanism that operates in the time scale of spontaneous sleep cycle.     

REM sleep deprivation impairs bar-press acquisition in rats

Brief REM sleep deprivation immediately after training temporarily retarded bar-press acquisition, abolished observational learning of the bar-press habit, and prevented adaptation to a shift from a CRF to a DRL schedule. These results support the information-processing model of REM sleep function.     

REM sleep deprivation impairs latent extinction in rats

Preextinction exposure to some aspects of the nonreward condition has been shown to facilitate extinction of bar pressing. Deprivation of REM sleep immediately following preextinction experience blocked this facilitation. REM sleep appears to be necessary for assimilation of the preextinction experience.     

Effects of age on recovery of body weight following REM sleep deprivation of rats

Chronically enforced rapid eye (paradoxical) movement sleep deprivation (REM-SD) of rats leads to a host of pathologies, of which hyperphagia and loss of body weight are among the most readily observed. In recent years, the etiology of many REM-SD-associated pathologies have been elucidated, but one unexplored area is whether age affects outcomes. In this study, male Sprague-Dawley rats at 2, 6, and 12 months of age were REM sleep-deprived with the platform (flowerpot) method for 10-12 days. Two-month-old rats resided on 7-cm platforms, while 10-cm platforms were used for 6- and 12-month-old rats; rats on 15-cm platforms served as tank controls (TCs). Daily changes in food consumption (g/kg(0.67)) and body weight (g) during baseline, REM-SD or TCs, and post-experiment recovery in home cages were determined. Compared to TCs, REM-SD resulted in higher food intake and decreases in body weight. When returned to home cages, food intake rapidly declined to baseline levels. Of primary interest was that rates of body weight gain during recovery differed between the age groups. Two-month-old rats rapidly restored body weight to pre-REM-SD mass within 5 days; 6-month-old rats were extrapolated by linear regression to have taken about 10 days, and for 12-month-old rats, the estimate was about 35 days. The observation that restoration of body weight following its loss during REM-SD may be age-dependent is in general agreement with the literature on aging effects on how mammals respond to stress.     

Negative transfer abolished by REM sleep deprivation in rats

Brief deprivation of REM sleep (REMD) immediately following inhibitory avoidance training abolished negative transfer in an active avoidance situation without impairing retention of the inhibitory avoidance response. REMD beginning 3 hr after inhibitory training had no effect. A reminder treatment (brief placement in the apparatus) between 30 min and 24 hr before active avoidance training counteracted the REMD impairment of negative transfer. The reminder treatment was not impaired by subsequent REMD.     

Swimming immobility of REM sleep deprived rats reared in different environments

This study tested the hypothesis that environmental rearing treatments which alter the REM sleep levels of rats affect swimming immobility, an adaptive, REM sleep sensitive behavior. At weaning, 72 female Sprague-Dawley rats were maintained in either an enriched, an impoverished, or a social control environment for 32–33 days. They were then placed in either a REM sleep depriving platform-in-water condition or in one of two control conditions (large platform or dry control) for 4 days before being scored for swimming immobility during a 10-min swimming test. A 3 (environments) × 3 (platforms) ANOVA revealed a main effect for environments, F(2,63)=5.20, p<0.01. Enriched rats exhibited a behavioral advantage over impoverished rats under the large platform control condition, F(1,63)=6.58, p<0.025, and under the dry control condition, F(1,63)=6.14, p<0.025. However, under the REM depriving condition, their behavioral advantage was virtually eliminated, F(1,63), p<1. The conclusion that the REM sleep levels of the rat groups probably determined their swimming immobility scores is discussed.     

Rapid eye movement sleep deprivation does not affect fear memory reconsolidation in rats

There is increasing evidence that sleep may be involved in memory consolidation. However, there remain comparatively few studies that have explored the relationship between sleep and memory reconsolidation. At present study, we tested the effects of rapid eye movement sleep deprivation (RSD) on the reconsolidation of cued (experiment 1) and contextual (experiment 2) fear memory in rats. Behaviour procedure involved four training phases: habituation, fear conditioning, reactivation and test. Rats were subjected to 6 h RSD starting either immediately after reactivation or 6 h later. The control rats were returned to their home cages immediately after reactivation and left undisturbed. Contrary to those hypotheses speculating a potential role of sleep in reconsolidation, we found that post-reactivation RSD whether from 0 to 6 h or 6 to 12 h had no effect on the reconsolidation of both cued and contextual fear memory. However, our present results did not exclude the potential roles of non-rapid eye movement sleep in the reconsolidation of fear memory or sleep in the reconsolidation of other memory paradigms.     

A selective serotonin reuptake inhibitor reduces REM sleep in the homing pigeon

Avian and mammalian 'rapid eye movement' sleep (REM sleep) resemble each other in several aspects. However, the question of whether REM sleep has a shared evolutionary ancestry in birds and mammals has yet to be thoroughly explored. The brain regions and neurotransmitter systems involved in the generation of mammalian REM sleep are phylogenetically ancient, and are also found in extant birds and reptiles. Several pharmacological experiments in birds indicate that similar neural substrates are involved in the regulation of avian and mammalian sleep. However, because the drugs used in these studies generally resulted in non-specific sleep loss, the neurochemical regulation of avian REM sleep in particular remains uncertain. The selective serotonin reuptake inhibitor (SSRI) zimelidine is known to reduce REM sleep in mammals. If avian REM sleep is similarly regulated by serotonin, it would be expected that an acute dose of a SSRI should also reduce avian REM sleep. To investigate a putative role of serotonin in the regulation of avian REM sleep, changes in sleep electroencephalogram (EEG) and behavior were recorded in five pigeons (Columba livia) after the administration of an acute dose of zimelidine. Our results demonstrate that the effects of zimelidine on avian REM sleep are comparable to those observed in mammals, indicating that serotonin may serve a similar function in the control of avian and mammalian REM sleep.     

The light/dark difference in meal size in the laboratory rat on a standard diet is abolished during REM sleep deprivation

Using a modified flowerpot technique, by which it was possible to use test animals as their own controls, the meal patterns of eight adult male rats were recorded before, during and after rapid eye movement sleep (REMs) deprivation. The results demonstrated that the prominent light/dark (LD) difference in meal size, typical of the baseline meal pattern, was abolished during REMs deprivation. This equalization was entirely due to reduction in meal size during the dark hours. After termination of REMs deprivation the size of the dark meals increased almost to the baseline level. However, the LD difference was not restored since the size of the light meals was also significantly increased. Changes in meal frequency were confined to the period of REMs deprivation. The possible role of REMs as a modulator of meal size in relation to the LD cycle of illumination is discussed.     

Effects of REM deprivation on the lordosis response induced by gonadal steroids in ovariectomized rats

Ovariectomized rats were submitted to REM sleep deprivation (REMd) using the water tank technique and their behavioral responsiveness (lordosis) to gonadal steroids was tested. In Experiment 1, animals received 2 micrograms of estradiol benzoate (EB) followed by 2 mg of progesterone (P) 44 hours later. Several REMd periods (12, 72, 96 and 120 hr) were applied, all ending four hr after P. REMd animals showed significantly lower lordosis quotients (LQ) than undisturbed sleep animals regardless of the duration of the deprivation period. In Experiment 2, animals received a single dose of EB (2 micrograms) and were REMd for 120 hours. Animals were tested daily to evaluate their LQ. EB, at this dose level, failed to elicit significant lordosis behavior in undisturbed sleep rats. REMd rats gradually increased their LQ values reaching maximal levels at 72 hours. Adrenalectomized control groups receiving the same hormonal treatment responded similarly to the experimental groups, thus discarding the participation of adrenal steroids in these effects. The present results show that REMd differentially affects the response to E and P in ovariectomized rats, enhancing the former and inhibiting the latter.     

Intrahippocampal administration of anandamide increases REM sleep

A nascent literature has postulated endocannabinoids (eCBs) as strong sleep-inducing lipids, particularly rapid-eye-movement sleep (REMs), nevertheless the exact mechanisms behind this effect remain to be determined. Anandamide and 2-arachidonyl glycerol, two of the most important eCBS, are synthesized in the hippocampus. This structure also expresses a high concentration of cannabinoid receptor 1 (CB1). Recent extensive literature supports eCBs as important regulators of hippocampal activity. It has also been shown that these molecules vary their expression on the hippocampus depending on the light–dark cycle. In this context we decided to analyze the effect of intrahippocampal administration of the eCB anandamide (ANA) on the sleep–waking cycle at two points of the light–dark cycle. Our data indicate that the administration of ANA directly into the hippocampus increases REMs in a dose dependent manner during the dark but not during the light phase of the cycle. The increase of REMs was blocked by the CB1 antagonist AM251. This effect was specific for the hippocampus since ANA administrations in the surrounding cortex did not elicit any change in REMs. These results support the idea of a direct relationship between hippocampal activity and sleep mechanisms by means of eCBs. The data presented here show, for the first time that eCBs administered into the hippocampus trigger REMs and support previous studies where chemical stimulation of limbic areas triggered sleep.     

The pendulum technique for paradoxical sleep deprivation in rats

A new technique for paradoxical sleep (PS) deprivation in rats is presented. Animals are prevented from entering into PS by allowing them to sleep for only brief periods of time. This is accomplished by an apparatus which moves the animals' cages backwards and forwards like a pendulum. At the extremes of the motion postural imbalance is produced in the animals forcing them to walk downwards to the other side of their cages. A minimal amount of PS and a moderate amount of slow wave sleep (SWS) were detected during a deprivation period of 72 hrs. Following the deprivation treatment the recovery of sleep was monitored for 3 hrs; at the beginning of the light period for one group and at the beginning of the dark period for a second group. The sleep-waking patterns of two baseline groups were established at the time when the recovery sleep was examined in the deprivation groups. The deprivation treatment resulted in a significant increase in the amount of PS and a significant decrease in the amount of SWS. The extent of PS increase was similar in both deprivation groups, in spite of a large difference in the amount of SWS. The decrease of SWS mainly occurred during recovery sleep in the light. It was observed that sleep in the dark differs from sleep in the light in behavioural aspects.     

Sleepiness and REM Sleep Recurrence: The Effects of Stage 2 and REM Sleep Awakenings

Determinants of daytime sleepiness include sleep length, sleep continuity, and circadian factors. Sleep stage composition has not been seen as influencing subsequent daytime functioning; however, earlier studies did not focus explicitly on sleepiness. The present experiment studied the effects of selective sleep-stage restriction on an objective measure of sleep tendency, and explored the relationship between sleepiness and subsequent REM recurrence during REM deprivation. Daytime sleep latency was measured by a modified Multiple Sleep Latency Test prior to and following two nights of awakenings from either REM or Stage 2 sleep in 16 normal young adults. Sleep latency following these awakenings was also measured. REM sleep and Stage 2 awakenings produced comparable levels of sleepiness, both during the Awakening Nights and subsequent daytime Multiple Sleep Latency Testing. Pooling the groups, daytime and nocturnal sleepiness measures were correlated within individuals. In the REM-Awakening Group, Pre-Awakening daytime sleepiness was associated with the tendency for REM sleep to recur following experimental awakenings. Comparable levels of sleepiness may result from nonspecific processes such as sleep curtailment and fragmentation, or alternatively from separate REM and Stage 2 mechanisms. The relationship between REM sleep and sleepiness is discussed in the context of both state and trait models.     

Quantification of electromyographic activity during REM sleep in multiple muscles in REM sleep behavior disorder

STUDY OBJECTIVES: The aim of our study was to determine which muscle or combination of muscles (either axial or limb muscles, lower or upper limb muscles, or proximal or distal limb muscles) provides the highest rates of rapid eye movement (REM) sleep phasic electromyographic (EMG) activity seen in patients with REM sleep behavior disorder (RBD). SETTING: Two university hospital sleep disorders centers. PARTICIPANTS: Seventeen patients with idiopathic RBD (n = 8) and RBD secondary to Parkinson disease (n = 9). INTERVENTIONS: Not applicable. MEASUREMENTS AND RESULTS: Patients underwent polysomnography, including EMG recording of 13 different muscles. Phasic EMG activity in REM sleep was quantified for each muscle separately. A mean of 1459.6 +/- 613.8 three-second REM sleep mini-epochs were scored per patient. Mean percentages of phasic EMG activity were mentalis (42 +/- 19), flexor digitorum superficialis (29 +/- 13), extensor digitorum brevis (23 +/- 12), abductor pollicis brevis (22 +/- 11), sternocleidomastoid (22 +/- 12), deltoid (19 +/- 11), biceps brachii (19 +/- 11), gastrocnemius (18 +/- 9), tibialis anterior (right, 17 +/- 12; left, 16 +/- 10), rectus femoris (left, 11 +/- 6; right, 9 +/- 6), and thoraco-lumbar paraspinal muscles (6 +/- 5). The mentalis muscle provided significantly higher rates of excessive phasic EMG activity than all other muscles but only detected 55% of all the mini-epochs with phasic EMG activity. Simultaneous recording of the mentalis, flexor digitorum superficialis, and extensor digitorum brevis muscles detected 82% of all mini-epochs containing phasic EMG activity. This combination provided higher rates of EMG activity than any other 3-muscle combination. Excessive phasic EMG activity was more frequent in distal than in proximal muscles, both in upper and lower limbs. CONCLUSION: Simultaneous recording of the mentalis, flexor digitorum superficialis, and extensor digitorum brevis muscles provided the highest rates of REM sleep phasic EMG activity in subjects with RBD.