Why is paradoxical sleep a paradox

It has been demonstrated to be effective and has no risks of side effects. So, the adjective paradoxical may be used in three distinct ways in reference to topics in sleep medicine. It described a state of sleep that is better known as REM sleep. It refers to a type of insomnia in which sleep is misinterpreted as wakefulness. Finally, it is a useful behavioral technique in which the intention paradoxically becomes an effort to stay awake, rather than to fall asleep.

No matter how it is used, understanding sleep can be enhanced by defining these sorts of terms. If you need additional assistance with your insomnia, find a CBTI specialist in your area and finally put an end to your insomnia.

It may also help to have an evaluation by a board-certified sleep medicine physician who can arrange further testing and treatment. Tossing and turning night over night can have a big impact on your quality of life. Our free guide can help you get the rest you need. Sign up for our newsletter and get it free. Your Privacy Rights. To change or withdraw your consent choices for VerywellHealth. At any time, you can update your settings through the "EU Privacy" link at the bottom of any page.

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I Accept Show Purposes. Was this page helpful? Thanks for your feedback! Sign Up. What are your concerns? Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. This result further supports the hypothesis that the postsynaptic dopaminergic receptors are in a state of supersensitivity.

Alternatively, these data may indicate that pre-synaptic dopaminergic activity was augmented by the above-described treatment regimen.

Ghosh et al. Tufik b reported that such a response was not due to a modification in DA turnover or levels, since it was demonstrated that animals treated with L-DOPA and injected with apomorphine failed to show aggressive behavior.

In a later study, it was shown that the increase in apomorphine-induced stereo-typy and aggression in PSD rats was reversed by DA agonist pretreatment Troncone et al. Interaction between the DA and norepinephrine NOR systems, which was achieved through modulation of the DA drug regimen, induced aggressive behavior in PSD rats that were pretreated with adrenergic drugs.

This result indicates that NOR had a slight inhibitory action on the aggressiveness elicited by dopaminomimetic agents in PSD rats Troncone and Tufik The reduced level of aggression could be due to a small increase in DA release associated with a lack of secondary noradrenergic inhibition rather than to a lack of NOR activity.

This situation would evidence a role for beta-adrenoceptors in the modulation of this behavior. This tissue has been shown to be subsensitive to NOR, which is reflected by evaluation of in vitro cyclic-AMP synthesis Troncone et al.

A large body of evidence indicates that drug-induced yawning in rats is a behavioral consequence of dopaminergic autoreceptor stimulation, which results in decreased DA synthesis and release, impaired dopaminergic transmission, and consequent removal of the inhibition of cholinergic neurons exerted by DA neurons Yamada and Furukawa Thus, yawning behavior seems to involve both dopaminergic inhibition and cholinergic activation.

By evaluating animals after a recovery period of 24h, Neumann et al. It seems that interference on the dopa dopaminergic system occurs more strongly and at an earlier time than on cholinergic system.

With respect to the evidence mentioned above, these findings led to the hypothesis that PSD induces an upregulation of dopaminergic receptors Tufik et al. Nunes et al.

They found that PSD increased D 2 but not D 1 receptor binding in the brain, suggesting that the unregulated D 2 receptors are responsible for the previously reported changes in apomorphine-induced behaviors after PSD. This finding further supports the early studies on behavioral effects of dopaminergic stimulants in PSD animals Tufik et al. However, the decrease in yawning behavior induced by cholinergic agonists Tufik et al. Again, an autoradiographic study showed that PSD resulted in a generalized down regulation of M 2 -type muscarinic receptors in the brain of a rat, corroborating the notion that pontine M 2 -type receptors may participate, but do not necessarily play an integral role, in the development of PSD effects Nunes et al.

Some evidence suggests that PSD enhances serotonergic transmission. Bearing this in mind, direct examination of 5-HT receptor binding after PSD was restricted to early studies that used a non-selective ligand [3H]5-HT in a limited number of brain areas. These studies showed that binding to 5-HT 1a was not significantly altered by PSD in any of the brain areas examined. However, there was an overall trend toward decreased binding in the target paradoxically sleep deprived group.

Orexins are a newly discovered class of neuropeptides that regulate feeding and vigilance. Initially recognized for their importance in appetite control, orexins also called hypocretins are also involved in regulating sleep, arousal, and cardiovascular function.

Loss of orexin appears to be the primary cause of narcolepsy Kilduff and Peyron , Sutcliffe and de Lecea Expression of orexins is restricted to a discrete region of the hypothalamus, but the terminal projections of orexin-producing cells are widely distributed throughout the brain. In the rat, orexin induces a dose-dependent increase in wakefulness when it is injected intracerebroventricularly Piper et al. The densest projection of orexinergic cells in the rat is in the locus coeruleus Horvath et al.

Pedrazzoli et al. Decreased cerebral spinal fluid orexin levels were also observed at ZT8 after 24h of PS rebound. These results suggest that PSD activates and that rebound inhibits the orexin system. The authors suggested that increased orexin tone during PSD might be important for some of the effects of PSD, such as antidepressant effects, hyperphagia, and increased sympathetic activity. Another experiment performed by D'Almeida et al. The OX 1 R mRNA levels increased in more than 30 different regions, particularly in the amygdala and hypothalamus in the rebound group compared to control and sleep deprived groups.

Changes in OX 2 R mRNA levels were also seen only in the sleep rebound group, but the levels were decreased rather than increased, and they were predominantly confined to the cerebral cortex. These observations suggest that continued sleep deprivation progressively increases prepro-orexin mRNA levels and alters orexin receptor expression. These effects are not immediately reversed by sleep recovery, indicating a lasting activation of the orexinergic system.

Collectively, the overall changes in brain neurotransmitters after PSD may indicate that the mechanisms involve in the process of sleep recovery. Sleep deprivation of short duration or prolonged for several days alters the expression of distinct categories of genes in the brain, including immediate-early genes, such as transcription factors; genes that encode proteins involved in metabolic processes, neuronal plasticity, and the stress response; and genes that encode neurotransmitters, hormone receptors and transporters, and enzymes Cirelli et al.

In addition, it has been shown that the pattern of changes is consistent across species Cirelli and in distinct brain regions Cirelli et al. These differentially expressed transcripts include genes from many functional classes, including metabolic processes, the circadian sleep-wake cycle, the response to a stimulus, regulation of cell proliferation, and signaling pathways.

However, as occurs with a number of behavioral and physiological parameters, the expression levels of the remaining Noteworthy, DNA damage is an important step in events leading to genomic instability. We recently conducted an experiment demonstrating that DNA damage was preferentially induced in the brain and blood cells of paradoxically sleep deprived rats, whereas no detectable changes were observed in the liver or heart cells Andersen et al.

This study represents a relevant contribution to the understanding of the potential health risks associated with sleep deprivation. Collectively, these results suggest that PSD elicits a pattern of gene expression that is similar to those observed for other paradigms of sleep deprivation, and that PSD has characteristics that might be related to the regulation of PS.

In addition, 24h of sleep recovery was not sufficient for complete reversal of the effects caused by prolonged periods of PSD of a number of behavioral and physiological parameters Andersen et al.

This study corroborates our results, which indicate that there is less variation in the gene expression in the brain compared to other tissues, such as blood and cavernosum, following PSD Lee et al. This finding suggests that multiple neurotransmitter systems modulate this behavior. PSD for 96h results in nearly complete suppression of yawning induced by dopaminergic and cholinergic agonists Tufik et al. Since the activity of both of these neurotransmitter systems is also altered by stress De Kloet , animals were chronically exposed to different stress modalities.

The evaluation of yawning induced by dopaminergic and cholinergic drugs showed that immobilization caused suppression of this behavior, whereas forced swimming and foot shock increased the number of yawns. These findings suggest that yawning is differentially altered by constant and intermittent stressors Tufik et al.

Neither single nor repeated treatment with DEXA altered apomorphine-induced yawning. A single injection of DEXA, however, caused an increased number of yawns induced by pilocarpine. Repeated treatment with DEXA led to a decreased number of yawns induced by pilocarpine. The authors concluded that dopaminergic and cholinergic systems are distinctly altered by DEXA in terms of yawning behavior. The data suggest that cannabinoid agonists inhibited yawning induced by cholinergic and dopaminergic agonists.

In addition, the increased frequency of spontaneous yawning following cessation of chronic administration of a cannabinoid agonist may be of importance as a withdrawal sign for these drugs Nakamura-Palacios et al.

Cannabis also induces aggressive behavior in PSD rats. This effect is probably related to brain catecholamines, as DA may play an agonist role and NOR an inhibitory role Carlini et al. Sleep has roles in learning and memory processes at several levels Stickgold and Walker Two main lines of evidence support this hypothesis in rodents.

Firstly, PS following the acquisition of learning tasks leads to increases in the number and duration of episodes and PS density Smith and Wong Secondly, many studies report an impaired acquisition when PSD is performed before or after the training period for several learning tasks Smith , Silva et al.

PSD performed before the training period resulted in acquisition deficits that were not task-specific. This is because the procedure affected inhibitory avoidance and an appetite-motivated task Stern In contrast, using appetitive motivation, no effect on accuracy of Tmaze discrimination was found with PSD Hicks and Paulus The nature of the task might be one factor that accounts for these discrepancies. To determine whether PSD administered prior to training would have differential effects on two aversively motivated tasks classical conditioning of fear and inhibitory avoidance , Bueno et al.

The data show that PSD administered 24 or 72h before the training session had no effect on either task. However, when the period of deprivation was extended to 96h before the training session, acquisition of inhibitory avoidance was impaired, but no effect on classically conditioned fear was observed.

Thus, the authors concluded that PSD had differential effects on the two tasks, both aversively motivated and trained at the same time and under the same conditions. Moreover, the study on the effects of pharmacological interference with the cholinergic system on PSD-induced memory impairment show that activation of this system during the period of deprivation can prevent memory deficits induced by PSD Bueno et al.

In , Silva and Frussa-Filho proposed the use of the plus-maze discriminative avoidance task PMDAT , which is a behavioral paradigm that has the advantage of independently evaluate learning, memory, and anxiety as well as motor activity. PM-DAT complies with ethical protocols since there is no foot shock, which is imposed by classical avoidance tests.

Recently, Alvarenga et al. Our results demonstrate that PSD induced impairment in the acquisition, consolidation and retrieval of a discriminative avoidance task.

In the three experimental conditions, a 24h sleep recovery period was effective in abolishing the PSD cognitive effects, but was ineffective in modifying them per se. In addition, PSD produced significant alterations in anxiety-like behavior and locomotor activity, which may be related to the impairment in retrieval but not in acquisition or consolidation.

This study strengthened the critical role of PS but not sleep rebound in all the phases of learning and memory formation. In addition, it suggests that PSD effects on acquisition and consolidation do not seem to be related to other behavioral alterations induced by this procedure.

Consequently, speculations about the effect of the exercise on sleep due to sleep deprivation have been raised Martins et al. From our data, it can be assumed that PSD induced significant but heterogeneous effects in animals. For instance, PSD increased grooming, but it had no effect on stereotyped behaviors, locomotion, or the elevated plus maze test. Importantly, it significantly decreased rearing behavior, which is associated with potentiation of stereotypy and exploratory activity Andersen et al.

In addition, another study showed that single platform PSD rats had reduced locomotor activity and augmented anxiety-like behavior Suchecki et al. Recently, Martins and colleagues pointed out that PSD increased gnawing behavior undirected to feeding, supporting the view that spontaneous oral stereotypy, rather than hunger, is the major cause of increases in food removed from feeders in rats deprived of sleep for up to 96 hours.

In mice, sleep deprivation for 72h, achieved by the multiple platform method, induces increased anxiety as evaluated by the PM-DAT and in the conventional plusmaze decreased time spent in the open arms Silva et al. This anxiogenic effect was not observed after 24h of sleep deprivation. As mentioned, PSD results in several behavioral alterations in rats that are likewise induced by dopaminergic agonists Tufik et al.

DA plays a key role in the modulation of this behavior Bitran and Hull Morden and co-workers reported increased sexual performance in PSD male rats.

In another study, however, four days of PSD did not significantly alter male sexual performance Hicks et al. In this context, we have consistently demonstrated the facilitatory effects of PSD on genital reflexes penile erection, or PE, and ejaculation, or EJ in rats Andersen et al.

Indeed, combined administration of PSD and cocaine elicited genital reflexes much more markedly than did administration of PSD or cocaine alone Andersen and Tufik Although a number of factors are involved in a complex phenomenon such as PE, the authors suggest that the previously documented DA receptor supersensitivity induced by PSD may be an important contributor to the potentiation of genital reflexes by cocaine after sleep deprivation. Importantly, other dopaminergic drugs, such as cocaine Andersen et al.

The period of exposure to PSD seems to interfere with the responses of genital reflexes. More than 96h of PSD decreased genital reflexes, as observed at and hours Andersen et al. Interestingly, hormone levels seem to play a critical role in these erectile events for review, see Andersen and Tufik , Indeed, PSD decreases the level of testosterone, whereas progesterone levels were increased in both young and old groups, suggesting that, although sexual function commonly decreases with age, testosterone alone cannot be considered the main hormone involved in sexual activity Andersen et al.

Thus far, little attention has been given to whether sleep is differentially regulated between genders and the magnitude of the consequences of sleep loss. Studies have documented that, while healthy women appear to have better sleep quality than men, they report more sleep problems, including inadequate sleep time and insomnia Bixler et al.

Moreover, nightmares were reported to be twice as frequent in women Ohayon et al. The reasons for such discrepancies are attributed to hormonal fluctuations over the menstrual and estrous cycles, a factor that has been associated with sleep variations in both humans and rats Hachul et al. In particular, alterations in reproductive hormone release coincidental with sleep have been suggested as a manifestation of entrained links between CNS regulation and endocrine function.

Notably, our results demonstrate that female rats submitted to PSD in the diestrous phase PSD-diestrous had their estrous cycles disrupted during the recovery period. This was evidenced by a constant diestrus during the first week of recovery. In addition, the PSD-diestrous phase exhibited higher concentrations of corticosterone and lower estrogen levels than the respective control rats.

These data indicate that PSD may modulate ovarian hormone released through alterations in hormonal-neurochemical systems. Sleep has been described to provide an antioxidative function Reimund , which leads to the hypothesis that sleep deprivation is associated with an accumulation of free radicals.

It is known that PSD induces a number of alterations in systemic and brain energy metabolism Bergmann et al. It is possible that these effects occur as a result of reactive oxygen species ROS accumulation. A number of studies have reported that ROS are involved in the pathogenesis of several diseases and psychological stress Halliwell and Gutteridge D'Almeida and coworkers have studied the oxidative stress status following PSD.

First, they described a reduction in total glutathione GSH levels in the whole brain; however, a number of antioxidants were found to be unchanged in the brain after PSD D'Almeida et al. Twice daily administration of melatonin during the PSD period, and equivalent dosing in controls, resulted in similarly lowered hypothalamic GSH levels, indicating that the antioxidant properties of melatonin were not able to preserve hypothalamic GSH levels after PSD, and that exogenous melatonin may lead to decreases in hypothalamic GSH levels and further the decrease induced by PSD in this brain region D'Almeida et al.

Reduced GSH levels, a key indicator of oxidative stress, have been shown to precipitate apoptotic cell death in the brain under different conditions Tan et al. These findings suggest that the oxidative stress that develops in the brains of rats submitted to PSD does not result in cell loss.

Considering the stressful nature of the PSD method, which is associated with the disruption of various physiological processes, D'Almeida's group described that plasma homocysteine an intermediate amino acid in methionine-cysteine metabolism was reduced in PSD rats as compared with the cage group, and did not revert to normal levels after 24 or 48h of recovery. Whatever they dream about, they have the same kind of REM stage as sighted people do. After comparing the two, we can see that REM and paradoxical sleep are exactly the same thing!

They both feature specific reactions in particular areas of the brain, at a certain time in the sleeping cycle. In addition to that, both of them have atonia, or sleep paralysis. The Headphones Designed For Sleep. What Is A Paradox? Are they really the same thing? There are a few things that happen in the brain during REM sleep specifically, though. Our Brainwaves Resemble A Waking State From stage 1 to stage 4 of our sleep cycle, we move from a waking state to deep sleep.

They begin to resemble the brain waves we had when we were still awake. Amygdala: this is the part of the brain that links our senses and our emotions.

Hippocampus: this is responsible for long-term memory and recollection. Cingulate gyrus: this area controls muscle movement in response to stimulus. Anterior cingulate gyrus. This area of the brain deals with attention and motivation. This may account for why dreams are so vivid and things change so quickly.

Secondary visual cortices. These areas of the brain process visual information after the eyes have transferred it to the primary visual cortex. We Dream REM sleep is where most of our dreaming happens.

We do dream during other stages, but REM is where most dreaming happens. While the brain resembles that of an awake brain, the body is the opposite during REM sleep. Sleep Paralysis The scientific term for sleep paralysis is atonia. You can imagine what sort of things may go wrong if your body was working at full capacity! Those muscle movements that are essential for survival carry on.

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