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.

Rapid Eye Movement Sleep

Abstract: Eyelid Condition at Birth: Relationship to Adult Mammalian Sleep-waking Patterns, E Aserinsky Phylogeny and Evolution of Rapid Eye Movement (REM) Sleep, M G Frank Ontogenesis of REM Sleep, M Segawa Initiation of Rapid Eye Movement Sleep: Beyond the Brainstem, A R Morrison, L D Sanford, and R J Ross Muscle Atonia in REM Sleep, Y -Y Lai and J M Siegel PGO Wave Generation: Mechanism and Functional Significance, S Datta Norepinephrine and REM Sleep, P-H Luppi, D Gervasoni, C Peyron, C Rampon, B Barbagli, R Boissard, and P Fort New Directions for the Study of Cholinergic REM Sleep Generation: Specifying Pre- and Postsynaptic Mechanisms, M L Capece, H A Baghdoyan, and R Lydic Functional Role of Serotonin 5-HT1 and 5-HT2 Receptor in the Regulation of REM Sleep, J M Monti and D Monti Possible Role of GABA in the Regulation of REM Sleep with Special Reference to REM-OFF Neurons, B N Mallick, S Kaur, S K Jha, and J M Siegel Nitric Oxide: A Diffusible Modulator of Physiological Traits and Behavioral States, T O Leonard and R Lydic Neurotransmitters Changes and REM Sleep, T Kodama Spatio-Temporal Distribution of Neuronal Activities and REM Sleep, S Inoue, U K Saha, and T Musha Different Physiological Properties of Two Populations of PS-on Neurons in the Mesopontine Tegmentum, Y Koyama, Y Kayama, and K Sakai Hormones and REM Sleep, F Obal Jr and J M Krueger Endogenous Sleep Substances and REM Sleep, S Inoue, K Honda, M Kimura, and S-Q Zhang Brain Energy, Production, and Sleep Occurrence, R Cespuglio, H Faradji-Prevautel, and L Netchiporouk Rapid Eye Movement Sleep: From Cerebral Metabolism to Functional Brain Mapping, P Maquet and C Phillips REM Sleep and Apnea, D W Carley and M Radulovacki Thermoregulatory Control of the nonREM-REM Sleep Cycle, R Szymusiak, Md Noor Alam, and D McGinty REM Sleep Across Age and Sex, K Mishima, T Shimizu, and Y Hishikawa The Function of Fetal/Neonatal REM Sleep, M Mirmiran and Y G H Maas REM Sleep Deprivation Alters Factors Affecting Neuronal Excitability: Role of Norepinephrine and Its Possible Mechanism of Action, B N Mallick, H V A Adya, and s Thankachan REM Sleep Deprivation and Behavioral Changes, G W Vogel Cellular and Molecular Changes Occurring During REM Sleep, O Prospero-Garcia, L Navarro, E Murillo-Rodriguez, M Sanchez-Alavez, R Guzman-Marin, M Mendez-Diaz, M Gomez-Chavarin, A Jimenez-Anguiano, and R Drucker-Colin Intensity of REM Sleep, K Takahashi Why We Believe What We Believe About REM-Sleep Regulation, H Benington Hypothesis on REM Sleep from the Viewpoint of Neuronal Dynamics, M Nakao and M Yamamoto

REM Sleep Behavior Disorder in Parkinson's Disease and Other Synucleinopathies

Abstract: Rapid eye movement sleep behavior disorder is characterized by dream enactment and complex motor behaviors during rapid eye movement sleep and rapid eye movement sleep atonia loss (rapid eye movement sleep without atonia) during polysomnography. Rapid eye movement sleep behavior disorder may be idiopathic or symptomatic and in both settings is highly associated with synucleinopathy neurodegeneration, especially Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and pure autonomic failure. Rapid eye movement sleep behavior disorder frequently manifests years to decades prior to overt motor, cognitive, or autonomic impairments as the presenting manifestation of synucleinopathy, along with other subtler prodromal "soft" signs of hyposmia, constipation, and orthostatic hypotension. Between 35% and 91.9% of patients initially diagnosed with idiopathic rapid eye movement sleep behavior disorder at a sleep center later develop a defined neurodegenerative disease. Less is known about the long-term prognosis of community-dwelling younger patients, especially women, and rapid eye movement sleep behavior disorder associated with antidepressant medications. Patients with rapid eye movement sleep behavior disorder are frequently prone to sleep-related injuries and should be treated to prevent injury with either melatonin 3-12 mg or clonazepam 0.5-2.0 mg to limit injury potential. Further evidence-based studies about rapid eye movement sleep behavior disorder are greatly needed, both to enable accurate prognostic prediction of end synucleinopathy phenotypes for individual patients and to support the application of symptomatic and neuroprotective therapies. Rapid eye movement sleep behavior disorder as a prodromal synucleinopathy represents a defined time point at which neuroprotective therapies could potentially be applied for the prevention of Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and pure autonomic failure. © 2017 International Parkinson and Movement Disorder Society.

REM sleep behavior disorder is related to striatal monoaminergic deficit in MSA

Abstract: Objective: To explore the neurochemical basis of REM sleep behavior disorder (RBD) in multiple-system atrophy (MSA). Methods: In 13 patients with probable MSA, nocturnal, laboratory-based polysomnography was used to rate the severity of REM atonia loss by the percentage of REM sleep with tonically increased electromyographic (EMG) activity and the percentage of REM sleep with phasic EMG bursts. PET with (+)-[ 11 C]dihydrotetrabenazine ([ 11 C]DTBZ) was employed to measure the density of striatal monoaminergic terminals and SPECT with (−)-5-[ 123 I]iodobenzovesamicol ([ 123 I]IBVM) to measure the density of thalamic cholinergic terminals. Data in the patient group were compared with data from 15 normal control subjects scanned with [ 11 C]DTBZ and 12 with [ 123 I]IBVM. Results: Age and gender distributions were similar in patient and normal control groups. The MSA subjects showed decreased mean [ 11 C]DTBZ binding in the striatum ( p 123 I]IBVM binding in the thalamus ( p 11 C]DTBZ binding was inversely correlated with the severity of REM atonia loss ( p = 0.003). Thalamic [ 123 I]IBVM binding, however, was not correlated to the severity of REM atonia loss. Conclusion: Decreased nigrostriatal dopaminergic projections may contribute to RBD in MSA.

Subthreshold excitatory activity and motoneuron discharge during REM periods of active sleep

Abstract: A striking paradox of the rapid eye movement periods of active sleep, which are typically characterized by the exacerbation of somatomotor atonia, is the occurrence of muscle twitches and jerks. The purpose of this study was to examine the specific motoneuron membrane potential processes responsible for these myoclonic patterns of activity. In lumbar motoneurons, examined intracellularly in the cat prepared for long-term study, these processes consisted of recurrent depolarizing membrane potential shifts and spontaneous action potentials that were either full-sized or of partial amplitude. In addition, the invasion of antidromically induced spikes into the soma was often blocked. Hyperpolarizing potentials were evident in the intervals between spontaneous spikes. Hyperpolarization was also observed immediately before depolarization and spike activity, in contrast to the gradual depolarization of the motoneuron membrane potential that always occurred during wakefulness. Thus, during rapid eye movement periods, in conjunction with muscle twitches and jerks, a strong excitatory input is superimposed on a background of inhibitory input. The unique patterns of membrane potential change that arise thus seem to result from the simultaneous coactivation of excitatory and inhibitory processes.

Sleep enhances explicit recollection in recognition memory.

Abstract: Recognition memory is considered to be supported by two different memory processes, i.e., the explicit recollection of information about a previous event and an implicit process of recognition based on an acontextual sense of familiarity. Both types of memory supposedly rely on distinct memory systems. Sleep is known to enhance the consolidation of memories, with the different sleep stages affecting different types of memory. In the present study, we used the process-dissociation procedure to compare the effects of sleep on estimates of explicit (recollection) and implicit (familiarity) memory formation on a word-list discrimination task. Subjects studied two lists of words before a 3-h retention interval of sleep or wakefulness, and recognition was tested afterward. The retention intervals were positioned either in the early night when sleep is dominated by slow-wave sleep (SWS), or in the late night, when sleep is dominated by REM sleep. Sleep enhanced explicit recognition memory, as compared with wakefulness (P < 0.05), whereas familiarity was not affected by sleep. Moreover, explicit recognition was particularly enhanced after sleep in the early-night retention interval, and especially when the words were presented with the same contextual features as during learning, i.e., in the same font (P < 0.05). The data indicate that in a task that allows separating the contribution of explicit and implicit memory, sleep particularly supports explicit memory formation. The mechanism of this effect appears to be linked to SWS.