Showing papers on "Rapid eye movement sleep published in 2008"

Bruxism physiology and pathology: an overview for clinicians*

Abstract: Awake bruxism is defined as the awareness of jaw clenching. Its prevalence is reported to be 20% among the adult population. Awake bruxism is mainly associated with nervous tic and reactions to stress. The physiology and pathology of awake bruxism is unknown, although stress and anxiety are considered to be risk factors. During sleep, awareness of tooth grinding (as noted by sleep partner or family members) is reported by 8% of the population. Sleep bruxism is a behaviour that was recently classified as a 'sleep-related movement disorder'. There is limited evidence to support the role of occlusal factors in the aetiology of sleep bruxism. Recent publications suggest that sleep bruxism is secondary to sleep-related micro-arousals (defined by a rise in autonomic cardiac and respiratory activity that tends to be repeated 8-14 times per hour of sleep). The putative roles of hereditary (genetic) factors and of upper airway resistance in the genesis of rhythmic masticatory muscle activity and of sleep bruxism are under investigation. Moreover, rhythmic masticatory muscle activity in sleep bruxism peaks in the minutes before rapid eye movement sleep, which suggests that some mechanism related to sleep stage transitions exerts an influence on the motor neurons that facilitate the onset of sleep bruxism. Finally, it remains to be clarified when bruxism, as a behaviour found in an otherwise healthy population, becomes a disorder, i.e. associated with consequences (e.g. tooth damage, pain and social/marital conflict) requires intervention by a clinician.

Sleep disturbances in patients with schizophrenia : impact and effect of antipsychotics.

Abstract: Difficulties initiating or maintaining sleep are frequently encountered in patients with schizophrenia. Disturbed sleep can be found in 30–80% of schizophrenic patients, depending on the degree of psychotic symptomatology. Measured by polysomnography, reduced sleep efficiency and total sleep time, as well as increased sleep latency, are found in most patients with schizophrenia and appear to be an important part of the pathophysiology of this disorder. Some studies also reported alterations of stage 2 sleep, slow-wave sleep (SWS) and rapid eye movement (REM) sleep variables, i.e. reduced REM latency and REM density. A number of sleep parameters, such as the amount of SWS and the REM latency, are significantly correlated to clinical variables, including severity of illness, positive symptoms, negative symptoms, outcome, neurocognitive impairment and brain structure. Concerning specific sleep disorders, there is some evidence that schizophrenic patients carry a higher risk of experiencing a sleep-related breathing disorder, especially those demonstrating the known risk factors, including being overweight but also long-term use of antipsychotics. However, it is still unclear whether periodic leg movements in sleep or restless legs syndrome (RLS) are found with a higher or lower prevalence in schizophrenic patients than in healthy controls. There are no consistent effects of first-generation antipsychotics on measuresof sleep continuity and sleep structure, including the percentage of sleep stages or sleep and REM latency in healthy controls. In contrast to first-generation antipsychotics, the studied atypical antipsychotics (clozapine, olanzapine, quetiapine, risperidone, ziprasidone and paliperidone) demonstrate a relatively consistent effect on measures of sleep continuity, with an increase in either total sleep time (TST) or sleep efficiency, and individually varying effects on other sleep parameters, such as an increase in REM latency observed for olanzapine, quetiapine and ziprasidone, and an increase in SWS documented for olanzapine and ziprasidone in healthy subjects. The treatment of schizophrenic patients with first-generation antipsychotics is consistently associated with an increase in TST and sleep efficiency, and mostly an increase in REM latency, whereas the influence on specific sleep stages is more variable. On the other hand, withdrawal of such treatment is followed by a change in sleep structure mainly in the opposite direction, indicating a deterioration of sleep quality. On the background of the rather inconsistent effects of first-generation antipsychotics observed in healthy subjects, it appears possible that the high-potency drugs exert their effects on sleep in schizophrenic patients, for the most part, in an indirect way by suppressing stressful psychotic symptomatology. In contrast, the available data concerning second-generation antipsychotics (clozapine, olanzapine, risperidone and paliperidone) demonstrate a relatively consistent effect on measures of sleep continuity in patients and healthy subjects, with an increase in TST and sleep efficiency or a decrease in wakefulness. Additionally, clozapine and olanzapine demonstrate comparable influences on other sleep variables, such as SWS or REM density, in controls and schizophrenic patients. Possibly, the effects of second-generation antipsychotics observed on sleep in healthy subjects and schizophrenic patients might involve the action of these drugs on symptomatology, such as depression, cognitive impairment, and negative and positive symptoms. Specific sleep disorders, such as RLS, sleep-related breathing disorders, night-eating syndrome, somnambulism and rhythm disorders have been described as possible adverse effects of antipsychotics and should be considered in the differential diagnosis of disturbed or unrestful sleep in this population.

Theta and gamma coordination of hippocampal networks during waking and rapid eye movement sleep.

Abstract: Rapid eye movement (REM) sleep has been considered a paradoxical state because, despite the high behavioral threshold to arousing perturbations, gross physiological patterns in the forebrain resemble those of waking states. To understand how intrahippocampal networks interact during REM sleep, we used 96 site silicon probes to record from different hippocampal subregions and compared the patterns of activity during waking exploration and REM sleep. Dentate/CA3 theta and gamma synchrony was significantly higher during REM sleep compared with active waking. In contrast, gamma power in CA1 and CA3-CA1 gamma coherence showed significant decreases in REM sleep. Changes in unit firing rhythmicity and unit-field coherence specified the local generation of these patterns. Although these patterns of hippocampal network coordination characterized the more common tonic periods of REM sleep (approximately 95% of total REM), we also detected large phasic bursts of local field potential power in the dentate molecular layer that were accompanied by transient increases in the firing of dentate and CA1 neurons. In contrast to tonic REM periods, phasic REM epochs were characterized by higher theta and gamma synchrony among the dentate, CA3, and CA1 regions. These data suggest enhanced dentate processing, but limited CA3-CA1 coordination during tonic REM sleep. In contrast, phasic bursts of activity during REM sleep may provide windows of opportunity to synchronize the hippocampal trisynaptic loop and increase output to cortical targets. We hypothesize that tonic REM sleep may support off-line mnemonic processing, whereas phasic bursts of activity during REM may promote memory consolidation.

A causal role for brain-derived neurotrophic factor in the homeostatic regulation of sleep

Abstract: Slow-wave activity (SWA), the EEG power between 0.5 and 4 Hz during non-rapid eye movement (NREM) sleep, is one of the best characterized markers of sleep need, because it increases as a function of preceding waking duration and decreases during sleep, but the underlying mechanisms remain unknown. We hypothesized that SWA is high at sleep onset because it reflects the occurrence, during the previous waking period, of widespread synaptic potentiation in cortical and subcortical areas. Consistent with this hypothesis, we recently showed that the more rats explore, the stronger is the cortical expression of BDNF during wakefulness, and the larger is the increase in SWA during the subsequent sleep period. There is compelling evidence that BDNF plays a causal role in synaptic potentiation, and exogenous application of BDNF in vivo is sufficient to induce long-term increases in synaptic strength. We therefore performed cortical unilateral microinjections of BDNF in awake rats and measured SWA during the subsequent sleep period. SWA during NREM sleep was higher in the injected hemisphere relative to the contralateral one. The effect was reversible within 2 h, and did not occur during wakefulness or rapid eye movement sleep. Asymmetries in NREM SWA did not occur after vehicle injections. Furthermore, microinjections, during wakefulness, of a polyclonal anti-BDNF antibody or K252a, an inhibitor of BDNF TrkB receptors, led to a local SWA decrease during the following sleep period. These effects were also reversible and specific for NREM sleep. These results show a causal link between BDNF expression during wakefulness and subsequent sleep regulation.

Subjective and objective sleep quality and aging in the sleep heart health study

Abstract: OBJECTIVES: To examine the extent to which subjective and objective sleep quality are related to age independent of chronic health conditions. DESIGN: Cross-sectional study. SETTING: The Sleep Heart Health Study (SHHS) is a multicenter study designed to determine the cardiovascular consequences and the natural history of sleep disordered breathing. PARTICIPANTS: Five thousand four hundred seven community-dwelling adults who participated in the SHHS (mean age 63, range 45–99; 52% women). MEASUREMENTS: Unattended home polysomnography (PSG) and sleep questionnaires. RESULTS: Older age was associated with shorter sleep time, diminished sleep efficiency, and more arousals in men and women. In men, age was independently associated with more Stage 1 and Stage 2 sleep and less slow-wave (Stage 3 to 4) and rapid eye movement sleep. In women, older age was less strongly associated according to linear trend with sleep stage. Conversely, poor subjective sleep quality was not associated with older age in men, but older women had more trouble falling asleep, and there was a trend toward older women having more problems with waking up during the night and waking up too early. Associations between self-report and directly measured sleep time and sleep latency were low to moderate across age groups (correlation coefficient=0.06–0.32). CONCLUSION: Older age was more strongly associated with poorer sleep according to PSG in men than women, yet the subjective report of poor sleep with older age was stronger in women. The higher prevalence of chronic health conditions, including sleep apnea, in older adults did not explain changes of sleep parameters with aging and age–sex differences in these relationships.

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

Abstract: RAPID EYE MOVEMENT (REM) SLEEP BEHAVIOR DISORDER (RBD) IS A PARASOMNIA CHARACTERIZED BY DREAM-ENACTING BEHAVIORS ASSOCIATED WITH unpleasant dreams and loss of normal REM sleep muscle atonia.1 The International Classification of Sleep Disorders-2 established that the diagnosis of RBD requires demonstration of REM sleep without atonia by polysomnography,2 mainly because other sleep disorders can mimic the clinical features of RBD.3 The International Classification of Sleep Disorders-2 defined REM sleep without atonia as the “electromyographic (EMG) finding of excessive amounts of sustained or intermittent elevation of submental EMG tone or excessive phasic submental or (upper or lower) limb EMG twitching.”2 This definition has several limitations. First, a precise definition of “excessive amounts of tonic and phasic EMG activity” was not provided, since normal values of these measures are unknown. Second, it is not stated how the tonic and phasic EMG activity have to be measured. Third, it is unclear which muscle or combination of muscles of the body (either axial or extremity muscles, lower or upper extremity muscles, or proximal or distal extremity muscles) provides the highest rates of abnormal REM sleep EMG activity in RBD. Previous studies in RBD have evaluated the EMG activity in several combinations of muscles, including (1) exclusively the mentalis or the submentalis,4–12 (2) the mentalis or submentalis plus left and right anterior tibialis,13,14 and (3) mentalis or submentalis plus right and left tibialis anterior, and either brachioradialis,15,16 biceps brachii,17–19 extensor digitorum,20,21 or carpi radialis.22 The aim of our study was to determine which muscle or combination of muscles provides the highest rates of phasic EMG activity occurring during REM sleep in patients with RBD.

Sleeping outside the box: electroencephalographic measures of sleep in sloths inhabiting a rainforest

Abstract: The functions of sleep remain an unresolved question in biology. One approach to revealing sleep's purpose is to identify traits that explain why some species sleep more than others. Recent compara...

Glycinergic and GABAA-Mediated Inhibition of Somatic Motoneurons Does Not Mediate Rapid Eye Movement Sleep Motor Atonia

Abstract: A hallmark of rapid eye movement (REM) sleep is a potent suppression of postural muscle tone. Motor control in REM sleep is unique because it is characterized by flurries of intermittent muscle twitches that punctuate muscle atonia. Because somatic motoneurons are bombarded by strychnine-sensitive IPSPs during REM sleep, it is assumed that glycinergic inhibition underlies REM atonia. However, it has never been determined whether glycinergic inhibition of motoneurons is indeed responsible for triggering the loss of postural muscle tone during REM sleep. Therefore, we used reverse microdialysis, electrophysiology, and pharmacological and histological methods to determine whether glycinergic and/or GABAA-mediated neurotransmission at the trigeminal motor pool mediates masseter muscle atonia during REM sleep in rats. By antagonizing glycine and GABAA receptors on trigeminal motoneurons, we unmasked a tonic glycinergic/GABAergic drive at the trigeminal motor pool during waking and non-rapid eye movement (NREM) sleep. Blockade of this drive potently increased masseter muscle tone during both waking and NREM sleep. This glycinergic/GABAergic drive was immediately switched-off and converted into a phasic glycinergic drive during REM sleep. Blockade of this phasic drive potently provoked muscle twitch activity in REM sleep; however, it did not prevent or reverse REM atonia. Muscle atonia in REM even persisted when glycine and GABAA receptors were simultaneously antagonized and trigeminal motoneurons were directly activated by glutamatergic excitation, indicating that a powerful, yet unidentified, inhibitory mechanism overrides motoneuron excitation during REM sleep. Our data refute the prevailing hypothesis that REM atonia is caused by glycinergic inhibition. The inhibitory mechanism mediating REM atonia therefore requires reevaluation.

Selective 5HT2A and 5HT6 receptor antagonists promote sleep in rats

Abstract: Study objectives Serotonin (5-HT) has long been implicated in the control of sleep and wakefulness. This study evaluated the hypnotic efficacy of the 5-HT6 antagonist RO4368554 (RO) and the 5-HT2A receptor antagonist MDL100907 (MDL) relative to zolpidem. Design A randomized, repeated-measures design was utilized in which Wistar rats received intraperitoneal injections of RO (1.0, 3.0, and 10 mg/kg), MDL (0.1, 1.0 and 3.0 mg/kg), zolpidem (10 mg/kg), or vehicle in the middle of the dark (active) period. Electroencephalogram, electromyogram, body temperature (Tb) and locomotor activity were analyzed for 6 hours after injection. Measurements and results RO, MDL, and zolpidem all produced significant increases in sleep and decreases in waking, compared with vehicle control. All 3 doses of MDL produced more consolidated sleep, increased non-rapid eye movement sleep (NREM) sleep, and increased electroencephalographic delta power during NREM sleep. The highest dose of RO (10.0 mg/kg) produced significant increases in sleep and decreases in waking during hour 2 following dosing. These increases in sleep duration were associated with greater delta power during NREM sleep. ZO Zolpidem induced sleep with the shortest latency and significantly increased NREM sleep and delta power but also suppressed rapid eye movement sleep sleep; in contrast, neither RO nor MDL affected rapid eye movement sleep. Whereas RO did not affect Tb, both zolpidem and MDL reduced Tb relative to vehicle-injected controls. Conclusions These results support a role for 5-HT2A receptor modulation in NREM sleep and suggest a previously unrecognized role for 5-HT6 receptors in sleep-wake regulation.

Sleep-wake regulation is altered in leptin-resistant (db/db) genetically obese and diabetic mice

Abstract: Recent epidemiological and clinical studies indicate that the control of sleep-wake states may be an important factor in the regulation of energy metabolism. Leptin is a peripherally synthesized hormone that has critical signaling properties in the brain for the control of long-term energy homeostasis. In this study, we examined the hypothesis that leptin signaling exerts a role in sleep-wake regulation and that leptin may represent an important mechanistic link in the coordination of sleep-wake states and metabolism. Sleep-wake patterns were recorded in a genetic mouse model of obesity and diabetes, the db/db mouse, which harbors a mutation in a particular isoform of the leptin receptor (long form, LRb). We found that db/db mice exhibit a variety of alterations in sleep regulation, including an increase in overall sleep time, a dramatic increase in sleep fragmentation, attenuated diurnal rhythmicity in rapid eye movement sleep and non-rapid eye movement EEG delta power (a measure of sleep homeostatic drive), and a decrease in the compensatory response to acute (i.e., 6 h) sleep deprivation. The db/db mice also generated low amounts of locomotor activity and a reduction in the diurnal rhythm of activity. These results indicate that impaired leptin signaling has deleterious effects on the regulation of sleep amount, sleep architecture, and temporal consolidation of these arousal states. In summary, leptin may represent an important molecular component in the integration of sleep, circadian rhythms, and energy metabolism.

Sleep deprivation can inhibit adult hippocampal neurogenesis independent of adrenal stress hormones

Abstract: Sleep deprivation (SD) can suppress cell proliferation in the hippocampal dentate gyrus of adult male rodents, suggesting that sleep may contribute to hippocampal functions by promoting neurogenesis. However, suppression of cell proliferation in rats by the platform-over-water SD method has been attributed to elevated corticosterone (Cort), a potent inhibitor of cell proliferation and nonspecific correlate of this procedure. We report here results that do not support this conclusion. Intact and adrenalectomized (ADX) male rats were subjected to a 96-h SD using multiple- and single-platform methods. New cells were identified by immunoreactivity for 5-bromo-2'-deoxyuridine (BrdU) or Ki67 and new neurons by immunoreactivity for BrdU and doublecortin. EEG recordings confirmed a 95% deprivation of rapid eye movement (REM) sleep and a 40% decrease of non-REM sleep. Cell proliferation in the dentate gyrus was suppressed by up to 50% in sleep-deprived rats relative to apparatus control or home cage control rats. This effect was also observed in ADX rats receiving continuous low-dose Cort replacement via subcutaneous minipumps but not in ADX rats receiving Cort replacement via drinking water. In these latter rats, Cort intake via water was reduced by 60% during SD; upregulation of cell proliferation by reduced Cort intake may obscure inhibitory effects of sleep loss on cell proliferation. SD had no effect on the percentage of new cells expressing a neuronal phenotype. These results demonstrate that the Cort replacement method is critical for detecting an effect of SD on cell proliferation and support a significant role for sleep in adult neurogenesis.

Rapid eye movement sleep deprivation contributes to reduction of neurogenesis in the hippocampal dentate gyrus of the adult rat.

Abstract: THE SUBGRANULAR CELL LAYER IN THE DENTATE GYRUS (DG) OF THE ADULT HIPPOCAMPUS CONTAINS PROGENITOR CELLS, WHICH HAVE THE POTENTIAL TO proliferate and differentiate into neurons. These progenitors mature locally into granule cells of the DG, sending axonal projections to area CA3 and dendrites into the molecular layer.1.2 Adult neurogenesis has been demonstrated in birds and several mammals, including humans. The processes of cell proliferation, migration, maturation, and survival are all subject to modulation by experiential events.3 Stress is an important negative regulator of cell proliferation.4,5 Previously we reported that 96 hours of total sleep deprivation (TSD) affects neurogenesis in the rat DG by reducing cell proliferation in the subgranular cell layer, and the percentage of new cells later expressing a neuronal marker.6,7 The inhibitory effects of extended sleep deprivation have been confirmed.8 However, mammalian sleep is physiologically heterogeneous. The two primary stages of mammalian sleep, non-rapid eye movement (NREM) and rapid eye movement (REM) sleep, have very different, even opposite, electrophysiologic and metabolic properties, compared with waking, and could have different effects on neurogenesis. Revealing the relative impact of REM and NREM sleep on neurogenesis is a necessary step in understanding the mechanisms underlying suppression of neurogenesis in response to sleep loss. The aim of the present study was to assess the effect of REM sleep deprivation (REMD) on neurogenesis in the DG of the adult rat. To achieve REM deprivation, rats lived on a treadmill that was briefly activated when REM was detected by fast Fourier transform analysis of the electroencephalogram (EEG) and electromyogram (EMG) activity. Yoked control (YC) animals lived on the same treadmill and were subjected to the same treadmill movements.

The effects of gender and age on REM-related sleep-disordered breathing.

Abstract: Sleep disordered breathing occurring predominantly in rapid eye movement REM sleep (rapid-eye-movement-related sleep-disordered breathing, REM SDB) is present in 10 to 36% of patients undergoing polysomnography (PSG) for suspected obstructive sleep apnea (O'Connor et al. in Am J Respir Crit Care Med 161:1465-1472, 2000; Resta et al. in J Respir Medicine 99:91-96, 2005; Haba-Rubio et al. in Chest 128:3350-3357, 2005; Juvelekian and Golish, American Academy of Sleep Medicine, abstract, 2004). We hypothesize that REM SDB is an age-related condition in women and, additionally, more prevalent in women than in men. Subjects with REM SDB were identified retrospectively among 1,540 obstructive sleep apnea (OSA) patients with an apnea-hypopnea index (AHI) >or= 5. Inclusion criteria for REM SDB were age >18, AHI >or= 5, NREM AHI 2. PSG data included sleep latency, REM latency, total sleep time (TST), AHI, REM AHI, NREM AHI, and sleep stage percentages. Demographic data and medical and psychiatric histories were also obtained. Statistical comparisons were made between men and women and women older and younger than 55 years, a marker for menopausal status. Two hundred twenty-one subjects fulfilled the criteria for REM SDB, yielding a prevalence of 14.4%. Overall, female apneics had a significantly higher prevalence of REM SDB than did men (24.5 vs 7.9%; p < 0.001). Younger women had a significantly higher prevalence than did older women (27.2 vs 18.6%; p = 0.008); younger men had a significantly higher prevalence of REM SDB than did older men (9.9 vs 4.5%; p = 0.002). Women were significantly older and more obese than were men. Younger women were more likely to be depressed and were significantly more obese than were older women. REM SDB is more prevalent in women than in men and more prevalent in men and women younger than 55 than those older than 55. In this population, women are more obese and older than men, while younger women were more obese than older women. These descriptive distinctions suggest differences in mechanism which may depend on gender and age.

Lack of Effects of Pramipexole on REM Sleep Behavior Disorder in Parkinson Disease

Abstract: PARKINSON DISEASE (PD) IS A NEURODEGENERATIVE DISORDER ASSOCIATED WITH LOSS OF THE DOPAMINERGIC CELLS IN THE SUBSTANTIA NIGRA resulting in bradykinesia, tremor, and rigidity. These classical motor symptoms are responsive to dopaminergic agents. In PD, the degenerative process also involves non-dopaminergic neuronal areas beyond the substantia nigra such as the lower brainstem, the amygdala, and the cortex. Impairment of these brain areas in PD account for the occurrence of several non-motor symptoms, including dysautonomia and dementia, which do not respond to dopamine replacement therapy.1 REM sleep behavior disorder (RBD) is a frequent feature of PD that is characterized by dream-enacting behaviors, unpleasant dreams, and loss of muscle atonia during REM sleep.2,3 It is unknown if RBD in PD results from dopaminergic deficiency. To assess whether dopaminergic dysfunction plays a major role in the pathogenesis of RBD in PD, we prospectively examined the therapeutic effect of pramipexole, a D2-D3 dopamine receptor agonist, on RBD features in patients with PD.

Searching for a Marker of REM Sleep Behavior Disorder: Submentalis Muscle EMG Amplitude Analysis during Sleep in Patients with Narcolepsy/Cataplexy

Abstract: Study Objectives: To evaluate the amplitude of submentalis muscle EMG activity during sleep in patients with narcolepsy/cataplexy with or without REM sleep behavior disorder (RBD).

The Developmental Decrease in REM Sleep: The Role of Transmitters and Electrical Coupling

Abstract: A NUMBER OF RECENT REVIEWS PROVIDE DETAILED DESCRIPTIONS OF THE ORGANIZATION OF THE NEUROLOGIC SUBSTRATES CONTROLLING SLEEP-WAKE systems.1–6 The reader is also referred to an extensive consideration of rapid eye movement (REM) sleep.7 Our recent mini-review focused on developmental events related to the decrease in REM sleep, including its relationship to other developmental changes, the role of blood flow, some factors that may influence its progress, and its potential role in brain development.8 Briefly, the part of the brain controlling sleep-wake states and most responsible for inducing REM sleep is the reticular activating system (RAS), especially its cholinergic component. The RAS triggers changes in state mainly via its ascending projections to the intralaminar thalamus (ILT) to modulate thalamocortical systems in both waking and REM sleep, while simultaneously modulating REM sleep and postural muscle tone via its descending projections to the pontomedullary reticular formation. Since that review, a more complete survey of the transmitter systems that affect these neurons has been completed, and the role of electrical coupling as a novel mechanism in sleep-wake control has been discovered. We will describe the organization of sleep-wake control systems in the adult and then deal with development.

Abnormal sleep and sleepiness in Parkinson's disease.

Abstract: Purpose of review Sleep problems are frequent and disabling in patients with Parkinson's disease. Recent data provide major advances in the mechanisms and consequences of rapid eye movement sleep behavior disorders, insomnia and narcolepsy-like daytime sleepiness. Recent findings A large series confirms that rapid eye movement sleep behavior disorders may precede parkinsonism or dementia (particuarly, but not exclusively, Lewy bodies dementia) for several years. In Parkinson's disease, rapid eye movement sleep behavior disorders expose patients to higher risks of dementia and hallucinations. Surprisingly, parkinsonism disappears during rapid eye movement sleep behavior disorders, suggesting basal ganglia are bypassed. The interest for structures controlling atonia during rapid eye movement sleep switches from the pedunculopontine nuclei to the locus subcoeruleus. The neuropathology of hypothalamus in Parkinson's disease indicates a massive hypocretin loss, probably underlying the narcolepsy phenotype. The benefit of the new, 24-h long acting ropinirole and transdermal rotigotine on sleep and sleepiness is modest. Eventually, the dopamine release in the mesocorticolimbic pathway is increased during rapid eye movement sleep, supporting its role in dopaminergic-induced vivid dreams. Summary In clinical practice, rapid eye movement sleep behavior disorders should be looked at as heralding neurodegenerative diseases in patients with mild cognitive impairment and as a risk factor for dementia and hallucinations in patients with Parkinson's disease.

Rapid Eye Movement Sleep in Relation to Overweight in Children and Adolescents

Abstract: Context Short sleep duration is associated with obesity, but few studies have examined the relationship between obesity and specific physiological stages of sleep.

Characterization of GABAergic neurons in rapid-eye-movement sleep controlling regions of the brainstem reticular formation in GAD67-green fluorescent protein knock-in mice.

Abstract: Recent experiments suggest that brainstem GABAergic neurons may control rapid-eye-movement (REM) sleep. However, understanding their pharmacology/physiology has been hindered by difficulty in identification. Here we report that mice expressing green fluorescent protein (GFP) under the control of the GAD67 promoter (GAD67-GFP knock-in mice) exhibit numerous GFP-positive neurons in the central gray and reticular formation, allowing on-line identification in vitro. Small (10−15 μm) or medium-sized (15−25 μm) GFP-positive perikarya surrounded larger serotonergic, noradrenergic, cholinergic and reticular neurons, and >96% of neurons were double-labeled for GFP and GABA, confirming that GFP-positive neurons are GABAergic. Whole-cell recordings in brainstem regions important for promoting REM sleep [subcoeruleus (SubC) or pontine nucleus oralis (PnO) regions] revealed that GFP-positive neurons were spontaneously active at 3−12 Hz, fired tonically, and possessed a medium-sized depolarizing sag during hyperpolarizing steps. Many neurons also exhibited a small, low-threshold calcium spike. GFP-positive neurons were tested with pharmacological agents known to promote (carbachol) or inhibit (orexin A) REM sleep. SubC GFP-positive neurons were excited by the cholinergic agonist carbachol, whereas those in the PnO were either inhibited or excited. GFP-positive neurons in both areas were excited by orexins/hypocretins. These data are congruent with the hypothesis that carbachol-inhibited GABAergic PnO neurons project to, and inhibit, REM-on SubC reticular neurons during waking, whereas carbachol-excited SubC and PnO GABAergic neurons are involved in silencing locus coeruleus and dorsal raphe aminergic neurons during REM sleep. Orexinergic suppression of REM during waking is probably mediated in part via excitation of acetylcholine-inhibited GABAergic neurons.

Physiological sleep-dependent changes in arterial blood pressure: central autonomic commands and baroreflex control.

Abstract: Sleep is a heterogeneous behaviour As a first approximation, it is subdivided objectively into two states: non-rapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS) The mean value and variability of arterial blood pressure (ABP) decrease physiologically from wakefulness to NREMS In REMS, there may be a further decrease or increase in mean ABP as well as phasic hypertensive events, which enhance the variability of ABP The reduced mean ABP during NREMS results from a decrease in either heart rate or sympathetic vasoconstrictor tone During REMS, sympathetic activity to the different cardiovascular effectors undergoes a substantial repatterning Thus, the mean ABP in REMS reflects a balance between changes in cardiac output and constriction or dilatation of different vascular beds In both sleep states, the phasic changes in ABP are driven by bursts of vasoconstriction, which may be accompanied by surges of heart rate The available evidence supports the hypothesis that the sleep-dependent changes in ABP, either tonic or phasic, result from the integration between cardiovascular reflexes and central autonomic commands that are specific to each sleep state

Sleep-wake behavior and responses to sleep deprivation of mice lacking both interleukin-1β receptor 1 and tumor necrosis factor-α receptor 1

Abstract: Data indicate that interleukin (IL)-1 beta and tumor necrosis factor-alpha (TNFalpha) are involved in the regulation of non-rapid eye movement sleep (NREMS). Previous studies demonstrate that mice lacking the IL-1 beta type 1 receptor spend less time in NREMS during the light period, whereas mice lacking the p55 (type 1) receptor for TNFalpha spend less time in NREMS during the dark period. To further investigate roles for IL-1 beta and TNFalpha in sleep regulation we phenotyped sleep and responses to sleep deprivation of mice lacking both the IL-1 beta receptor 1 and TNFalpha receptor 1 (IL-1R1/TNFR1 KO). Male adult mice (IL-1R1/TNFR1 KO, n=14; B6129SF2/J, n=14) were surgically instrumented with EEG electrodes and with a thermistor to measure brain temperature. After recovery and adaptation to the recording apparatus, 48 h of undisturbed baseline recordings were obtained. Mice were then subjected to 6h sleep deprivation at light onset by gentle handling. IL-1R1/TNFR1 KO mice spent less time in NREMS during the last 6h of the dark period and less time in rapid eye movement sleep (REMS) during the light period. There were no differences between strains in the diurnal timing of delta power during NREMS. However, there were strain differences in the relative power spectra of the NREMS EEG during both the light period and the dark period. In addition, during the light period relative power in the theta frequency band of the REMS EEG differed between strains. After sleep deprivation, control mice exhibited prolonged increases in NREMS and REMS, whereas the duration of the NREMS increase was shorter and there was no increase in REMS of IL-1R1/TNFR1 KO mice. Delta power during NREMS increased in both strains after sleep deprivation, but the increase in delta power during NREMS of IL-1R1/TNFR1 KO mice was of greater magnitude and of longer duration than that observed in control mice. These results provide additional evidence that the IL-1 beta and TNFalpha cytokine systems play a role in sleep regulation and in the alterations in sleep that follow prolonged wakefulness.