Cardiac autonomic nervous activity during different sleep stages in individuals with spinal cord injury: The influence of physical training.

OBJECTIVE: The present study assessed the influence of physical training on cardiac autonomic activity in individuals with spinal cord injury (SCI) during different sleep stages. METHODS: Twenty-six volunteers were allocated into three groups: 9 sedentary individuals without SCI (control, CON); 8 sedentary tetraplegic individuals with chronic SCI (SED-SCI); 9 physically trained tetraplegic individuals with chronic SCI (TR-SCI). All participants underwent nocturnal polysomnography to monitor sleep stages: wakefulness, non-rapid eye movement (NREM) sleep (N1, N2, and N3 stages), and REM sleep. The electrocardiography data obtained during this exam were extracted to analyze the heart rate variability (HRV). RESULTS: Sleep stages influenced HRV in the time [RR interval and root mean square of successive RR interval differences (RMSSD)] and frequency [low-frequency (LF) and high-frequency (HF) powers and LF-to-HF ratio] domains (P < 0.05). SED-SCI individuals showed unchanged HRV compared to CON (P > 0.05). When comparing the TR-SCI and SED-SCI groups, no significant differences in HRV were reported in the time domain (P > 0.05). However, in the frequency domain, more accentuated HF power was observed in TR-SCI than in SED-SCI individuals during the N2 and N3 stages and REM sleep (P < 0.05). Moreover, TR-SCI had higher HF power than CON during the N3 stage (P < 0.05). CONCLUSIONS: TR-SCI individuals have greater HF power, indicative of parasympathetic modulation, than sedentary (injured or not injured) individuals during different sleep stages. Therefore, enhanced parasympathetic activity induced by physical training may improve cardiac autonomic modulation during sleep in individuals with chronic SCI.

Selective REM sleep restriction in mice using a device designed for tunable somatosensory stimulation.

BACKGROUND: Sleep perturbation is widely used to investigate the physiological mechanisms that mediate sleep-wake dynamics, and to isolate the specific roles of sleep in health and disease. However, state-of-the-art methods to accomplish sleep perturbation in preclinical models are limited in their throughput, flexibility, and specificity. NEW METHOD: A system was developed to deliver vibro-tactile somatosensory stimulation aimed at controlled, selective sleep perturbation. The frequency and intensity of stimulation can be tuned to target a variety of experimental applications, from sudden arousal to sub-threshold transitions between light and deep stages of NREM sleep. This device was activated in closed-loop to selectively interrupt REM sleep in mice. RESULTS: Vibro-tactile stimulation effectively and selectively interrupted REM sleep - significantly reducing the average REM bout duration relative to matched, unstimulated baseline recordings. As REM sleep was repeatedly interrupted, homeostatic mechanisms prompted a progressively quicker return to REM sleep. These effects were dependent on the parameters of stimulation applied. COMPARISON WITH EXISTING METHODS: Existing sleep perturbation systems often require moving parts within the cage and/or restrictive housing. The system presented is unique in that it interrupts sleep without invading the animal's space. The ability to vary stimulation parameters is a great advantage over existing methods, as it allows for adaptation in response to habituation and/or circadian/homeostatic changes in arousal threshold. CONCLUSIONS: The proposed method of stimulation demonstrates feasibility in affecting mouse sleep within a standard home cage environment, thus limiting environmental stress. Furthermore, the ability to tune frequency and intensity of stimulation allows for graded control over the extent of sleep perturbation, which potentially expands the utility of this technology beyond applications related to sleep.

Sleep physiology in patients with epilepsy: Influence of seizures on rapid eye movement (REM) latency and REM duration.

OBJECTIVE: A well-established bidirectional relationship exists between sleep and epilepsy. Patients with epilepsy tend to have less efficient sleep and shorter rapid eye movement (REM) sleep. Seizures are far more likely to arise from sleep transitions and non-REM sleep compared to REM sleep. Delay in REM onset or reduction in REM duration may have reciprocal interactions with seizure occurrence. Greater insight into the relationship between REM sleep and seizure occurrence is essential to our understanding of circadian patterns and predictability of seizure activity. We assessed a cohort of adults undergoing evaluation of drug-resistant epilepsy to examine whether REM sleep prior to or following seizures is delayed in latency or reduced in quantity. METHODS: We used a spectrogram-guided approach to review the video-electroencephalograms of patients' epilepsy monitoring unit admissions for sleep scoring to determine sleep variables. RESULTS: In our cohort of patients, we found group- and individual-level delay of REM latency and reduced REM duration when patients experienced a seizure before the primary sleep period (PSP) of interest or during the PSP of interest. A significant increase in REM latency and decrease in REM quantity were observed on nights where a seizure occurred within 4 h of sleep onset. No change in REM variables was found when investigating seizures that occurred the day after the PSP of interest. Our study is the first to provide insight about a perisleep period, which we defined as 4-h periods before and after the PSP. SIGNIFICANCE: Our results demonstrate a significant relationship between seizures occurring prior to the PSP, during the PSP, and in the 4-h perisleep period and a delay in REM latency. These findings have implications for developing a biomarker of seizure detection as well as longer term seizure risk monitoring.

Impact of endogenous analgesia triggered by acupuncture, stress, or noxious stimulation on REM sleep-deprived rats.

Poor sleep increases pain, at least in part, by disrupting endogenous pain modulation. However, the efficacy of endogenous analgesia in sleep-deprived subjects has never been tested. To assess this issue, we chose three different ways of triggering endogenous analgesia: (1) acupuncture, (2) acute stress, and (3) noxious stimulation, and compared their ability to decrease the pronociceptive effect induced by REM-SD (Rapid Eye Movement Sleep Deprivation) with that to decrease inflammatory hyperalgesia in the classical carrageenan model. First, we tested the ability of REM-SD to worsen carrageenan-induced hyperalgesia: A low dose of carrageenan (30 µg) in sleep-deprived Wistar rats resulted in a potentiated hyperalgesic effect that was more intense and longer-lasting than that induced by a higher standard dose of carrageenan (100 µg) or by REM-SD alone. Then, we found that (1) acupuncture, performed at ST36, completely reversed the pronociceptive effect induced by REM-SD or by carrageenan; (2) immobilization stress completely reversed the pronociceptive effect of REM-SD, while transiently inhibited carrageenan-induced hyperalgesia; (3) noxious stimulation of the forepaw by capsaicin also reversed the pronociceptive effect of REM-SD and persistently increased the nociceptive threshold above the baseline in carrageenan-treated animals. Therefore, acupuncture, stress, or noxious stimulation reversed the pronociceptive effect of REM-SD, while each intervention affected carrageenan-induced hyperalgesia differently. This study has shown that while sleep loss may disrupt endogenous pain modulation mechanisms, it does not prevent the activation of these mechanisms to induce analgesia in sleep-deprived individuals.

Which structure generates paradoxical (REM) sleep: The brainstem, the hypothalamus, the amygdala or the cortex?

Paradoxical or Rapid eye movement (REM) sleep (PS) is a state characterized by REMs, EEG activation and muscle atonia. In this review, we discuss the contribution of brainstem, hypothalamic, amygdalar and cortical structures in PS genesis. We propose that muscle atonia during PS is due to activation of glutamatergic neurons localized in the pontine sublaterodorsal tegmental nucleus (SLD) projecting to glycinergic/GABAergic pre-motoneurons localized in the ventro-medial medulla (vmM). The SLD PS-on neurons are inactivated during wakefulness and slow-wave sleep by PS-off GABAergic neurons localized in the ventrolateral periaqueductal gray (vPAG) and the adjacent deep mesencephalic reticular nucleus. Melanin concentrating hormone (MCH) and GABAergic PS-on neurons localized in the posterior hypothalamus would inhibit these PS-off neurons to initiate the state. Finally, the activation of a few limbic cortical structures during PS by the claustrum and the supramammillary nucleus as well as that of the basolateral amygdala would also contribute to PS expression. Accumulating evidence indicates that the activation of these limbic structures plays a role in memory consolidation and would communicate to the PS-generating structures the need for PS to process memory. In summary, PS generation is controlled by structures distributed from the cortex to the medullary level of the brain.

A new perspective on positive symptoms: expression of damage or self-defence mechanism of the brain?

Usually, positive neurological symptoms are considered as the consequence of a mere, afinalistic and abnormal increase in function of specific brain areas. However, according to the Theory of Active Inference, which argues that action and perception constitute a loop that updates expectations according to a Bayesian model, the brain is rather an explorer that formulates hypotheses and tests them to assess the correspondence between internal models and reality. Moreover, the cerebral cortex is characterised by a continuous "conflict" between different brain areas, which constantly attempt to expand in order to acquire more of the limited available computational resources, by means of their dopamine-induced neuroplasticity. Thus, it has recently been suggested that dreams, during rapid eye movement sleep (REMS), protect visual brain areas (deprived of their stimuli during rest) from being conquered by other normally stimulated ones. It is therefore conceivable that positive symptoms also have a functional importance for the brain. We evaluate supporting literature data of a 'defensive' role of positive symptoms and the relevance of dopamine-induced neuroplasticity in the context of neurodegenerative and psychiatric diseases. Furthermore, the possible functional significance of idiopathic REMS-related behavioural disorder as well as phantom limb syndrome is examined. We suggest that positive neurological symptoms are not merely a passive expression of a damage, but active efforts, related to dopamine-induced plasticity, to maintain a correct relationship between the external world and its brain representation, thus preventing healthy cortical areas from ousting injured ones.

Auditory stimulation during REM sleep modulates REM electrophysiology and cognitive performance.

REM sleep is critical for memory, emotion, and cognition. Manipulating brain activity during REM could improve our understanding of its function and benefits. Earlier studies have suggested that auditory stimulation in REM might modulate REM time and reduce rapid eye movement density. Building on this, we studied the cognitive effects and electroencephalographic responses related to such stimulation. We used acoustic stimulation locked to eye movements during REM and compared two overnight conditions (stimulation and no-stimulation). We evaluated the impact of this stimulation on REM sleep duration and electrophysiology, as well as two REM-sensitive memory tasks: visual discrimination and mirror tracing. Our results show that this auditory stimulation in REM decreases the rapid eye movements that characterize REM sleep and improves performance on the visual task but is detrimental to the mirror tracing task. We also observed increased beta-band activity and decreased theta-band activity following stimulation. Interestingly, these spectral changes were associated with changes in behavioural performance. These results show that acoustic stimulation can modulate REM sleep and suggest that different memory processes underpin its divergent impacts on cognitive performance.

Monitoring differences in the function of the autonomic nervous system in patients with chronic insomnia using a wearable device.

STUDY OBJECTIVES: to characterize possible differences in the function of the ANS in patients with chronic insomnia compared to a control group, using a wearable device, in order to determine whether those findings allow diagnosing this medical entity. METHODS: Thirty-two patients with chronic insomnia and nineteen patients without any sleep disorder, as a control group, were recruited prospectively. Both groups of patients underwent an in-patient night with simultaneous polysomnography and wearable device recording Empatica E4 a diverse array of physiological signals, including electrodermal activity, temperature, accelerometry, and photoplethysmography, providing a comprehensive resource for in-depth sleep analysis. RESULTS: In polysomnography, patients suffering from insomnia showed a significant decrease in sleep efficiency and total sleep time, prolonged sleep latency, and increased wakefulness after sleep onset. Accelerometry results were statistically significant differences in the three axis (x, y, z) just in stage N3, no differences were observed between both groups in REM sleep. The lowest temperature was reached in REM sleep in both groups. Peripheral temperature did not decrease during the different sleep phases compared to wakefulness in insomnia, unlike in the control group. Heart rate was higher in patients with insomnia than in controls during wakefulness and sleep stage. Heart rate variability was lower in stage N3 and higher in REM sleep compared to wakefulness in both groups. Sweating was significantly higher in patients with insomnia compared to the control group, as indicated by Skin Conductance Variability values and Sudomotor Nerve. CONCLUSIONS: Our study suggests that patients with insomnia have increased sympathetic activity during sleep, showing a higher heart rate. Temperature and sweating significantly influence the different sleep phases.

Recurrent Isolated Sleep Paralysis.

Recurrent isolated sleep paralysis has a 7.6% lifetime prevalence of at least one episode in the general population. Episodes resolve spontaneously and are benign. Sleep paralysis represents a dissociate state, with persistence of the rapid eye movement (REM)-sleep muscle atonia in the waking state. The intrusion of alpha electroencephalogram into REM sleep is followed by an arousal response and then by persistence of REM atonia into wakefulness. Predisposing factors include irregular sleep-wake schedules, sleep deprivation, and jetlag. No drug treatment is required. Patients should be informed about sleep hygiene. Cognitive behavioral therapy may be useful in cases accompanied by anxiety and frightening hallucinations.

Rapid Eye Movement Sleep Behavior Disorder: Clinical Presentation and Diagnostic Criteria.

Rapid eye movement (REM) sleep behavior disorder (RBD) classically presents with repetitive complex motor behavior during sleep with associated dream mentation. The diagnosis requires a history of repetitive complex motor behaviors and polysomnographic demonstration of REM sleep without atonia (RSWA) or capturing dream enactment behaviors. RSWA is best evaluated in the chin or flexor digitorum superficialis muscles. The anterior tibialis muscle is insufficiently accurate to be relied upon solely for RBD diagnosis. RBD may present with parkinsonism or cognitive impairment or may present in isolation. Patients should be monitored for parkinsonism, autonomic failure, or cognitive impairment.

Somnotate: A probabilistic sleep stage classifier for studying vigilance state transitions.

Electrophysiological recordings from freely behaving animals are a widespread and powerful mode of investigation in sleep research. These recordings generate large amounts of data that require sleep stage annotation (polysomnography), in which the data is parcellated according to three vigilance states: awake, rapid eye movement (REM) sleep, and non-REM (NREM) sleep. Manual and current computational annotation methods ignore intermediate states because the classification features become ambiguous, even though intermediate states contain important information regarding vigilance state dynamics. To address this problem, we have developed "Somnotate"-a probabilistic classifier based on a combination of linear discriminant analysis (LDA) with a hidden Markov model (HMM). First we demonstrate that Somnotate sets new standards in polysomnography, exhibiting annotation accuracies that exceed human experts on mouse electrophysiological data, remarkable robustness to errors in the training data, compatibility with different recording configurations, and an ability to maintain high accuracy during experimental interventions. However, the key feature of Somnotate is that it quantifies and reports the certainty of its annotations. We leverage this feature to reveal that many intermediate vigilance states cluster around state transitions, whereas others correspond to failed attempts to transition. This enables us to show for the first time that the success rates of different types of transition are differentially affected by experimental manipulations and can explain previously observed sleep patterns. Somnotate is open-source and has the potential to both facilitate the study of sleep stage transitions and offer new insights into the mechanisms underlying sleep-wake dynamics.

A mammal and bird's-eye-view of the pupil during sleep and wakefulness.

Besides regulating the amount of light that reaches the retina, fluctuations in pupil size also occur in isoluminant conditions during accommodation, during movement and in relation to cognitive workload, attention and emotion. Recent studies in mammals and birds revealed that the pupils are also highly dynamic in the dark during sleep. However, despite exhibiting similar sleep states (rapid eye movement [REM] and non-REM [NREM] sleep), wake and sleep state-dependent changes in pupil size are opposite between mammals and birds, due in part to differences in the type (striated vs. smooth) and control of the iris muscles. Given the link between pupil dynamics and cognitive processes occurring during wakefulness, sleep-related changes in pupil size might indicate when related processes are occurring during sleep. Moreover, the divergent pupillary behaviour observed between mammals and birds raises the possibility that changes in pupil size in birds are a readout of processes not reflected in the mammalian pupil.

Contemporary diagnostic visual and automated polysomnographic REM sleep without atonia thresholds in isolated REM sleep behavior disorder.

STUDY OBJECTIVES: Accurate diagnosis of isolated rapid eye movement (REM) sleep behavior disorder (iRBD) is crucial due to its injury potential and neurological prognosis. We aimed to analyze visual and automated REM sleep without atonia (RSWA) diagnostic thresholds applicable in varying clinical presentations in a contemporary cohort of patients with iRBD using submentalis (SM) and individual bilateral flexor digitorum superficialis (FDS) and anterior tibialis electromyography limb recordings during polysomnography. METHODS: We analyzed RSWA in 20 patients with iRBD and 20 age-, REM-, apnea-hypopnea index-matched controls between 2017 and 2022 for phasic burst durations, density of phasic, tonic, and "any" muscle activity (number of 3-second mini-epochs containing phasic or tonic muscle activity divided by the total number of REM sleep 3-second mini-epochs), and automated Ferri REM atonia index (RAI). Group RSWA metrics were comparatively analyzed. Receiver operating characteristic curves determined optimized area under the curve (AUC) and maximized specificity and sensitivity diagnostic iRBD RSWA thresholds. RESULTS: All mean RSWA metrics were higher in patients with iRBD than in controls (P < .05), except for selected anterior tibialis measures. Optimized, maximal specificity AUC diagnostic cutoffs for coprimary outcomes were: SM "any" 6.5%, 14.0% (AUC = 92.5%) and combined SM+FDS "any" 15.1%, 27.4% (AUC = 95.8%), while SM burst durations were 0.72, and 0.72 seconds (AUC 90.2%) and FDS RAI = 0.930, 0.888 (AUC 92.8%). CONCLUSIONS: This study provides evidence for current quantitative RSWA diagnostic thresholds in chin and individual 4 limb muscles applicable in different iRBD clinical settings and confirms the key value of SM or SM+FDS to assure accurate iRBD diagnosis. Evolving iRBD recognition underscores the necessity of continuous assessment with future large, prospective, well-harmonized, multicenter polysomnographic analyses. CITATION: Leclair-Visonneau L, Feemster JC, Bibi N, et al. Contemporary diagnostic visual and automated polysomnographic REM sleep without atonia thresholds in isolated REM sleep behavior disorder. J Clin Sleep Med. 2024;20(2):279-291.

REM parameters in drug-free major depressive disorder: A systematic review and meta-analysis.

Previous studies revealed that rapid eye movement (REM) parameters, such as REM latency (RL) and REM density (RD) could be used as electrophysiological markers of depression. Yet these finding should be re-tested in a comorbid-free and drug-free sample. The present systematic review and meta-analysis was conducted to investigate whether drug-free and comorbid-free patients with unipolar depression differentiate from controls with respect to the RL and RD. The PubMed and Web of Science databases were screened from inception to 23 January 2023 for case-control studies comparing RL and RD of patients with unipolar depression and controls. The primary outcome was the standard mean difference. The data were fitted with a random-effects model. Meta-regressions were conducted to investigate patient characteristics and effect size. Publication bias assessment was checked by Egger's Regression and funnel plot asymmetry. Among 43 articles accepted as eligible, 46 RL and 22 RD measurements were included in the meta-analysis. The results indicated shortened RL and increased RD in the patient group than controls. Neither Egger's regression nor funnel plot asymmetry were significant for publication bias. In conclusion, our results tested within drug-free and comorbid-free samples are in line with the literature.

Linking brain structure, cognition, and sleep: insights from clinical data.

STUDY OBJECTIVES: To use relatively noisy routinely collected clinical data (brain magnetic resonance imaging (MRI) data, clinical polysomnography (PSG) recordings, and neuropsychological testing), to investigate hypothesis-driven and data-driven relationships between brain physiology, structure, and cognition. METHODS: We analyzed data from patients with clinical PSG, brain MRI, and neuropsychological evaluations. SynthSeg, a neural network-based tool, provided high-quality segmentations despite noise. A priori hypotheses explored associations between brain function (measured by PSG) and brain structure (measured by MRI). Associations with cognitive scores and dementia status were studied. An exploratory data-driven approach investigated age-structure-physiology-cognition links. RESULTS: Six hundred and twenty-three patients with sleep PSG and brain MRI data were included in this study; 160 with cognitive evaluations. Three hundred and forty-two participants (55%) were female, and age interquartile range was 52 to 69 years. Thirty-six individuals were diagnosed with dementia, 71 with mild cognitive impairment, and 326 with major depression. One hundred and fifteen individuals were evaluated for insomnia and 138 participants had an apnea-hypopnea index equal to or greater than 15. Total PSG delta power correlated positively with frontal lobe/thalamic volumes, and sleep spindle density with thalamic volume. rapid eye movement (REM) duration and amygdala volume were positively associated with cognition. Patients with dementia showed significant differences in five brain structure volumes. REM duration, spindle, and slow-oscillation features had strong associations with cognition and brain structure volumes. PSG and MRI features in combination predicted chronological age (R2 = 0.67) and cognition (R2 = 0.40). CONCLUSIONS: Routine clinical data holds extended value in understanding and even clinically using brain-sleep-cognition relationships.

The effects of acute exercise and a nap on heart rate variability and memory in young sedentary adults.

Recent evidence suggests that the autonomic nervous system can contribute to memory consolidation during sleep. Whether fluctuations in cardiac autonomic activity during sleep following physical exercise contribute to the process of memory consolidation has not been studied. We assessed the effects of a non-rapid eye movement (NREM) nap following acute exercise on cardiac autonomic regulation assessed with heart rate variability (HRV) to examine if HRV influences memory processes. Fifty-six (59% female) healthy young adults (23.14 ± 3.74 years) were randomly allocated to either the exercise plus nap (ExNap, n = 27) or nap alone (NoExNap, n = 29) groups. The ExNap group performed a 40-minute moderate-intensity cycling, while the NoExNap group was sedentary prior to learning 45 neutral pictures for a later test. Subsequently, participants underwent a 60-minute NREM nap while measuring EKG, followed by a visual recognition test. Our results indicated that heart rate did not significantly differ between the groups (p = .243), whereas vagally mediated HRV indices were lower in the ExNap group compared to the NoExNap group (p < .05). There were no significant differences in sleep variables between the groups (p > .05). Recognition accuracy was significantly higher in the ExNap group than in the NoExNap group (p = .027). In addition, the recognition accuracy of the ExNap group was negatively associated with vagally mediated HRV (p < .05). Pre-nap acute exercise appears to attenuate parasympathetic activity and to alter the relationship between memory and cardiac autonomic activity.

English translation of the first study reporting cyclical periods of increased respiration and eye and body motility during sleep in infants in 1926, with commentary.

This is the first English translation of the work Periodic phenomena in the sleep in children, published in 1926 in the Journal Novoe v refleksologii i fiziologii nervnoi sistemy (Vol. 2, pp. 338-345) by Maria Denisova and Nicholai Figurin; it is the first study to report data on what is currently termed rapid eye movement (REM) sleep. The authors acquired continuous quantitative respiration data, as well as, eye and body movements during sleep in children for up to 6 hours, and discovered several novel features of sleep cycles in healthy infants from birth to about 1 year of age. First, the study reports cyclical periods of increased respiration and eye and body movements, with rapid ocular movements visible under relaxed eyelids (separation: 0.5-1 mm). These observations suggest atonia of REM sleep. Second, the length of the complete cycle (alternating active and quiet sleep phases or states) is about 50 minutes, an estimate that is consistent with later work. Third, the study identifies infant-specific ordering of sleep states, with the active phase beginning after sleep onset, followed by the quiescence phase. Importantly, these published data on sleep cycles precede all published studies related to the state now termed REM sleep by about 30 years (i.e. publishing in Science and in the Journal of Applied Physiology in the 1950s by Eugene Aserinski and Nathaniel Kleitman). In the historical commentary accompanying this translation, the findings of those later works are carefully compared to the original data on respiration and ocular and body motility cycles during sleep in infants, first reported and published by Denisova and Figurin (1926).

Altered parasympathetic activity during sleep and emotionally arousing wakefulness in frequent nightmare recallers.

Nightmare disorder is characterized by dysfunctional emotion regulation and poor subjective sleep quality reflected in pathophysiological features such as abnormal arousal processes and sympathetic influences. Dysfunctional parasympathetic regulation, especially before and during rapid eye movement (REM) phases, is assumed to alter heart rate (HR) and its variability (HRV) of frequent nightmare recallers (NM). We hypothesized that cardiac variability is attenuated in NMs as opposed to healthy controls (CTL) during sleep, pre-sleep wakefulness and under an emotion-evoking picture-rating task. Based on the polysomnographic recordings of 24 NM and 30 CTL participants, we examined HRV during pre-REM, REM, post-REM and slow wave sleep, separately. Additionally, electrocardiographic recordings of resting state before sleep onset and under an emotionally challenging picture-rating task were also analyzed. Applying repeated measures analysis of variance (rmANOVA), a significant difference was found in the HR of NMs and CTLs during nocturnal segments but not during resting wakefulness, suggesting autonomic dysregulation, specifically during sleep in NMs. As opposed to the HR, the HRV values were not significantly different in the rmANOVA in the two groups, implying that the extent of parasympathetic dysregulation on a trait level might depend on the severeness of dysphoric dreaming. Nonetheless, in the group comparisons, the NM group showed increased HR and reduced HRV during the emotion-evoking picture-rating task, which aimed to model the nightmare experience in the daytime, indicating disrupted emotion regulation in NMs under acute distress. In conclusion, trait-like autonomic changes during sleep and state-like autonomic responses to emotion-evoking pictures indicate parasympathetic dysregulation in NMs.

Regulation of REM sleep in mice: The role of dopamine and serotonin function in the basolateral amygdala.

Animals have a sleep cycle that involves the repetitive occurrence of non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. In a previous study, we discovered that a transient increase in dopamine (DA) levels in the basolateral amygdala (BLA) during NREM sleep terminates NREM sleep and initiates REM sleep by acting on Drd2-positive neurons (Hasegawa et al., 2022). In this study, we identified the neurons activated by the transient increase of DA in the BLA and found that chemogenetic excitation of these neurons increased REM sleep. Additionally, we demonstrated that acute inhibition of serotonin (5HT) in the BLA elicited a transient increase in DA in the BLA, which triggered REM sleep.

Role of the substantia nigra pars reticulata in sleep-wakefulness: A review of research progress.

Sleep is a complex physiological process that includes two main stages: non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. During mammalian sleep, especially REM sleep, skeletal muscles are suppressed to varying degrees, and corresponding movements are inhibited. The synchronous occurrence of sleep and motor inhibition suggests they may share the same neural circuits. Recently, the substantia nigra pars reticulata (SNr) has attracted attention for its potential dual role in regulating sleep-wake cycles and movement. In this review, the SNr's role is surveyed by examining existing research reports regarding its involvement in sleep-wake regulation and motor control. By focusing on the SNr, the goal is to shed light on its dual role intricacies and stimulate further inquiry into potential interactions between sleep and movement regulation, thus aiming to explore sleep-wake regulatory mechanisms and offer novel directions for subsequent scientific investigation.