Rapid Eye Movement Research Articles

Dysfunctional hippocampal-prefrontal network underlies a multidimensional neuropsychiatric phenotype following early-life seizure.

Brain disturbances during development can have a lasting impact on neural function and behavior. Seizures during this critical period are linked to significant long-term consequences such as neurodevelopmental disorders, cognitive impairments, and psychiatric symptoms, resulting in a complex spectrum of multimorbidity. The hippocampus-prefrontal cortex (HPC-PFC) circuit emerges as a potential common link between such disorders. However, the mechanisms underlying these outcomes and how they relate to specific behavioral alterations are unclear. We hypothesized that specific dysfunctions of hippocampal-cortical communication due to early-life seizure would be associated with distinct behavioral alterations observed in adulthood. Here, we performed a multilevel study to investigate behavioral, electrophysiological, histopathological, and neurochemical long-term consequences of early-life Status epilepticus in male rats. We show that adult animals submitted to early-life seizure (ELS) present working memory impairments and sensorimotor disturbances, such as hyperlocomotion, poor sensorimotor gating, and sensitivity to psychostimulants despite not exhibiting neuronal loss. Surprisingly, cognitive deficits were linked to an aberrant increase in the HPC-PFC long-term potentiation (LTP) in a U-shaped manner, while sensorimotor alterations were associated with heightened neuroinflammation, as verified by glial fibrillary acidic protein (GFAP) expression, and altered dopamine neurotransmission. Furthermore, ELS rats displayed impaired HPC-PFC theta-gamma coordination and an abnormal brain state during active behavior resembling rapid eye movement (REM) sleep oscillatory dynamics. Our results point to impaired HPC-PFC functional connectivity as a possible pathophysiological mechanism by which ELS can cause cognitive deficits and psychiatric-like manifestations even without neuronal loss, bearing translational implications for understanding the spectrum of multidimensional developmental disorders linked to early-life seizures.

Dysfunctional hippocampal-prefrontal network underlies a multidimensional neuropsychiatric phenotype following early-life seizure

Brain disturbances during development can have a lasting impact on neural function and behavior. Seizures during this critical period are linked to significant long-term consequences such as neurodevelopmental disorders, cognitive impairments, and psychiatric symptoms, resulting in a complex spectrum of multimorbidity. The hippocampus-prefrontal cortex (HPC-PFC) circuit emerges as a potential common link between such disorders. However, the mechanisms underlying these outcomes and how they relate to specific behavioral alterations are unclear. We hypothesized that specific dysfunctions of hippocampal-cortical communication due to early-life seizure would be associated with distinct behavioral alterations observed in adulthood. Here, we performed a multilevel study to investigate behavioral, electrophysiological, histopathological, and neurochemical long-term consequences of early-life Status epilepticus in male rats. We show that adult animals submitted to early-life seizure (ELS) present working memory impairments and sensorimotor disturbances, such as hyperlocomotion, poor sensorimotor gating, and sensitivity to psychostimulants despite not exhibiting neuronal loss. Surprisingly, cognitive deficits were linked to an aberrant increase in the HPC-PFC long-term potentiation (LTP) in a U-shaped manner, while sensorimotor alterations were associated with heightened neuroinflammation, as verified by glial fibrillary acidic protein (GFAP) expression, and altered dopamine neurotransmission. Furthermore, ELS rats displayed impaired HPC-PFC theta-gamma coordination and an abnormal brain state during active behavior resembling rapid eye movement (REM) sleep oscillatory dynamics. Our results point to impaired HPC-PFC functional connectivity as a possible pathophysiological mechanism by which ELS can cause cognitive deficits and psychiatric-like manifestations even without neuronal loss, bearing translational implications for understanding the spectrum of multidimensional developmental disorders linked to early-life seizures.

Prediction of Co-Occurrence of Lewy Body Disease with Alzheimer's Disease.

Identifying the coexistence of Lewy body (LB) pathology with Alzheimer's disease (AD) in clinical practice is important in the era of anti-amyloid-β antibody therapy. However, few studies have predicted the presence of comorbid LB pathology with AD using indicative biomarkers of dementia with Lewy bodies or by collecting detailed clinical symptoms. We report the clinical progression of a 67-year-old patient diagnosed with AD who developed rapid eye movement sleep disorder-like symptoms and transient visual hallucinations 10 years after AD onset and was considered to have comorbid LB pathology based on imaging indicative biomarkers of dementia with Lewy bodies.

Alpha-synuclein pathology in isolated rapid eye movement sleep behaviour disorder: a meta-analysis.

Accumulating evidence indicates that patients with isolated rapid eye movement sleep behaviour disorder (iRBD), a prodromal stage of synucleinopathies, show abnormal deposition of misfolded alpha-synuclein (a-Syn) in peripheral tissues. The clinical utility of testing for a-Syn in iRBD is unclear. This meta-analysis focused on the utility of testing for the abnormal a-Syn phosphorylated at Ser129 (p-syn) and a-Syn seeding activity (a-Syn seed amplification assays [aSyn-SAA]). Following an electronic database search, 15 studies were included that provided at a minimum data on test positivity in participants with iRBD. Test positivity from cerebrospinal fluid (CSF) was 80% (95% confidence interval [CI] 68-88%, I2 = 71%) and for skin was 74.8% (95% CI 53.2-88.5%, I2 = 64%) for aSyn-SAA and 78.5% (95% CI 70.4-84.9%, I2 = 14%) for p-syn. The phenoconversion rate ratio of biopsy-positive versus biopsy-negative iRBD was 1.28 (95% CI 0.68-2.41, I2 = 0%). Skin as a source had a specificity of 99% (95% CI 95-100%, I2 = 0%; p = 0.01 compared to CSF). As a test, p-syn, had a specificity of 100% (95% CI 93-100%, I2 = 0%; p < 0.001) compared to aSyn-SAA. The odds ratio of a-Syn test positivity in iRBD versus other RBDs was 112 (95% CI 20-629, I2 = 0%). These results demonstrate clinically significant test positivity in iRBD and favour skin over CSF as the source of a-Syn pathological analysis, and p-syn over aSyn-SAA as the testing method. Overall, these findings indicate that testing for a-Syn could help in differentiating iRBD from RBD secondary to other conditions.

Simulated quick returns in a laboratory context and effects on sleep and pre-sleep arousal between shifts: a crossover controlled trial

This trial presents a laboratory model investigating the effect of quick returns (QRs, <11 h time off between shifts) on sleep and pre-sleep arousal. Using a crossover design, 63 participants worked a simulated QR condition (8 h time off between consecutive evening- and day shifts) and a day-day (DD) condition (16 h time off between consecutive day shifts). Participants slept at home and sleep was measured using a sleep diary and sleep radar. Compared to the DD condition, the QR condition reduced subjective and objective total sleep time by approximately one hour (both p < .001), reduced time in light- (p < .001), deep- (p = .004), rapid eye movement (REM, p < .001), percentage of REM sleep (p = .023), and subjective sleep quality (p < .001). Remaining sleep parameters and subjective pre-sleep arousal showed no differences between conditions. Results corroborate previous field studies, validating the QR model and indicating causal effects of short rest between shifts on common sleep parameters and sleep architecture.

Relationship between OSA pathophysiological phenotypes and treatment response to mandibular advancement devices: a pilot study.

To assess whether critical pathophysiological phenotypes predict treatment response in patients with obstructive sleep apnea (OSA) using a mandibular advancement device (MAD). Thirty-one OSA patients were treated with a MAD. Individuals were categorized and graded into four pathophysiological phenotypes based on polysomnographic features (anatomical, ventilatory control, arousal threshold and muscle responsiveness). Morphoanthropometric data were additionally assessed. Patients were classified as responders or nonresponders. Associations between polysomnographic phenotypes and treatment response were documented, as was morphoanthropometric data and their impact on therapeutic success. There was a male predominance (64.5%), with a median age of 49 years (25p:40; 75p:55), BMI=27.4 kg/m2 (26; 28.8) and apnea-hypopnea index (AHI) of 18.2 (25p:11.7; 75p: 27.6). The majority of patients treated with a MAD (58%) were good responders (68.0% mild and moderate versus 16.7% severe). Treatment response was associated with shorter intermolar and interpremolar distances in the lower arch (p = 0.0092 and 0.0129). Rapid eye movement sleep AHI (REMAHI) and MAD-related treatment response were inversely correlated (p = 0.0013). Favorable anatomical (p = 0.0339) and low muscle response (p = 0.0447) phenotypes were correlated with outcomes. According to our results, a favorable response occurred in a better 'anatomical phenotype' and in the worse 'muscular responsiveness phenotype' according to polysomnographic data. Furthermore, other favorable predictors, such as a REMAHI <16 and a smaller distance between lower molars and premolars, were found. These findings indicate that clinical and polysomnographic aspects can discriminate phenotypes that may guide decisions on MAD treatment for OSA.

Purkinje cell dysfunction causes disrupted sleep in ataxic mice.

Purkinje cell dysfunction disrupts movement and causes disorders such as ataxia. Recent evidence suggests that Purkinje cell dysfunction may also alter sleep regulation. Here, we used an ataxic mouse model generated by silencing Purkinje cell neurotransmission (L7Cre;Vgatfx/fx) to better understand how cerebellar dysfunction impacts sleep physiology. We focused our analysis on sleep architecture and electrocorticography (ECoG) patterns based on their relevance to extracting physiological measurements during sleep. We found that circadian activity is unaltered in the mutant mice, although their sleep parameters and ECoG patterns are modified. The L7Cre;Vgatfx/fx mutant mice have decreased wakefulness and rapid eye movement (REM) sleep, while non-rapid eye movement (NREM) sleep is increased. The mutants have an extended latency to REM sleep, which is also observed in human ataxia patients. Spectral analysis of ECoG signals revealed alterations in the power distribution across different frequency bands defining sleep. Therefore, Purkinje cell dysfunction may influence wakefulness and equilibrium of distinct sleep stages in ataxia. Our findings posit a connection between cerebellar dysfunction and disrupted sleep and underscore the importance of examining cerebellar circuit function in sleep disorders.

Modulatory effects of low-intensity retinal ultrasound stimulation on rapid and non-rapid eye movement sleep.

Prior investigations have established that the manipulation of neural activity has the potential to influence both rapid eye movement and non-rapid eye movement sleep. Low-intensity retinal ultrasound stimulation has shown effectiveness in the modulation of neural activity. Nevertheless, the specific effects of retinal ultrasound stimulation on rapid eye movement and non-rapid eye movement sleep, as well as its potential to enhance overall sleep quality, remain to be elucidated. Here, we found that: In healthy mice, retinal ultrasound stimulation: (i) reduced total sleep time and non-rapid eye movement sleep ratio; (ii) changed relative power and sample entropy of the delta (0.5-4Hz) in non-rapid eye movement sleep; and (iii) enhanced relative power of the theta (4-8Hz) and reduced theta-gamma coupling strength in rapid eye movement sleep. In Alzheimer's disease mice with sleep disturbances, retinal ultrasound stimulation: (i) reduced the total sleep time; (ii) altered the relative power of the gamma band during rapid eye movement sleep; and (iii) enhanced the coupling strength of delta-gamma in non-rapid eye movement sleep and weakened the coupling strength of theta-fast gamma. The results indicate that retinal ultrasound stimulation can modulate rapid eye movement and non-rapid eye movement-related neural activity; however, it is not beneficial to the sleep quality of healthy and Alzheimer's disease mice.

Altered Cortical Information Interaction During Respiratory Events in Children with Obstructive Sleep Apnea-Hypopnea Syndrome.

Obstructive sleep apnea-hypopnea syndrome (OSAHS) significantly impairs children's growth and cognition. This study aims to elucidate the pathophysiological mechanisms underlying OSAHS in children, with a particular focus on the alterations in cortical information interaction during respiratory events. We analyzed sleep electroencephalography before, during, and after events, utilizing Symbolic Transfer Entropy (STE) for brain network construction and information flow assessment. The results showed a significant increase in STE after events in specific frequency bands during N2 and rapid eye movement (REM) stages, along with increased STE during N3 stage events. Moreover, a noteworthy rise in the information flow imbalance within and between hemispheres was found after events, displaying unique patterns in central sleep apnea and hypopnea. Importantly, some of these alterations were correlated with symptom severity. These findings highlight significant changes in brain region coordination and communication during respiratory events, offering novel insights into OSAHS pathophysiology in children.

The CCJR® Gerard A. Engh Excellence in Knee Research Award: Remote Monitoring of Sleep Disturbance Following Total Knee Arthroplasty: A Cautionary Note

BackgroundSleep disturbances are common after total knee arthroplasty (TKA). Despite the rising popularity of wearables to track sleep, little evidence exists in the arthroplasty literature regarding their efficacy. We aimed to correlate validated wearable sleep metrics with patient-reported sleep quality following TKA. MethodsPatients undergoing primary TKA were consecutively enrolled. Patients used a wearable device preoperatively and 90 days postoperatively to track five previously-validated measures of sleep. Each month, they rated their sleep quality. Wearable sleep data was correlated with patient-reported sleep quality using a point biserial correlation test. Categorical data were compared using Chi-square tests. A total of 110 patients were included. ResultsPreoperatively, 20.8% of patients reported “fairly bad” or “very bad” sleep; this increased to 44.4% 30 days postoperatively, then decreased to 26.5% 60 days postoperatively, and to 20.2% 90 days postoperatively. At 30 days postoperatively, time in bed, time asleep, and minutes of rapid eye movement sleep weakly correlated with patient-reported sleep quality (correlations 0.356, 0.345, and 0.345, respectively; P < .001). Sleep quality did not correlate with any wearable metric collected 60 or 90 days postoperatively. ConclusionsPatient-reported sleep quality following TKA initially worsened postoperatively, then improved to preoperative levels by 90 days. Time in bed, time asleep, and rapid eye movement sleep minutes only weakly correlated with patient-reported sleep quality at 30 days; no other correlations were detected. Surgeons that utilize remote monitoring following TKA should be aware that surrogate measures generated from these devices may correlate weakly, if at all, with the patient-reported outcome of the parameter being studied.

Effectiveness of a grid mattress on adults' sleep quality and health: A quasi-experimental intervention study.

Despite that 93% of people indicate that a mattress plays a pivotal role in achieving high-quality sleep, there is a scarcity of research investigating the influence of mattresses on sleep quality, pain, and mood in nonclinical poor sleepers. The purpose was to examine the effectiveness of a pressure-releasing medium-firm grid mattress on sleep and health outcomes (e.g., mood, pain, daytime fatigue) of adults with nonclinical insomnia symptoms using a quasi-experimental design. Participants were 39 adults (mean age = 45.29) with nonclinical insomnia (i.e., occasional sleeplessness). Following 1 week of baseline assessments on their current mattress, they slept on a pressure-relieving grid mattress for 8 weeks. Participants completed self-report assessments of the Pittsburgh Sleep Quality Index, Berlin Questionnaire, Insomnia Severity Index, Restorative Sleep Questionnaire, Perceived Stress Scale, Profile of Mood States, Daytime Fatigue Scale, Pain and Sleep Questionnaire, and Brief Pain Inventory at Baseline and Weeks 1, 2, 3, 4, and 8. Participants continually wore an Oura Ring to objectively assess sleep and daytime activity. The data were collected from January 2022 to April 2022 and were stored electronically. Repeated-measures analyses of variance were used to analyze mean time differences. Self-reported sleep quality, perceived pain, perceived stress, mood, and daytime fatigue improved significantly from Baseline to Week 8, p's < 0.05. Objective Oura Ring validated the self-reported sleep and daytime activity outcomes with improvements in sleep duration, time awake during the night, light sleep, deep sleep, and total sleep time, p's < 0.05. No significant time effects were evidenced for rapid eye movement sleep. No adverse events were reported. The grid mattress is a simple, noninvasive, and nonpharmacological intervention that improved adults sleep quality and health. Controlled trials are encouraged to examine the effects of this mattress in a variety of populations and environments.

Idiopathic Rapid Eye Movement Sleep Behavior Disorder (iRBD) Shares Similar Fecal Short-Chain Fatty Acid Alterations with Multiple System Atrophy (MSA) and Parkinson's Disease (PD).

Idiopathic rapid eye movement sleep behavior disorder (iRBD) is considered as a prodromal stage of synucleinopathies. Fecal short-chain fatty acid (SCFA) changes in iRBD and the relationships with synucleinopathies have never been investigated. To investigate fecal SCFA changes among iRBD, multiple system atrophy (MSA), and Parkinson's disease (PD), and evaluate their relationships. Fecal SCFAs and gut microbiota were measured in 29 iRBD, 42 MSA, 40 PD, and 35 normal controls (NC) using gas chromatography-mass spectrometry and 16S rRNA gene sequencing. Compared with NC, fecal SCFA levels (propionic, acetic, and butyric acid) were lower in iRBD, MSA, and PD. Combinations of these SCFAs could differentiate NC from iRBD (AUC 0.809), MSA (AUC 0.794), and PD (AUC 0.701). Decreased fecal SCFAs were associated with the common reducing SCFA-producing gut microbiota in iRBD, MSA, and PD. iRBD shares similar fecal SCFA alterations with MSA and PD, and the combination of these SCFAs might be a potential synucleinopathies-related biomarker. © 2024 International Parkinson and Movement Disorder Society.

Sleep loss and emotion: A systematic review and meta-analysis of over 50 years of experimental research.

In a largely sleep-deprived society, quantifying the effects of sleep loss on emotion is critical for promoting psychological health. This preregistered systematic review and meta-analysis quantified the effects of various forms of sleep loss on multiple aspects of emotional experiences. Eligible studies used experimental reductions of sleep via total sleep deprivation, partial sleep restriction, or sleep fragmentation in healthy populations to examine effects on positive affect, negative affect, general mood disturbances, emotional reactivity, anxiety symptoms, and/or depressive symptoms. In total, 1,338 effect sizes across 154 studies were included (N = 5,717; participant age range = 7-79 years). Random effects models were conducted, and all forms of sleep loss resulted in reduced positive affect (standardized mean difference [SMD] = -0.27 to -1.14), increased anxiety symptoms (SMD = 0.57-0.63), and blunted arousal in response to emotional stimuli (SMD = -0.20 to -0.53). Findings for negative affect, reports of emotional valence in response to emotional stimuli, and depressive symptoms were mixed and depended on the type of sleep loss. Nonlinear effects for the amount of sleep loss as well as differences based on the stage of sleep restricted (i.e., rapid eye movement sleep or slow-wave sleep) were also detected. This study represents the most comprehensive quantitative synthesis of experimental sleep and emotion research to date and provides strong evidence that periods of extended wakefulness, shortened sleep duration, and/or nighttime awakenings adversely influence human emotional functioning. Findings provide an integrative foundation for future research on sleep and emotion and elucidate the precise ways that inadequate sleep may impact our daytime emotional lives. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

An EEG Signature of MCH Neuron Activities Predicts Cocaine Seeking

BackgroundIdentifying biomarkers that predict substance use disorder (SUD) propensity may better strategize anti-addiction treatment. The melanin-concentrating hormone (MCH) neurons in the lateral hypothalamus (LH) critically mediates interactions between sleep and substance use; however, their activities are largely obscured in surface electroencephalogram (EEG) measures, hindering the development of biomarkers. MethodsSurface EEG signals and real-time Ca2+ activities of LH MCH neurons (Ca2+MCH) were simultaneously recorded in male and female adult rats. Mathematical modeling and machine learning were then applied to predict Ca2+MCH using EEG derivatives. The robustness of the predictions was tested across sex and treatment conditions. Finally, features extracted from the EEG-predicted Ca2+MCH either before or after cocaine experience were used to predict future drug-seeking behaviors. ResultsAn EEG waveform derivative – a modified theta-to-delta ratio (EEG Ratio) – accurately tracks real-time Ca2+MCH in rats. The prediction was robust during rapid eye movement sleep (REMS), persisted through REMS manipulations, wakefulness, circadian phases, and was consistent across sex. Moreover, cocaine self-administration and long-term withdrawal altered EEG Ratio suggesting shortening and circadian redistribution of synchronous MCH neuron activities. In addition, features of EEG Ratio indicative of prolonged synchronous MCH neuron activities predicted lower subsequent cocaine seeking. EEG Ratio also exhibited advantages over conventional REMS measures for the predictions. ConclusionsThe identified EEG Ratio may serve as a non-invasive measure for assessing MCH neuron activities in vivo and evaluating REMS; it may also serve as a potential biomarker predicting drug use propensity.

A Comparative Study of Architecture and Quality of Sleep among Juvenile Myoclonic Epilepsy Patients and Healthy Individuals Attending Tertiary Care Hospital in Central India

&#x0D; &#x0D; &#x0D; &#x0D; Background and Objective: Primary sleep disorders are common in patients with epilepsy. Seizures, epileptiform discharges, and antiepileptic drugs alter the sleep architecture of patients with juvenile myoclonic epilepsy (JME). We evaluated sleep architecture and its quality in these patients.&#x0D; Materials and Methods: Thirty patients with JME (11 men and 19 women with mean age of 21.10 ± 4.55 years) and 30 healthy controls underwent overnight polysomnography (PSG). Sleep quality and daytime sleepiness were assessed using Pittsburgh Sleep Quality Index (PSQI) and Epworth Sleepiness Scale (ESS), respectively.&#x0D; Results: Myoclonus and generalized tonic-clonic seizures (GTCS) were present in all patients with JME, while absence seizures were in 13.3%. Sleep deprivation was the most frequent precipitating factor for seizures (56.6%) followed by fatigue, sound, and photic stimulation. Patients with JME reported a statistically significant drop in sleep efficiency (P&lt;0.001) with prolonged sleep onset latency (P&lt;0.001). There was prolongation in the N1 stage of non-rapid eye movement (NREM) sleep (P=0.002), and reduction in the N2 stage of NREM (P&lt;0.001) and rapid eye movement (REM) sleep (P&lt;0.001). The median PSQI score was higher in patients with JME, suggesting poor sleep quality (P&lt;0.001), and the daytime sleepiness was not different as indicated by the similar median ESS score (P=0.033).&#x0D; Conclusion: Our results suggest a significant alteration in the sleep architecture of patients with JME with reduced sleep efficiency and poor sleep quality. The possible role of the disease itself is suggested for these alterations as a simi- lar trend was also observed in drug naïve patients.&#x0D; &#x0D; &#x0D; &#x0D;

Brain Functional Connectivity Changes in Rapid Eye Movement Sleep Behavior Disorder

The idiopathic rapid eye movement sleep behavior disorder (iRBD) has been reported as prodromal biomarker for neurodegenerative synucleinopathies. To early detect neurodegeneration in preclinical stage, pathophysiological changes of iRBD have been studied in many ways including structural magnetic resonance imaging (MRI), functional MRI (fMRI), and connectivity analyses. This review summarizes functional connectivity studies using resting-state fMRI in iRBD patients focused on motor-related network, compensatory mechanism of synucleinopathies, cognitive dysfunction, and non-motor symptoms.

Exploring the Intersection of Narcolepsy and Attention Deficit Hyperactivity Disorder: Similarities, Differences, and Clinical Implications

Narcolepsy and attention deficit hyperactivity disorder (ADHD) are distinct neurobiological conditions characterized by overlapping symptoms, including excessive daytime sleepiness and cognitive dysfunction. Despite their differences in etiology and pathophysiology, recent studies have highlighted a potential association between the two disorders, with a significant prevalence of ADHD symptoms observed in narcolepsy patients. This narrative review explores the similarities and differences between narcolepsy and ADHD, focusing on their shared symptomatology, neurobiological mechanisms, challenges in diagnosis, and treatment implications. While both disorders exhibit disruptions in dopaminergic and noradrenergic neurotransmitter systems, differential diagnosis remains challenging due to overlapping clinical presentations. Polysomnography findings, such as appearance of sleep onset rapid eye movements in narcolepsy patients, provide important distinctions that enable accurate diagnosis. Treatment strategies often involve stimulant medications for symptom management; however, nonpharmacological interventions, such as cognitive behavioral therapy, have been shown to have the potential to improve patient outcomes. Clinicians must consider the possibility of coexisting narcolepsy in ADHD patients and vice versa to ensure appropriate treatment selection and optimal patient care. Further research is needed to refine diagnostic criteria, elucidate the complex interplay between the two disorders, and develop personalized therapeutic approaches. A multidisciplinary approach involving sleep specialists, neurologists, psychiatrists, and psychologists is essential to address the diverse biopsychosocial needs of patients with concurrent narcolepsy and ADHD.

Crocin (bioactive compound of Crocus sativus L.) potently restores REM sleep deprivation-induced manic- and obsessive-compulsive-like behaviors in female rats.

Rapid-eye movement (REM) sleep deprivation (SD) can induce manic-like behaviors including hyperlocomotion. On the other hand, crocin (one of the main compounds of Crocus sativus L. or Saffron) may be beneficial in the improvement of mental and cognitive dysfunctions. Also, crocin can restore the deleterious effects of SD on mental and cognitive processes. In this study, we investigated the effect of REM SD on female rats' behaviors including depression- and anxiety-like behaviors, locomotion, pain perception, and obsessive-compulsive-like behavior, and also, the potential effect of crocin on REM SD effects. We used female rats because evidence on the role of REM SD in modulating psychological and behavioral functions of female (but not male) rats is limited. REM SD was induced for 14 days (6h/day), and crocin (25, 50, and 75 mg/kg) was injected intraperitoneally. Open field test, forced swim test, hot plate test, and marble burying test were used to assess rats' behaviors. The results showed REM SD-induced manic-like behavior (hyperlocomotion). Also, REM SD rats showed decreased anxiety- and depression-like behavior, pain subthreshold (the duration it takes for the rat to feel pain), and showed obsessive compulsive-like behavior. However, crocin at all doses partially or fully reversed REM SD-induced behavioral changes. In conclusion, our results suggested the possible comorbidity of OCD and REM SD-induced manic-like behavior in female rats or the potential role of REM SD in the etiology of OCD, although more studies are needed. In contrast, crocin can be a possible therapeutic choice for decreasing manic-like behaviors.

Sleep and Thermoregulation in Birds: Cold Exposure Reduces Brain Temperature but Has Little Influence on Sleep Time and Sleep Architecture in Jackdaws (Coloeus monedula).

Birds have an electrophysiological sleep state that resembles mammalian rapid-eye-movement (REM) sleep. However, whether its regulation and function are similar is unclear. In the current experiment, we studied REM sleep regulation in jackdaws (Coloeus monedula) by exposing the birds to low ambient temperature, a procedure that selectively suppresses REM sleep in mammals. Eight jackdaws were equipped with electrodes to record brain activity and neck muscle activity and a thermistor to record cortical brain temperature. Recordings covered a three-day period starting with a 24 h baseline day at an ambient temperature of 21 °C, followed by a 12 h cold night at 4 °C, after which the ambient temperature was restored to 21 °C for the remaining recovery period. Cold exposure at night caused a significant drop in brain temperature of 1.4 °C compared to the baseline night. However, throughout the cold night, jackdaws expressed NREM sleep and REM sleep levels that were not significantly different from the baseline. Also, EEG spectral power during NREM sleep was unaffected by cold exposure. Thus, while cold exposure had a clear effect on brain temperature in jackdaws, it did not have the same REM sleep suppressing effect reported for mammals. These findings suggest that the REM-sleep-like state in birds, unlike REM sleep in mammals, is protected against the influence of low temperature.

Ozone rectal insufflation mitigates chronic rapid eye movement sleep deprivation-induced cognitive impairment through inflammation alleviation and gut microbiota regulation in mice

A range of sleep disorders has the potential to adversely affect cognitive function. This study was undertaken with the objective of investigating the effects of ozone rectal insufflation (O3-RI) on cognitive dysfunction induced by chronic REM sleep deprivation, as well as elucidating possible underlying mechanisms. O3-RI ameliorated cognitive dysfunction in chronic REM sleep deprived mice, improved the neuronal damage in the hippocampus region and decreased neuronal loss. Administration of O3-RI may protect against chronic REM sleep deprivation induced cognitive dysfunction by reversing the abnormal expression of Occludin and leucine-rich repeat and pyrin domain-containing protein 3 inflammasome as well as interleukin-1β in the hippocampus and colon tissues. Moreover, the microbiota diversity and composition of sleep deprivation mice were significantly affected by O3-RI intervention, as evidenced by the reversal of the Firmicutes/Bacteroidetes abundance ratio and the relative abundance of the Bacteroides genus. In particular, the relative abundance of the Bacteroides genus demonstrated a pronounced correlation with cognitive impairment and inflammation. Our findings suggested that O3-RI can improve cognitive dysfunction in sleep deprivation mice, and its mechanisms may be related to regulating gut microbiota and alleviating inflammation and damage in the hippocampus and colon.