Deep Slow Wave Sleep Research Articles

Le sommeil d’un performeur de l’extrême. Dormir huit jours et sept nuits, assis, sans bouger, enfermé dans une sculpture

Sleep in extreme situations has been little studied. The artist Abraham Poincheval (AP) is known for his performances in confined spaces. For his show at the Perrotin Gallery in Paris, he was enclosed for 8days and 7nights in a metal sculpture of his body in a seated position, with his head facing a work by Hans Hartung at the end of a cone system placed in front of his eyes which occluded all other visual stimuli. The interior of the metal structure was not padded and there was no head support. His sleep and internal temperature were continuously recorded using polysomnography (Grael, Compumedics) and an orally swallowed temperature sensitive capsule (Bodycap) with temperature sampling every 2min. AP slept an average of 355.1min/24h, composed of light slow-wave sleep (N1: 47.1min, N2: 192.2min), deep slow-wave sleep (N3: 100.4min), and REM sleep 4,3 % (15.4min). Sleep, although mostly nocturnal, was split into periods of no more than 20min. Deep sleep was therefore remarkably resistant to the uncomfortable experimental conditions, while REM sleep was markedly impaired, lasting only a few short minutes and followed by rapid awakening. This is probably due to the head position within the sculpture which was unsupported, so REM sleep with its inherent muscle atonia led to involuntary head flexion and was impossible to sustain for long. The thermal minimum was between 5:17 a.m. and 6:35 a.m. The amplitude of the core temperature decreased by more than 30 % between the beginning and the end of the protocol. Despite the immobility induced by the confined experimental conditions, there was no desynchronization of circadian rhythms. The sleep time was surprisingly long given the conditions, and slow-wave sleep was relatively preserved with an amount typically found in normal subjects while REM sleep was markedly impaired. Slow-wave sleep is clearly preserved underlying its central role in physical and mental homeostasis. REM sleep is clearly more fragile. The reduction in REM sleep linked to position has been found in a study of sleep in the sitting position in airplanes where loss of muscle tonus in the neck fragments REM sleep. Techniques for selective REM sleep deprivation also use muscle atonia: one of the initial techniques of selective REM sleep deprivation relied on muscle atonia in REM causing a cat to fall from a small perch into water. In man, the lack of head support is clearly a source of REM fragmentation. However in the case of this study, we cannot exclude an effect of other factors, notably the meditative techniques used by the performer to maintain attention on the painting, described as a dream state punctuated by visual hallucinations. Surprisingly, despite physical isolation within the sculpture, AP's biological rhythms remained stable. However, the conditions were not those of complete isolation: noise, the presence of the public in the gallery who occasionally talked to AP through the sculpture, and variations in light during the day were all temporal cues. In addition, a heatwave during the performance raised the temperature in the room with reduced total sleep time on the hottest night. Although the phase of the circadian rhythm measured by the internal temperature did not change, the amplitude fell which is compatible with reduced physical activity. In conclusion, under physically constraining and uncomfortable sleep conditions, deep sleep is maintained while REM sleep is starkly reduced. From a homeostatic point of view, this means that over a short period of time, in a survival situation, energy recovery through deep slow-wave sleep takes priority over REM sleep.

Prediction of sleep indices using continuous data analysis of core body temperature variation

Human body temperature consists of skin temperature, which is easily affected by the external environment, and core body temperature, which is maintained constant to protect the functions of the body's center. Core body temperature is less susceptible to the external environment and is maintained constant in order to protect the functions of the internal organs. The deeper the sleep, the greater the decrease in body temperature. Upon entering sleep, the body temperature threshold is lowered and heat dissipation through the skin becomes more active. When sleep is deep slow-wave sleep, heat dissipation becomes very active, accompanied by sweating and a large drop in body temperature. Recently, it has become possible to continuously measure human core body temperature using infrared sensors. Therefore, we attempted to actually measure the phenomenon in which core body temperature reaches a minimum value around 4:00 a.m. using continuous measurement of human core body temperature.

Hyoid bone position as an indicator of severe obstructive sleep apnea

BackgroundThe objective of this study was to evaluate the relationship between hyoid bone position and severity of obstructive sleep apnea (OSA), and to investigate its value as a complementary diagnostic method.MethodsA total of 133 patients who were diagnosed as OSA with an apnea-hypopnea index ≥ 5 were included. Clinical examination, level I polysomnography (PSG) and lateral cephalographic analysis were done. Comprehensive PSG characteristics were compared according to hyoid bone position and the predictive power of the distance between the mandible and hyoid was assessed.ResultsThe distance between the hyoid bone and mandibular plane was significantly longer in the severe OSA group (p = 0.013). The distance from hyoid bone to third vertebrae (C3) and hyoid bone to mentum were also longer in the severe OSA group but the difference did not reach statistical significance. The distance between hyoid bone and mandibular plane was effective in predicting severe OSA, with a cut-off value of 19.45 mm (AUC = 0.623, p = 0.040). When grouped according to a distance cut-off value of 19.45 mm, those with a longer distance between the hyoid bone and mandibular plane showed more respiratory disturbance, lower oxygen saturation levels, less deep slow wave sleep, and more fragmented sleep with arousals.ConclusionsThe distance between the hyoid bone and mandibular plane derived from cephalometric analysis can be a valuable diagnostic parameter that can be easily applied in differentiating severe OSA patients.

Chaperone Hsp70 (HSPA1) Is Involved in the Molecular Mechanisms of Sleep Cycle Integration.

The molecular mechanisms of sleep cycle integration at the beginning and the end of the inactive period are not clear. Sleep cycles with a predominance of deep slow-wave sleep (SWS) seem to be associated with accelerated protein synthesis in the brain. The inducible Hsp70 chaperone corrects protein conformational changes and has protective properties. This research explores (1) whether the Hspa1 gene encoding Hsp70 protein activates during the daily rapid-eye-movement sleep (REMS) maximum, and (2) whether a lower daily deep SWS maximum affects the Hspa1 expression level during the subsequent REMS. Combining polysomnography in male Wistar rats, RT-qPCR, and Western blotting, we reveal a three-fold Hspa1 upregulation in the nucleus reticularis pontis oralis, which regulates REMS. Hspa1 expression increases during the daily REMS maximum, 5–7 h after the natural peak of deep SWS. Using short-term selective REMS deprivation, we demonstrate that REMS rebound after deprivation exceeds the natural daily maximum, but it is not accompanied by Hspa1 upregulation. The results suggest that a high proportion of deep SWS, usually observed after sleep onset, is a necessary condition for Hspa1 upregulation during subsequent REMS. The data obtained can inform the understanding of the molecular mechanisms integrating SWS and REMS and key biological function(s) of sleep.

Thalamo-Cortical and Thalamo-Thalamic Coupling During Sleep and Wakefulness in Rats.

Introduction: The thalamus, a heterogeneous brain structure, is involved in the generation of sleep-related thalamo-cortical oscillations. Higher order nuclei might possess a distinct function compared with first-order nuclei in brain communication. Here it is investigated whether this distinction can also be found during the process of falling asleep and deepening of slow-wave sleep. Methods: A nonlinear version of Granger causality was used to describe changes in directed network activity between the somatosensory cortex and rostral reticular thalamic nucleus (rRTN) and caudal reticular thalamic nucleus (cRTN), the higher order posterior (PO)- and anterior-thalamic nuclei (ATN), and the first-order ventral posteromedial thalamic nucleus (VPM) as assessed in local field potential recordings acquired during passive wakefulness (PW), light slow-wave sleep (LSWS), and deep slow-wave sleep (DSWS) in freely behaving rats. Surrogate statistics was used to assess significance. Results: Decreases in cortico-thalamo-cortical couplings were found. In contrast, multiple increases in intrathalamic couplings were observed. In particular, the rRTN increased its inhibition on the ATN from PW to LSWS, and this was further strengthened from LSWS to DSWS. The cRTN increased its coupling to VPM and PO from PW to LSWS, but the coupling from cRTN to VPM weakened at the transition from LSWS to DSWS, while its coupling to PO strengthened. Furthermore, intra-RTN coupling from PW to LSWS was differently changed compared with the change from LSWS to DSWS. Discussion: It can be inferred that higher order (ATN and PO) and first-order nuclei (VPM) are differentially inhibited during DSWS, which might be relevant for a proper functioning of sleep-related processes. Impact statement The functionally heterogeneous thalamus is affected by the different sleep/wake states. Changes in directed functional coupling between the thalamus and cortex and between functional different thalamic nuclei during the process of falling asleep and deepening to slow-wave sleep were investigated. It was revealed that the rostral and caudal subparts of the reticular thalamic nucleus, constituting the major source of intrathalamic inhibition, decouple from each other and show different coupling profiles with other thalamic nuclei. Specifically, higher order nuclei were found to be more inhibited than first-order nuclei during deep slow-wave sleep. These differences might be relevant for a proper coordination of sleep-related processes such as housekeeping, forgetting of irrelevant information, and consolidation of episodic memory.

Modulating effect of liposomal miR-101 on the processes of amyloidogenesis, smell, sleep and neuroinflammation in experimental Alzheimer's disease

The current therapy for Alzheimer's disease does not give patients a chance of recovery. Therefore, it is relevant to study the novel factors of influence, in particular microRNA, on the pathogenic mechanisms of amyloidosis. The aim of this work was to determine the effect of miR-101 on early predictors of amyloidosis in experimental Alzheimer's disease in animals. The study was carried out on 25 male rats of 14 months of age. A model of Alzheimer's disease was created by intrahippocampal administration of Aβ40 aggregates to animals. Ten days later, a 10-day course of nasal administration of miR-101 in liposomes was launched. The level of endogenous Aβ42 and cytokines (TNFα, IL-6 and IL-10) was determined in the supernatants of the nerve tissues of the target brain structures (hippocampus, olfactory bulbs, and olfactory tubercles). A neuroethological method of presenting smells of isovaleric acid and peanut butter was used to assess the olfactory system functional state in the experimental rats. In the course of polygraphic registration of the sleep-wakefulness cycle, the representation of wakefulness and individual sleep phases, as well as proportion of incomplete and complete sleep cycles were determined. It was shown that injection of Aβ40 aggregates into the hippocampus simulates an amyloidogenic state in the rat’s hippocampus and olfactory tubercles, but not in the olfactory bulbs. Moreover, a pro-inflammatory state was registered in the hippocampus of the animal brain (an increase in the concentration of pro-inflammatory cytokines TNFα and IL-6), while the cytokine level in the olfactory bulbs and tubercles did not change. When studying the functional state of olfactory analyzers in the rats with Alzheimer's disease, we revealed negative changes in behavioral response to the smell of isovaleric acid and peanut butter. In terms of somnograms, the Aβ40 toxicity caused reduction in the deep slow-wave sleep stage combined with deficiency of the paradoxical sleep phase, and predominance of incomplete sleep cycles. Nasal therapy with miR-101 in liposomes normalized the level of Aβ42 in the hippocampus and olfactory tubercles and decreased the level of proinflammatory cytokines in the hippocampus. MiR-101 prevented olfactory disfunctions in assessing smells of isovaleric acid and peanut butter, increased the ratio of deep slow-wave sleep and paradoxical sleep in the cycle structure and restored proportion of complete sleep cycles in animals. Thus, liposomal miR-101 has an anti-amyloidogenic and anti-inflammatory effect in rats with a model of Alzheimer's disease. It helps to restore the functional state of olfactory analyzer and optimize structural organization of the sleep-wakefulness cycle in sick animals.

Effects of propofol on sleep architecture and sleep–wake systems in rats

Previous studies have shown that the synchronization of electroencephalogram (EEG) signals is found during propofol-induced general anesthesia, which is similar to that of slow-wave sleep (SWS). However, a complete understanding is lacking in terms of the characteristics of EEG changes in rats after propofol administration and whether propofol acts through natural sleep circuits. Here, we examined the characteristics of EEG patterns induced by intraperitoneal injection of propofol in rats. We found that high (10 mg/kg) and medium (5 mg/kg) doses of propofol induced a cortical EEG of low-frequency, high-amplitude activity with rare electromyographic activity and markedly shortened sleep latency. The high dose of propofol increased deep slow-wave sleep (SWS2) to 4 h, as well as the number of large SWS2 bouts (>480 s), their mean duration and the peak of the power density curve in the delta range of 0.75–3.25 Hz. After the medium dose of propofol, the total number of wakefulness, light slow-wave sleep (SWS1) and SWS2 episodes increased, whereas the mean duration of wakefulness decreased. The high dose of propofol significantly increased c-fos expression in the ventrolateral preoptic nucleus (VLPO) sleep center and decreased the number of c-fos-immunoreactive neurons in wake-related systems including the tuberomammillary nucleus (TMN), perifornical nucleus (PeF), lateral hypothalamic nucleus (LH), ventrolateral periaqueductal gray (vPAG) and supramammillary region (SuM). These results indicated that the high dose of propofol produced high-quality sleep by increasing SWS2, whereas the medium dose produced fragmented and low-quality sleep by disrupting the continuity of wakefulness. Furthermore, sleep-promoting effects of propofol are correlated with activation of the VLPO cluster and inhibition of the TMN, PeF, LH, vPAG and SuM.

Modeling of chronic sleep restriction for translational studies

To develop of a chronic sleep restriction model in rats by repeated sleep deprivation using an orbital shaker and to determine whether this model leads to disturbances in sleep homeostatic mechanisms. Male Wistar rats (7-8 months old) underwent sleep restriction for five consecutive days: 3 h of sleep deprivation and 1 h of sleep opportunity repeating throughout each day. Polysomnograms were recorded telemetrically throughout the day before sleep restriction (baseline), on the 1st, 3rd, 5th day of sleep restriction and 2 days after the end of sleep restriction (recovery period). During the period of sleep restriction, the total amount of slow-wave sleep (SWS) and rapid eye movement (REM) sleep decreased by 61% and 55%, respectively, compared to baseline. On the first day of recovery, amount of SWS increased mainly in the dark (active) phase of the day, while REM sleep increased in both light and dark phases; there was no marked rebound of daily SWS amount, while REM sleep increased by 30% from baseline. On the first day of recovery, an elevation of EEG beta and sigma power in sleep states was observed mainly in the light phase of the day. The loss of deep SWS throughout the sleep restriction period increased from 50% on 1st day to 75% on 5th day. The level of deep SWS remained below the baseline by 15-20% on the two subsequent days of recovery. The findings suggest that homeostatic mechanisms of SWS are persistently impaired after 5-day chronic sleep restriction. Besides, a decline of wakefulness accompanied by an increase of SWS in the active phase of the recovery period indicates a disruption in circadian rhythm. The proposed model leads to the disruption of sleep homeostatic mechanisms, which, in turn, impede compensation of SWS loss caused by chronic insufficient sleep.

Abstract 17318: Cardioprotective Microbes and Restorative Sleep Are Reduced and Blood Pressure During Sleep is Increased When Rats Have Fragmented Sleep

Introduction: Sleep that is restless and fragmented impairs cardiovascular (CV) health. Using a rat model, we measured sleep characteristics and assessed bacterial communities in the gut microbiome. We hypothesized poor quality sleep to be associated with a reduction in cardioprotective microbiomes and adverse CV outcomes. Methods: Wistar Kyoto rats had normal sleep (n= 7, controls) or 8-hrs of fragmented sleep (n = 8) for 28 days. Implanted telemetry transmitters recorded blood pressure (BP), heart rate (HR), and cortical electroencephalogram (EEG) signals continuously. Fecal samples were collected daily; microbial composition was determined by 16S rRNA amplicon sequencing. Results: The sleep fragmented (SF) rats could not achieve deep slow-wave sleep (SWS) for 8-hrs each day—compared with controls, relative EEG delta power (a marker of the depth of sleep) was significantly lower (29±3% versus 39±3%, P = 0.04). In addition, SF was associated with a rise in BP and HR. The relative abundance of Parabacteroides (classified to genus level) and Tannerellaceae (classified to family level), both gram-negative anaerobic bacteria from the phylum Bacteroidetes, were decreased in SF rats during late-SF (intervention days 20 & 27), relative to controls. Elevated Parabacteroides levels (%) were significantly and inversely correlated with systolic (R= -0.002, P <0.001) and diastolic (R= -0.003, P <0.001) BP levels recorded during sleep in both groups of rats. Conclusions: Parabacteroides levels in the gut microbiome may contribute to changes in BP. Undesirable changes in sleep from SF are associated with reduced levels of Parabacteroides during the late-SF period in the gut microbiome, compared with controls. The Parabacteroides -BP associations and reactivity of this bacterium to disrupted sleep support Parabacteroides as an exciting cardioprotective biomarker to stratify and prevent negative CV outcomes provoked by SF.

Acute 5-HT2C Receptor Antagonist SB-242084 Treatment Affects EEG Gamma Band Activity Similarly to Chronic Escitalopram.

Serotonin 2C receptors (5-HT2CRs) are implicated in the pathomechanism and treatment of anxiety and depression. Recently, as a new biomarker of depression, alterations in the gamma power of the electroencephalogram (EEG) have been suggested. Chronic treatment with the selective serotonin reuptake inhibitor (SSRI) antidepressant escitalopram has been shown to cause sleep-wake stage-dependent alterations in gamma power. However, despite the antidepressant potency of 5-HT2CR-antagonists, there is no data available regarding the effects of selective 5-HT2CR-antagonists on gamma activity. Therefore, we investigate the acute effect of the 5-HT2CR-antagonist SB-242084 on gamma power in different vigilance stages when given in monotherapy, or in combination with chronic escitalopram treatment. We administered SB-242084 (1 mg/kg, intraperitoneally) or vehicle to EEG-equipped rats after a 21-day-long pretreatment with escitalopram (10 mg/kg/day, via osmotic minipumps) or vehicle. Frontoparietal EEG, electromyogram, and motor activity were recorded during the first 3 h of passive phase, after the administration of SB-242084. Quantitative EEG analysis revealed that acute SB-242084 increased gamma power (30–60 Hz) in light and deep slow-wave sleep, and passive wakefulness. However, in active wakefulness, rapid eye movement sleep, and intermediate stage, no change was observed in gamma power. The profile of the effect of SB-242084 on gamma power was similar to that produced by chronic escitalopram. Moreover, SB-242084 did not alter chronic escitalopram-induced effects on gamma. In conclusion, the similarity in the effect of the 5-HT2CR-antagonist and chronic SSRI on gamma power provides further evidence for the therapeutic potential of 5-HT2CR-antagonists in the treatment of depression and/or anxiety.

Can absence seizures be predicted by vigilance states?: Advanced analysis of sleep–wake states and spike–wave discharges' occurrence in rats

Spike–wave discharges (SWDs) are the main manifestation of absence epilepsy. Their occurrence is dependent on the behavioral state, and they preferentially occur during unstable vigilance periods. The present study investigated whether the occurrence of SWDs can be predicted by the preceding behavioral state and whether this relationship is different between the light and the dark phases of the 24-h day.Twenty-four-hour (12:12 light/dark phases) electroencephalographic (EEG) recordings of 12 Wistar Albino Glaxo, originally bred in Rijswijk (WAG/Rij) rats, a well-known genetic model of absence epilepsy, were analyzed and transformed into sequences of 2-s length intervals of the following 6 possible states: active wakefulness (AW), passive wakefulness (PW), deep slow-wave sleep (DSWS), light slow-wave sleep (LSWS), rapid eye movement (REM) sleep, and SWDs, given discrete series of categorical data. Probabilities of all transitions between states and Shannon entropy of transitions were calculated for the light and dark phases separately and statistically analyzed.Common differences between the light and the dark phases were found regarding the time spent in AW, LSWS, DSWS, and SWDs. The most probable transitions were that AW was preceded and followed by PW and vice versa regardless of the phase of the photoperiod. A similar relationship was found for light and deep slow-wave sleep. The most probable transitions to and from SWDs were AW and LSWS, respectively, with these transition likelihoods being consistent across both circadian phases. The second most probable transitions around SWDs appeared more variable between light and dark. During the light phase, SWDs occurred around PW and participated exclusively in sleep initiation; in the dark phase, SWDs were seen on both, ascending and descending steps towards and from sleep. Conditional Shannon entropy showed that AW and DSWS are the most predictable events, while the possible prediction horizon of SWDs is not larger than 4 s and despite the higher occurrence of SWDs in the dark phase, did not differ between phases.It can be concluded that although SWDs show a stable, strong circadian rhythm with a peak in number during the dark phase, their occurrence cannot be reliably predicted by the preceding behavioral state, except at a very short time base.

Spike–Wave Discharges and Sleep–Wake States during Circadian Desynchronization: No Effects of Agomelatine upon Re-Entrainment

Rapid changes in the light–dark cycle cause circadian desynchronization between rhythms of spike–wave discharges (SWDs) and motor activity in genetic epileptic rats, and this is accompanied by an increase in epileptic activity. Given the close relationship between absence seizures and sleep–wake states, the present study assessed firstly a putative relationship between vigilance rhythms and SWDs during re-synchronization, and secondly sleep–wake patterns responsible for increased epileptic activity. Lastly, in a view of existing evidence that melatonin and its agonists accelerate re-synchronization, the effects of different doses of agomelatine upon the speed of re-synchronization of different sleep–wake states and SWDs were investigated.Simultaneous electroencephalographic and electromyographic recordings were made in symptomatic WAG/Rij rats, before, during and 10 days following an 8 h light phase delay. Agomelatine was orally administered acutely and sub-chronically, during 10 post-shift days.The magnitude of the advance after the shift and the speed of re-synchronization were specific for various rhythms. Most prominent change was the increase in REM sleep duration during the dark phase. A post-shift increase in passive wakefulness and a reduction in deep slow-wave sleep coincided with an aggravation of SWDs during the light phase. Agomelatine showed neither an effect on sleep–wake parameters and SWDs, nor affected re-synchronization.The same speed of re-synchronization of SWDs and light slow-wave sleep suggests that both are controlled by a common circadian mechanism. The redistribution of SWDs and their increase in the light phase after the shift may be of importance for patients with absence epilepsy planning long trans-meridian flight across time zones.

Habituation of Somatosensory Event-Related Potentials in Subthreshold Rhythmic (1 Hz) Electrocutaneous Stimulation of the Arm during the Slow-Wave Stage of Daytime Sleep

Previous studies have shown that low-frequency subthreshold electrocutaneous stimulation of the arm during deep slow-wave sleep in humans improves sleep quality. The main cognitive processes are known to operate during sleep, and use of event-related potentials is the main method for analysis of these processes. The aims of the present work were to study the characteristics of somatosensory event-related potentials (sERP) on rhythmic (1 Hz) subthreshold electrocutaneous volley stimulation of the arm during the slow-wave stage of daytime sleep and to evaluate the potential for habituation of sERP to rhythmic stimulation during sleep. Subthreshold stimulation during sleep produced somatosensory event-related potentials (ERP) (group mean, n = 16) in which three long-latency components could be identifi ed, which were more marked in the frontal lead of the contralateral hemisphere. Comparison of sERP averaged from the beginning and end of the volley of stimuli (30 stimuli) demonstrated signifi cant decreases in the amplitudes of all sERP components by the end of the volley. It is suggested that the decrease in sERP amplitude in slow-wave sleep is due to the simplest form of stimulus-dependent nonassociative learning - habituation.

Effect of long-term deep slow-wave sleep deprivation on the reproductive system in male rats

Objective: To investigate the effect of long-term deep slow-wave sleep deprivation on the gonad axis, sperm abnormality rate, and structure of the testis in male rats and possible mechanisms. Methods: A total of 30 specific pathogen-free male Wistar rats aged 5 weeks were randomly divided into slow-wave sleep deprivation group 1 (SD1 group) , slow-wave sleep and sleep time deprivation group 2 (SD2 group) , and control group, with 10 rats in each group. The flower pot method was used to establish a model of sleep deprivation. In addition to 12-hour sleep deprivation at night, the rats in the SD1 group were given interference once every 24 minutes, and those in the SD2 group were deprived of sleep for 8 minutes every 24 minutes; the rats in the control group were given 12-hour light illumination and then placed in dark environment for 12 hours. All rats were sacrificed by exsanguination from the femoral artery, and the testis, the epididymis, and blood were collected for analysis. Sperm abnormality rate and sperm motility rate were measured, and cauda epididymal sperm counting was performed. ELISA was used to measure the serum levels of testosterone (T) , follicle-stimulating hormone (FSH) , and luteinizing hormone (LH) . Results: Compared with the control group, the SD2 group had a significant increase in organ coefficient of the epididymis (P<0.05) and a significant reduction in sperm motility rate (P<0.05) . There were significant differences between the SD1 group and the SD2 group in the increase in sperm abnormality rate (P<0.05) and the reduction in cauda epididymal sperm count (P<0.05) . The levels of FSH and T tended to increase, and the level of LH tended to decrease. Pathological examination showed degeneration and vacuolization of a small amount of spermatogenic cells in the SD1 group; in the SD2 group, there were significant degeneration, edema, and vacuolization of most spermatogenic cells, some spermatogenic cells were observed in the lumen, and there were no sperms in the lumen. Conclusion: Long-term deep slow-wave sleep deprivation impairs the structure of the testis, affects sperm motility rate and sex hormones, and increases the risk of sperm abnormality.

Acute and chronic escitalopram alter EEG gamma oscillations differently: relevance to therapeutic effects

Brain oscillations in the gamma frequency band of the electroencephalogram (EEG) have been implicated in several sensory and cognitive processes, and have also been associated with numerous neuropsychiatric disorders, including depression. The widely prescribed selective serotonin reuptake inhibitors (SSRIs), similarly to other antidepressants, are known to produce markedly different effects on sleep and behavioral measures with acute and chronic administration. Although there are studies examining the acute effect of escitalopram on slower (<30 Hz) oscillations, we hardly could find any data about the effect of the drug on higher-frequency EEG oscillations (>30 Hz) in different sleep-wake stages, particularly comparing the acute and chronic effects of the drug concerning gamma oscillations. Our aim was to investigate, how escitalopram affects gamma power in different sleep-wake stages, and to discover possible differential effects between acute and chronic treatment. EEG-equipped Wistar rats were treated with escitalopram or vehicle acutely (10 mg/kg, i.p.) or chronically (10 mg/kg/day for 21 days, osmotic minipumps) and frontoparietal EEG, electromyogram and motor activity were recorded during the first 3 h of passive phase. We found that acute and chronic escitalopram treatment affected gamma oscillations differently. While acute escitalopram caused a reduction in gamma power during rapid eye movement sleep (REMS) and intermediate stage of sleep (IS), chronic treatment caused an elevation in gamma power during non-REMS stages, namely in light and deep slow-wave sleep (SWS-1 and SWS-2, respectively) and in IS. However, gamma activity during active and passive wakefulness (AW and PW, respectively) was not influenced by either acute or chronic dosing of escitalopram. Furthermore, we found that in drug-free (vehicle-treated) rats, a relatively high gamma power was present during wakefulness and REMS, while a much lower power was measured during non-REMS stages. These findings indicate that acute and chronic administration of escitalopram alter gamma activity differently, moreover, in a sleep-wake stage dependent manner that may be related to differential therapeutic and/or side effects.

REM-sleep behavior disorder and sleepwalking in a patient with Parkinson's disease and essential tremor

REM-sleep behavior disorder (RBD), a form of parasomnia, is characterized by motor and/or speech activity during sleep corresponding to the dream content. RBD is currently considered as a marker of onset of neurodegenerative diseases (sinucleinopathies) and as a most specific early symptom of Parkinson's disease (PD). The authors describe a clinical case of a patient with the combination of essential tremor, initial signs of PD and RBD. A polysomnographic study has confirmed clinical signs of RBD and determined the disturbances of sleep architecture: the increase in falling asleep, number of awakenings, wakefulness during sleep, the absence of deep slow-wave sleep. The particular features of the patient were essential tremor and sleep walking.

Effects of Electrical Stimulation of the Oral Reticular Nucleus of the Pons on the Background of Different States in the Sleep–Waking Cycle in Krushinskii–Molodkina Rats

The effects of electrical stimulation of the oral reticular nucleus of the pons on behavior and brain activity in different states of the sleep–waking cycle were studied in Krushinskii–Molodkina rats, which have an inherited predisposition to audiogenic convulsions. Electrical stimulation of this structure at a frequency of 7 Hz on the background of deep slow-wave sleep induced a transition from slow- to fast-wave sleep. Analogous stimulation during fast-wave sleep had no effect on the electrogram patterns or spectra of the hippocampus or the visual, auditory, or somatosensory areas of the cortex and did not interrupt this state, though it did induce an almost twofold increase in the duration of its individual episodes. Electrical stimulation of the nucleus at 7 Hz during waking or shallow slow-wave sleep had no effect on behavior or electrogram patterns or spectral characteristics in the study structures and did not induce transition from one stage of the cycle to another. The results obtained here show that the state of the animals in the sleep–waking cycle is an important variable on which the effects of electrical stimulation of the oral reticular nucleus of the pons depend.

Slow-wave sleep and molecular chaperones

From ancient times the mankind has been interested in a topical issue: why is it necessary to spend about one-third of human life for sleep? This review considers the main data on the key function of slow-wave sleep (SWS) and the molecular mechanisms of its regulation; the basic conclusions are presented below as a summary and hypotheses. 1. SWS has an energy-conserving function developed simultaneously with the evolution of tachimetabolism and endothermy/homoiothermy. 2. The most significant reduction of energy demands in the brain occurs during the deep SWS (characterized by increased EEG-delta power), thus creating the optimal conditions for enhancing anabolic processes and realizing the key biological function of sleep--the increase in protein synthesis rate in the brain. 3. The conditions of the paradoxical sleep (PS) as an 'archeowakefulness' state, containing the elements of endogenous stress, seem to be acceptable for expression of chaperones required for repairing misfolded proteins newly synthesized during the deep SWS. 4. The close integration of two molecular systems, HSP70 and HSP40, contained in the sleep 'center' in the preoptic area of the hypothalamus, and their compensatory interrelations contribute significantly to the maintenance of sleep homeostasis and to implementation of its functions under non-stress conditions and during long-term deficiency of chaperones in the brain that is intrinsic for aging and various neuropathologies. 5. Occurring daily throughout the lifetime cyclical changes of the protein synthesis rate (during the deep SWS) and the expression of HSP70 chaperonez (during wakefulness and, possibly, during PS) are crucial for functions of homeothermic organisms, including recuperation of the nervous system's structure and functions.

Thalamic Atrophy Contributes to Low Slow Wave Sleep in Neuromyelitis Optica Spectrum Disorder.

Slow wave sleep abnormality has been reported in neuromyelitis optica spectrum disorder (NMOSD), but mechanism for such abnormality is unknown. To determine the structural defects in the brain that account for the decrease of slow wave sleep in NMOSD patients. Thirty-three NMOSD patients and 18 matched healthy controls (HC) were enrolled. Polysomnography was used to monitor slow wave sleep and three-dimensional T1-weighted MRIs were obtained to assess the alterations of grey matter volume. The percentage of deep slow wave sleep decreased in 93% NMOSD patients. Compared to HC, a reduction of grey matter volume was found in the bilateral thalamus of patients with a lower percentage of slow wave sleep (FWE corrected at cluster-level, p < 0.05, cluster size > 400 voxels). Furthermore, the right thalamic fraction was positively correlated with the decrease in the percentage of slow wave sleep in NMOSD patients (p < 0.05, FDR corrected, cluster size > 200 voxels). Our study identified that thalamic atrophy is associated with the decrease of slow wave sleep in NMOSD patients. Further studies should evaluate whether neurotransmitters or hormones which stem from thalamus are involved in the decrease of slow wave sleep.

Effects of Stimulation of the Inferior Colliculi in Krushinskii–Molodkina Rats

The effects of chemical and electrical stimulation of the central nucleus of the inferior colliculus on the generation and formation of convulsive manifestations and on the organization of sleep were studied in Krushinskii–Molodkina rats with an inherited predisposition to audiogenic convulsions. Microinjection of quinolinic acid (10 μg in 1 μl of distilled water) or electrical stimulation at a frequency of 70 Hz generated paroxysmal manifestations in the form of intense rotatory movement acts, similar to “wild running” of animals in the initial convulsion-free stage of audiogenic seizures. This provides grounds for suggesting that in Krushinskii–Molodkina rats the inferior colliculi are part of the neural network responsible for the generation and execution of the running stage during the formation of convulsive responses to sound stimuli. Application of these stimuli was also followed by a decrease in the total duration of fast-wave sleep during the poststimulus period. Conversely, electrical stimulation of the inferior colliculi at a frequency of 7 Hz on the background of deep slow-wave sleep induced episodes of fast-wave sleep in the rats; after 3–4 sessions of this stimulation producing this effect, there was an almost two-fold increase in the total duration of fastwave sleep during the post-stimulus period due to an increase in the number but not the duration of these episodes. These results provide evidence that the inferior colliculi in rats may have a modulatory effect on the functioning of the fast-wave sleep triggering system.