Human Prosocial Preferences Are Related to Slow-Wave Activity in Sleep.

Prosocial behavior is crucial for the smooth functioning of the society. Yet, individuals differ vastly in the propensity to behave prosocially. Here, we try to explain these individual differences under normal sleep conditions without any experimental modulation of sleep. Using a portable high-density EEG, we measured the sleep data in 54 healthy adults (28 females) during a normal night's sleep at the participants' homes. To capture prosocial preferences, participants played an incentivized public goods game in which they faced real monetary consequences. The whole-brain analyses showed that a higher relative slow-wave activity (SWA, an indicator of sleep depth) in a cluster of electrodes over the right temporoparietal junction (TPJ) was associated with increased prosocial preferences. Source localization and current source density analyses further support these findings. Recent sleep deprivation studies imply that sleeping enough makes us more prosocial; the present findings suggest that it is not only sleep duration, but particularly sufficient sleep depth in the TPJ that is positively related to prosociality. Because the TPJ plays a central role in social cognitive functions, we speculate that sleep depth in the TPJ, as reflected by relative SWA, might serve as a dispositional indicator of social cognition ability, which is reflected in prosocial preferences. These findings contribute to the emerging framework explaining the link between sleep and prosocial behavior by shedding light on the underlying mechanisms.

Alterations in microglial morphology concentrate in the habitual sleeping period of the mouse.

In nocturnal animals, waking appears during the dark period while maximal non-rapid-eye-movement sleep (NREMS) with electroencephalographic slow-wave-activity (SWA) takes place at the beginning of the light period. Vigilance states associate with variable levels of neuronal activity: waking with high-frequency activity patterns while during NREMS, SWA influences neuronal activity in many brain areas. On a glial level, sleep deprivation modifies microglial morphology, but only few studies have investigated microglia through the physiological sleep-wake cycle. To quantify microglial morphology (territory, volume, ramification) throughout the 24 h light-dark cycle, we collected brain samples from inbred C57BL male mice (n = 51) every 3 h and applied a 3D-reconstruction method for microglial cells on the acquired confocal microscopy images. As microglia express regional heterogeneity and are influenced by local neuronal activity, we chose to investigate three interconnected and functionally well-characterized brain areas: the somatosensory cortex (SC), the dorsal hippocampus (HC), and the basal forebrain (BF). To temporally associate microglial morphology with vigilance stages, we performed a 24 h polysomnography in a separate group of animals (n = 6). In line with previous findings, microglia displayed de-ramification in the 12 h light- and hyper-ramification in the 12 h dark period. Notably, we found that the decrease in microglial features was most prominent within the early hours of the light period, co-occurring with maximal sleep SWA. By the end of the light period, all features reached maximum levels and remained steadily elevated throughout the dark period with minor regional differences. We propose that vigilance-stage specific neuronal activity, and SWA, could modify microglial morphology.

Association between sleep slow-wave activity and in-vivo estimates of myelin in healthy young men.

Sleep has been suggested to contribute to myelinogenesis and associated structural changes in the brain. As a principal hallmark of sleep, slow-wave activity (SWA) is homeostatically regulated but also differs between individuals. Besides its homeostatic function, SWA topography is suggested to reflect processes of brain maturation. Here, we assessed whether interindividual differences in sleep SWA and its homeostatic response to sleep manipulations are associated with in-vivo myelin estimates in a sample of healthy young men. Two hundred twenty-six participants (18-31 y.) underwent an in-lab protocol in which SWA was assessed at baseline (BAS), after sleep deprivation (high homeostatic sleep pressure, HSP) and after sleep saturation (low homeostatic sleep pressure, LSP). Early-night frontal SWA, the frontal-occipital SWA ratio, as well as the overnight exponential SWA decay were computed over sleep conditions. Semi-quantitative magnetization transfer saturation maps (MTsat), providing markers for myelin content, were acquired during a separate laboratory visit. Early-night frontal SWA was negatively associated with regional myelin estimates in the temporal portion of the inferior longitudinal fasciculus. By contrast, neither the responsiveness of SWA to sleep saturation or deprivation, its overnight dynamics, nor the frontal/occipital SWA ratio were associated with brain structural indices. Our results indicate that frontal SWA generation tracks inter-individual differences in continued structural brain re-organization during early adulthood. This stage of life is not only characterized by ongoing region-specific changes in myelin content, but also by a sharp decrease and a shift towards frontal predominance in SWA generation.

Encephalopathy related to status epilepticus during slow sleep (ESES). Pathophysiological insights and nosological considerations.

Encephalopathy related to Status Epilepticus during slow Sleep (ESES) is a childhood epilepsy syndrome characterized by the appearance of cognitive, behavioral, and motor disturbances in conjunction with a striking activation of EEG epileptic abnormalities during non-REM sleep. After more than 50 years since the first description, the pathophysiological mechanisms underlying the appearance of encephalopathy in association with a sleep-related enhancement of epileptic discharges are incompletely elucidated. Recent experimental data support the hypothesis that the development of the ESES encephalopathic picture depends on a spike-induced impairment of the synaptic homeostasis processes occurring during normal sleep and that is particularly pronounced during the developmental age. During sleep, synaptic homeostasis is promoted by synaptic weakening/elimination after the increment of synaptic strength that occurs during wakefulness. The EEG can display modifications in synaptic strength by changes in sleep slow wave activity (SWA). Recent studies during active ESES have failed to show changes in sleep SWA, while these changes occurred again after recovery from ESES, thus supporting a spike-related interference on the normal homeostatic processes of sleep. This impairment, during the developmental period, can lead to disruption of cortical wiring and brain plastic remodeling, which lead to the, often irreversible, neuropsychological compromise typical of ESES. From the nosographic point of view, these pathophysiological data lend support to the maintenance of the term ESES, i.e., "encephalopathy related to status epilepticus during sleep". Indeed, this term conveys the concept that the extreme activation of epileptic discharges during sleep is directly responsible for the encephalopathy, hence the importance of defining this condition as an encephalopathy related to the exaggerated activation of epileptic activity during sleep. In this respect, ESES represents a genuine example of a "pure" epileptic encephalopathy in which sleep-related epileptic activity "per se" has a crucial role in determining the encephalopathic picture. This paper was presented at the 8th London-Innsbruck Colloquium on Status Epilepticus and Acute Seizures held in September 2022.

The sleep EEG topography in children and adolescents shows sex differences in language areas.

The topographic distribution of slow wave activity (SWA, EEG power between 0.75 and 4.5 Hz) during non-rapid eye movement (NREM) sleep was proposed to mirror cortical maturation with a typical age-related pattern. Here, we examined whether sex differences occur in SWA topography of children and adolescents (22 age-matched subjects, 11 boys, mean age 13.4 years, range: 8.7-19.4, and 11 girls, mean age 13.4 years, range: 9.1-19.0 years). In females, SWA during the first 60 min of NREM sleep was higher over bilateral cortical areas that are related to language functions, while in males SWA was increased over the right prefrontal cortex, a region also involved in spatial abilities. We conclude that cortical areas governing functions in which one sex outperforms the other exhibit increased sleep SWA and, thus, may indicate maturation of sex-specific brain function and higher cortical plasticity during development.