Sleep has been hypothesized to rebalance overall synaptic strength after ongoing learning during waking leads to net synaptic potentiation. If so, because synaptic strength and size are correlated, synapses on average should be larger after wake and smaller after sleep. This prediction was recently confirmed in mouse cerebral cortex using serial block-face electron microscopy (SBEM). However, whether these findings extend to other brain regions is unknown. Moreover, sleep deprivation by gentle handling was reported to produce hippocampal spine loss, raising the question of whether synapse size and number are differentially affected by sleep and waking. Here we applied SBEM to measure axon-spine interface (ASI), the contact area between pre-synapse and post-synapse, and synapse density in CA1 stratum radiatum. Adolescent YFP-H mice were studied after 6-8 h of sleep (S ϭ 6), spontaneous wake at night (W ϭ 4) or wake enforced during the day by novelty exposure (EW ϭ 4; males/females balanced). In each animal Ն425 ASIs were measured and synaptic vesicles were counted in ϳ100 synapses/mouse. Reconstructed dendrites included many small, nonperforated synapses and fewer large, perforated synapses. Relative to S, ASI sizes in perforated synapses shifted toward higher values after W and more so after EW. ASI sizes in nonperforated synapses grew after EW relative to S and W, and so did their density. ASI size correlated with presynaptic vesicle number but the proportion of readily available vesicles decreased after EW, suggesting presynaptic fatigue. Thus, CA1 synapses undergo changes consistent with sleep-dependent synaptic renormalization and their number increases after extended wake.

SUMMARYThis study sought to determine if there is any overlap between the two major NREM and REM parasomnias, i.e., sleepwalking/sleep terrors (SW/ST) and REM sleep behaviour disorder (RBD). We assessed adult patients with SW/ST using RBD screening questionnaires and determined if they had enhanced muscle tone during REM sleep.Conversely, we assessed RBD patients using the Paris Arousal Disorders Severity Scale (PADSS) and determined if they had more N3 awakenings. The 251 participants

Human foetuses and newborns smile first during sleep, before they smile while awake and interacting with caregivers. Whether smiling persists during adult sleep, and expresses inner joy, is yet unknown. Smiles were looked for during night‐time video‐polysomnography combined with electromyography of the zygomatic and orbicularis oculi muscles in 100 controls, 22 patients with sleepwalking and 52 patients with rapid eye movement (REM) sleep behaviour disorder. Autonomous reactions (heart rate and level of vasoconstriction) and the presence of rapid eye movements were examined during smiles and laughs. On visual examination of the face video clips synchronous with zygomatic contraction, 8% of controls smiled while asleep (7% in REM sleep and 1% in non‐REM sleep). Some patients with sleepwalking also smiled and laughed during N2 sleep and N3 parasomnia. Half of the patients with REM sleep behaviour disorder smiled and one‐third laughed, mostly during REM sleep. The 173 happy faces included mild smiles (24.8%), open‐mouth smiles (29.5%) and laughs (45.7%). More than half of the smiles were the Duchenne (genuine) type, including an active closure of the eyelids. Approximately half of the smiles and laughs were temporally associated with rapid eye movements. There was no increased heart rate variability during smiles and laughs. Two scenic behaviours including smiles and laughs suggested that the happy facial expression was associated with a happy dreaming scenario. Smiling and laughing occasionally persist during adult sleep. There are several lines of evidence suggesting that these happy emotional expressions reflect a true inner mirth.

Multiple evidence in rodents shows that the strength of excitatory synapses in the cerebral cortex and hippocampus is greater after wake than after sleep. The widespread synaptic weakening afforded by sleep is believed to keep the cost of synaptic activity under control, promote memory consolidation, and prevent synaptic saturation, thus preserving the brain’s ability to learn day after day. The cerebellum is highly plastic and the Purkinje cells, the sole output neurons of the cerebellar cortex, are endowed with a staggering number of excitatory parallel fiber synapses. However, whether these synapses are affected by sleep and wake is unknown. Here, we used serial block face scanning electron microscopy to obtain the full 3D reconstruction of more than 7000 spines and their parallel fiber synapses in the mouse posterior vermis. This analysis was done in mice whose cortical and hippocampal synapses were previously measured, revealing that average synaptic size was lower after sleep compared to wake with no major changes in synapse number. Here, instead, we find that while the average size of parallel fiber synapses does not change, the number of branched synapses is reduced in half after sleep compared to after wake, corresponding to ~16% of all spines after wake and ~8% after sleep. Branched synapses are harbored by two or more spines sharing the same neck and, as also shown here, are almost always contacted by different parallel fibers. These findings suggest that during wake, coincidences of firing over parallel fibers may translate into the formation of synapses converging on the same branched spine, which may be especially effective in driving Purkinje cells to fire. By contrast, sleep may promote the off-line pruning of branched synapses that were formed due to spurious coincidences.

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