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Cellular plasticity at the structural level and sleep at the behavioural level are both essential for memory formation. The link between the two is not well understood. A functional connection between adult neurogenesis and hippocampus-dependent memory consolidation during NREM sleep has been hypothesized but not experimentally shown. Here, we present evidence that during a three-day learning session in the Morris water maze task a genetic knockout model of adult neurogenesis (Cyclin D2−/−) showed changes in sleep macro- and microstructure. Sleep EEG analyses revealed a lower total sleep time and NREM fraction in Cyclin D2−/− mice as well as an impairment of sleep specific neuronal oscillations that are associated with memory consolidation. Better performance in the memory task was associated with specific sleep parameters in wild-type, but not in Cyclin D2−/− mice. In wild-type animals the number of proliferating cells correlated with the amount of NREM sleep. The lack of adult neurogenesis led to changes in sleep architecture and oscillations that represent the dialog between hippocampus and neocortex during sleep. We suggest that adult neurogenesis—as a key event of hippocampal plasticity—might play an important role for sleep-dependent memory consolidation and modulates learning-induced changes of sleep macro- and microstructure.

Objective Bipolar disorder is a severe mental disorder for which currently no reliable biomarkers exist. It has been shown that patients with schizophrenia but not with unipolar depression have a reduced density of fast sleep spindles during N2 sleep. The aim of this study was to assess fast sleep spindle density in euthymic patients with bipolar disorder. Methods Patients with bipolar disorder (n = 24) and healthy control subjects (n = 25) were assessed using all-night polysomnography. Sleep spindles within stage N2 sleep were identified by visual inspection and subdivided into fast (>13 Hz) and slow (≤13 Hz) spindles. All spindles were subsequently characterised by density, frequency, amplitude, duration and coherence. Results Euthymic patients with bipolar disorder were found to have a reduced density and a lower mean frequency of fast spindles. Slow spindle density and frequency did not differ between groups. There were no differences regarding amplitude, duration or coherence. Conclusions A reduction in fast spindle density during N2 sleep points towards thalamic dysfunction as a potential neurobiological mechanism of relevance in bipolar disorder. In addition, a reduced sleep spindle density could be interpreted as a common endophenotype shared with schizophrenia but not unipolar depression and may - if replicated - be of utility in early recognition and risk stratification.

Appearances of alpha waves in the sleep electrencephalogram indicate physiological, brief states of awakening that lie in between wakefulness and sleep. These microstates may also cause the loss in sleep quality experienced by individuals suffering from insomnia. To distinguish such pathological awakenings from physiological ones, differences in alpha-wave characteristics between transient awakening and wakefulness observed before the onset of sleep were studied. In polysomnographic datasets of sleep-healthy participants (n = 18) and patients with insomnia (n = 10), alpha waves were extracted from the relaxed, wake state before sleep onset, wake after sleep-onset periods and arousals of sleep. In these, alpha frequency and variability were determined as the median and standard deviation of inverse peak-to-peak intervals. Before sleep onset, patients with insomnia showed a decreased alpha variability compared with healthy participants (P

Background Simultaneous downregulation of the autonomic and central nervous system activity enables the gradual physiological state change from wakefulness to sleep onset. Dysregulation of central or autonomic arousal has been found in neurological ( Silvani et al., 2016 ) and psychiatric disorders ( Hegerl and Hensch, 2014 , Hegerl et al., 2012 , Schulz et al., 2016 , Schwabedal et al., 2016 ), often associated with dysregulated sleep-wake patterns. Aim We investigated the hypothesis that brain-autonomic co-regulation affects the attentive process in the transition from wakefulness to sleep onset. We propose that the degree to which autonomic and brain dynamics are correlated predicts the level of cortical excitability or inhibition and sleep onset behavior in this transition. To test our hypothesis, we explored electroencephalogram (EEG), electrocardiogram (ECG) and skin conductance data recorded during a 2-h resting state oddball experiment. Methods 39 healthy study participants underwent a 2-h resting EEG with eyes closed including ECG-derived heart rate (HR) and measurement of skin conductance level (SCL). The Vigilance Algorithm Leipzig (VIGALL 2.1) was used to assess brain arousal regulation based on automatic EEG-vigilance stage classification of 1-s EEG segments. These vigilance stages (=vigilance; V) were scored and cross-correlated with HR and SCL over a range of ±100 s, and a mean period of vigilance fluctuations was estimated from the frequency of maxima after low-pass filtering. Mean amplitudes of event-related potentials N100 and P200 to standard and deviant stimuli at Cz were calculated as indices of cortical excitability (N100) and cortical inhibition (P200) ( Cortoos et al., 2014 ). Results In all subjects, higher max cross-correlation coefficients (V-HR mean: r = 0.362, range: −0.069 to 0.762; SD = 0.192; V-SCL mean: r = 0.277, range: −0.299 to 0.629; SD = 0.211) were associated with longer mean periods of cortico-autonomic signals (V-HR: r = 0.462, p = .003; V-SCL: r = 0.516, p = .001). The cross-correlation of V with either HR and SCL partitioned the subjects into two groups (group no lag: n0 = 20, τ = 0; group lag: n1 = 19, τ (range) = −98 to −87) dependent on the time lag of maximal correlation. Subjects in n0, who fell asleep more often (indexed by the frequency of falling asleep: t37 = 2.49, p = .018) during the 2-h EEG compared to subjects in n1, had higher max cross-correlation coefficients (V-HR: t37 = 4.24, p = 1.43E−4; V-SCL: t37 = 5.02, p = 1.35E−5) and displayed an increased standard (t30.235 = 3.19, p = .003) and deviant P200 amplitude (t37 = 3.63, p = .001) compared to subjects in n1. No significant group differences were found for N100 amplitudes and KSS score either before or after the recording. Conclusion Healthy individuals with no time lag between cortical and autonomic signals showed a stronger brain-autonomic coupling and increased P200 amplitudes (indicating a higher level of cortical inhibition) compared to individuals with a temporal misalignment. This may explain differences in sleep-onset behavior between groups. Present results indicate possible diagnostic value in the assessment of brain-autonomic regulation, for example in disorders with sleep-related symptoms such as insomnia, dementia or depression.