, 1977) Finally, in humans, some sleep disorders (e g , sleep wa

, 1977). Finally, in humans, some sleep disorders (e.g., sleep walking) suggest the existence of “dissociated states” (Mahowald and Schenck, 2005), where some brain regions are “asleep” when others are simultaneously “awake. Given the recent evidence supporting local regulation of SWA, we hypothesized that sleep slow waves may occur locally such that neurons

alternate between active and inactive states at different times in different brain regions. To evaluate this possibility, simultaneous recordings of intracranial depth EEG and spiking activities of isolated units were obtained in 8–12 brain regions in the cortex and hippocampus of 13 individuals Y-27632 supplier undergoing presurgical clinical testing. Anti-diabetic Compound Library research buy The results provide direct evidence for local slow waves, revealing a continuum of global-local waves, with the majority of events being confined to specific regions. At one extreme, typical of early NREM sleep, high-amplitude slow waves were usually global, detectable with scalp EEG. At the other extreme, more typical of late NREM sleep, slow waves could be entirely local, where any region

could be active or inactive. In addition, we find that sleep spindles—the other EEG hallmark of NREM sleep—also occur mostly locally, establishing that the two fundamental sleep oscillations are mostly confined to local circuits. We also reveal a robust tendency of sleep slow waves to propagate from medial prefrontal cortex to the medial temporal lobe (MTL) and hippocampus. Both local occurrence and propagation of slow wave events reflect the underlying connectivity such that transitions into activity in a given region can be predicted by the activity of its afferent regions. We obtained full night heptaminol continuous polysomnographic sleep recordings in 13 neurosurgical patients, lasting 421 ± 20 min (mean ± SEM). Figure 1 illustrates the experimental setup and provides an overview of the data. Polysomnography included electrooculogram (EOG), electromyogram (EMG), scalp EEG, and video monitoring. Sleep-wake stages were scored as waking,

NREM sleep stages N1 through N3, and REM sleep according to established guidelines (Iber et al., 2007). Depth intracranial electrodes recorded activity in 129 medial brain regions in frontal and parietal cortices, parahippocampal gyrus, entorhinal cortex, hippocampus, and amygdala (Figure 1E; see Table S1A available online). We simultaneously recorded scalp EEG, depth EEG, multiunit activity (MUA), and neuronal spiking activity (Figure 1D) from a total of 600 units (355 single units and 245 multiunit clusters). Measures of overnight sleep in patients resembled normal sleep in individuals without epilepsy (Figure S1). Average (±SEM) sleep efficiency (sleep time per time in bed) was 82% ± 2%. NREM sleep, REM sleep, and wake after sleep onset (WASO) constituted 75% ± 2%, 13% ± 2%, and 12% ± 2% of sleep time, respectively.

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