Intrinsic cortical dynamics modulates the processing of sensory information and therefore may be critical for conscious perception. We tested this hypothesis by electroencephalographic recording of ongoing and stimulus-related brain activity during stepwise drug-induced loss of consciousness in healthy human volunteers. We found that progressive loss of consciousness was tightly linked to the emergence of a hypersynchronous cortical state in the alpha frequency range (8-14 Hz). This drug-induced ongoing alpha activity was widely distributed across the frontal cortex. Stimulus-related responses to median nerve stimulation consisted of early and midlatency response components in primary somatosensory cortex (S1) and a late component also involving temporal and parietal regions. During progressive sedation, the early response was maintained, whereas the midlatency and late responses were reduced and eventually vanished. The antagonistic relation between the late sensory response and ongoing alpha activity held for constant drug levels on the single-trial level. Specifically, the late response component was negatively correlated with the power and long-range coherence of ongoing frontal alpha activity. Our results suggest blocking of intracortical communication by hypersynchronous ongoing activity as a key mechanism for the loss of consciousness.

The <1Hz slow oscillation (SO) and spindles are hallmarks of mammalian non-rapid eye movement and slow wave sleep. Spindle activity occurring phase-locked to the SO is considered a candidate mediator of memory consolidation during sleep. We used source localization of magnetoencephalographic (MEG) and electroencephalographic (EEG) recordings from 11 sleeping human subjects for an in-depth analysis of the temporal and spatial properties of sleep spindles co-occurring with SOs. Slow oscillations and spindles were identified in the EEG and related to the MEG signal, providing enhanced spatial resolution. In the temporal domain, we confirmed a phase-locking of classical 12-15Hz fast spindle activity to the depolarizing SO up-state and of 9-12Hz slow spindle activity to the up-to-down-state transition of the SO. In the spatial domain, we show a broad spread of spindle activity, with less distinct anterior-posterior separation of fast and slow spindles than commonly seen in the EEG. We further tested a prediction of current memory consolidation models, namely the existence of a spatial bias of SOs over sleep spindles as a mechanism to promote localized neuronal synchronization and plasticity. In contrast to that prediction, a comparison of SOs dominating over the left vs. right hemisphere did not reveal any signs of a concurrent lateralization of spindle activity co-occurring with these SOs. Our data are consistent with the concept of the neocortical SO exerting top-down control over thalamic spindle generation. However, they call into question the notion that SOs locally coordinate spindles and thereby inform spindle-related memory processing.

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