Local Gamma Activity During Non-REM Sleep in the Context of Sensory Evoked K-Complexes.

Abstract

K-complexes (KCs) and Sleep Slow Oscillations (SSOs) are the EEG expression of neuronal bistability during deeper stages Non-REM sleep. They are characterized by a deep negative deflection lasting about half-a-second, sustained, at the cortical level, by a widespread and synchronized neuronal hyperpolarization (i.e., electrical silence). The phase of hyperpolarization is followed by a period of intense and synchronized neuronal firing (i.e., depolarization phase) resulting at the EEG level, in a large positive deflection (lasting about 0.5 s) and a concurrent high frequency activity (i.e., spindles). Both KCs and SSOs rather than being “local” phenomena, propagate over large sections of the cortex. These features suggest that bistability is a large-scale network phenomenon, possibly driven by a propagating excitatory activity and involving wide populations of synchronized neurons. We have recently shown that KCs and SSOs include a positive bump preceding the negative peak and that for sensory-evoked KCs this bump coincides with the P200 wave. We demonstrated that the P200 has a sensory-modality specific localization, as it is firstly elicited in the primary sensory areas related to the stimulus, which in turn receive projections from the thalamic core. We observed that the P200 acts as a propagating excitatory activity and hypothesized that it could play a key role in inducing the opening of K+ channels, and hence the cortical hyperpolarization. Here we demonstrate that the P200 is sustained by a high-frequency excitation bringing further support to its role in triggering bistability. We show that the P200 has a higher power density in gamma band as compared to the P900 coherently for all sensory modalities, and we confirm that the latter wave is crowned by higher activity in sigma-beta bands. Finally, we characterize the P200 gamma activity at the cortical level in terms of spatial localization and temporal dynamics, demonstrating that it emerges in sensory stimulus-specific primary areas and travels over the cortical mantle spreading toward fronto-central associative areas and fading concurrently with the N550 onset.