Circuit-level dynamics and propagation of slow wave activity modulate their interplay during the awakening process.

Slow-wave activity (SWA) in non-REM sleep and anesthesia is a hallmark of unconsciousness, but how it changes during the return to consciousness is unclear. Recording multi-area and laminar activity in mouse posterior parietal (PPC) and primary visual (V1) cortices during spontaneous awakening from isoflurane anesthesia, the authors show that spectral power is stronger in PPC (especially superficial layers) during deep unconsciousness but stronger in V1 upon awakening. Rostro-caudal (feedback-like) propagation of SWA is state-dependent, particularly in layer 5. Excitability of layer 2/3 neurons, suppressed at high isoflurane, recovers during awakening, when V1 and feedforward pathways reassert a strong role. SWA is a multiscale phenomenon with hierarchical and laminar properties.

Study at a glance

Abstract

Slow-wave activity (SWA) is a hallmark of the loss of consciousness in non-REM sleep and anesthesia. The mechanistic underpinnings of SWA, and its evolution when transitioning toward the conscious brain state is poorly understood. We address this topic by recording multi-area and laminar activity in posterior parietal (PPC) and primary visual (V1) cortices of mice spontaneously awakening from isoflurane anesthesia. Spectral power is stronger in PPC (especially in superficial layers) during deep unconsciousness, but stronger in V1 when awakening. Rostro-caudal (feedback-like) propagation of SWA also shows state-dependent modulation, particularly in layer 5. The excitability of layer 2/3 neurons, hindered at high isoflurane, recovers during awakening, when V1 and the feedforward pathway reacquire a strong role. Detailing the hierarchical and laminar properties of spontaneous traveling oscillations, we provide evidence that SWA is a multiscale phenomenon. Explicating the functional role of these processes is critical to understand the neuronal mechanisms of consciousness.