Rapid fragmentation of neuronal networks at the onset of propofol-induced unconsciousness
General anesthesia involves rapidly inducing a reversible coma by administering a large dose of a fast-acting drug, such as propofol. Previous research has demonstrated that propofol enhances inhibitory input to neurons throughout the spinal cord, brainstem, thalamus, and cortex. However, how these effects in single cells translate to larger-scale neural circuits and cause unconsciousness is not well understood. We recorded spiking activity from ensembles of single neurons and intracranial electrical activity during the induction of propofol general anesthesia in human subjects undergoing surgery. We found that loss of consciousness (LOC) corresponds to the abrupt onset of a slow cortical oscillation that marks a fragmentation of neuronal networks. These results identify the slow oscillation as a dramatic neural correlate of LOC and demonstrate that slow oscillation marks the transition into a brain state in which local neuronal networks are isolated, impairing both temporal and spatial communication throughout the cortex.
