The MIT news site (here) has an item on research by Patrick Purdon and others, Rapid fragmentation of neuronal networks at the onset of propofol-induced unconsciousness, published in PNAS. They found that communication between brain areas became very local under anesthetic.
By monitoring brain activity as patients were given a common anesthetic, the researchers were able to identify a distinctive brain activity pattern that marked the loss of consciousness. This pattern, characterized by very slow oscillation, corresponds to a breakdown of communication between different brain regions, each of which experiences short bursts of activity interrupted by longer silences.
This is another example of studying epileptic patients waiting for surgery with electrodes placed in their brains.
Using two different-sized electrodes, the researchers were able to obtain two different readings of brain activity. The larger electrodes, slightly bigger than a penny, were spaced about a centimeter apart and recorded the overall EEG, or brain-wave pattern. Smaller electrodes, in an array only 4 millimeters wide, recorded from individual neurons, marking the first time anyone has recorded from individual neurons in human patients as they lost consciousness. Between 50 and 100 electrodes were implanted in each patient, clustered in different regions.
The larger electrodes showed the fall into unconsciousness is an abrupt change to long waves of about 1 hertz in the EEG. But the small electrodes showed that individual neurons were still active.
Individual neurons revealed that within localized brain regions, neurons were active for a few hundred milliseconds, then shut off again for a few hundred milliseconds. This flickering of activity created the slow oscillation seen in the EEG. When one area was active, it was likely that another brain area that it was trying to communicate with was not active. Even when the neurons were on, they still couldnt send information to other brain regions. When consciousness is lost, there may still be information coming into the brain, but that information is remaining localized and doesnt get integrated into a coherent picture. Failure of information integration had previously been suggested as a possible mechanism for loss of consciousness, but no one was sure how that might happen. This finding really narrows it down quite a bit. It really does, in a very fundamental way, constrain the possibilities of what the mechanisms could be.
Here is the abstract:
The neurophysiological mechanisms by which anesthetic drugs cause loss of consciousness are poorly understood. Anesthetic actions at the molecular, cellular, and systems levels have been studied in detail at steady states of deep general anesthesia. However, little is known about how anesthetics alter neural activity during the transition into unconsciousness. We recorded simultaneous multiscale neural activity from human cortex, including ensembles of single neurons, local field potentials, and intracranial electrocorticograms, during induction of general anesthesia. We analyzed local and global neuronal network changes that occurred simultaneously with loss of consciousness. We show that propofol-induced unconsciousness occurs within seconds of the abrupt onset of a slow (<1 Hz) oscillation in the local field potential. This oscillation marks a state in which cortical neurons maintain local patterns of network activity, but this activity is fragmented across both time and space. Local (<4 mm) neuronal populations maintain the millisecond-scale connectivity patterns observed in the awake state, and spike rates fluctuate and can reach baseline levels. However, neuronal spiking occurs only within a limited slow oscillation-phase window and is silent otherwise, fragmenting the time course of neural activity. Unexpectedly, we found that these slow oscillations occur asynchronously across cortex, disrupting functional connectivity between cortical areas. We conclude that the onset of slow oscillations is a neural correlate of propofol-induced loss of consciousness, marking a shift to cortical dynamics in which local neuronal networks remain intact but become functionally isolated in time and space.