It’s a topic that has long captivated doctors, scientists and the public — what exactly happens in your brain when you’re oblivious on the operating table?
Some anesthesia drugs work in a straightforward manner by dampening down neurons in the brain. The mechanism of one anesthetic, however, has proved elusive: ketamine.
Ketamine is used often in patient care and in laboratory settings. The new paper examines the neurological mechanisms at work during ketamine anesthesia.
Co-senior authors Chestek and anesthesiologist George Mashour, M.D., Ph.D., led the research team, which took precise measurements down to the level of neurons in animal models.
“We found that general anesthesia reflects a communication breakdown in the cortex, even though sensory information is getting processed,” Mashour says. “But the processing appears to occur in isolated cognitive islands.”
Turns out, two adjacent parts of the brain that work together in the waking state simply stop talking to each other under general anesthesia. When awake, communication between the primary somatosensory cortex and the primary motor cortex is critical to normal function.
“This supports the idea that what anesthesia does to cause unconsciousness is interrupt communication between brain areas, stopping the processing of higher-level information,” says first author Karen Schroeder, a doctoral candidate in the U-M Department of Biomedical Engineering. “This was the first time anyone directly observed the interruption between the two areas using individual neurons.”