Does the posteromedial cortex play a primary role for the capacity for consciousness in rats?

Abstract

It remains unclear how specific cortical regions contribute to the brain’s overall capacity for consciousness. Clarifying this could help distinguish between theories of consciousness. Here, we investigate the association between markers of regionally specific (de)activation and the brain’s overall capacity for consciousness.We recorded electroencephalographic (EEG) responses to cortical electrical stimulation in 6 rats, and computed Perturbational Complexity Index state-transition (PCIST), which has been extensively validated as an index of the capacity for consciousness in humans. We also estimated the balance between activation and inhibition of specific cortical areas with the ratio between high and low frequency power (HF/LF) from spontaneous EEG activity at each electrode. We repeated these measurements during wakefulness, and under the influence of ketamine anaesthesia at two doses: the minimal dose needed to induce behavioural unresponsiveness and twice this dose.We found that PCIST was only slightly reduced from wakefulness to light ketamine anaesthesia, but dropped significantly down with deeper anaesthesia. The high-dose effect was selectively associated with reduced HF/LF ratio in the posteromedial cortex, which strongly correlated with PCIST. Conversely, behavioural unresponsiveness induced by light ketamine anaesthesia, was associated with similar spectral changes in frontal, but not posterior cortical regions.These findings seem to support the claim that the posteromedial cortex may play a primary role for the capacity for consciousness. Such region-specific associations between cortical activation and the overall capacity for consciousness must be accounted for by theories of consciousness.

Complexity and 1/f slope jointly reflect brain states

“…Next, we asked whether the impact of modifying E/I balance on the relationship between 1/f slope and LZc seen in our model could be reproduced in empirical electrophysiological data. We analyzed two open datasets, both obtained during resting-state and during increased cortical inhibition by propofol: a macaque monkey ECoG (48), and an epidural EEG in rats (49, 50).…”

“…We used an open EEG database (49) collected from two head - and body - restricted rats during wakefulness and propofol anesthesia (2 mg/kg/min). The EEG recording represents 3 minutes of spontaneous brain activity recorded with 16 EEG channels.…”