Anesthesia is featured by behavioral and physiological characteristics such as decreased sensory and motor function, loss of consciousness, etc. Some anesthetics such as dexmedetomidine (DEX), induce electroencephalogram signatures close to non-rapid eye movement sleep. Studies have shown that sleep is primarily driven by the activation of subcortical sleep-promoting neural pathways.
However, the neuronal level electrophysiology features of anesthesia and how they differ from sleep is still not fully understood.
In the present study, we recorded neuronal activity simultaneously from somatosensory cortex (S1) and motor cortex (M1) during awake, sleep, and DEX-induced anesthesia in rats.
The results show that DEX increased local field potential (LFP) power across a relatively wide band (1–25 Hz) in both S1 and M1. The coherence between S1 LFP and M1 LFP increased significantly in the delta and alpha bands. Power spectrum analysis during DEX-induced anesthesia revealed relatively high power in the delta and alpha bands, but low power in the theta and beta bands. Overall, the firing rate of individual neurons decreased after DEX. Correlation analysis of firing rate and LFP power indicate that more neurons were correlated, either positively or negatively, with LFPs during DEX-induced anesthesia compared to sleep.
Although these results showed enhancement of cortical LFP power in both DEX-induced anesthesia and sleep, different patterns of spike-field correlation suggest that the two states may be regulated by different cortical mechanisms.
Distinguishing anesthesia from sleep with neural oscillations could lead to more personalized, safer, and more effective approaches to managing consciousness in medical settings, with the potential for broad applications in neuroscience and clinical practice.