Abstract
General anesthesia is a drug-induced reversible state comprised of altered states of consciousness, amnesia, analgesia, and immobility. The medial frontal cortex (mPFC) has been discovered to modulate the level of consciousness through cholinergic and glutamatergic pathways. The optogenetic tools combined with in vivo electrophysiological recording were used to study the neural oscillatory modulation mechanisms in mPFC underlying the loss of consciousness (LOC) and emergence. We found that optogenetic activation of both cholinergic and glutamatergic neurons in the basal forebrain (BF) reversed the hypnotic effect of propofol and accelerated the emergence from propofol-induced unconsciousness. The cholinergic light-activation during propofol anesthesia increased the power in the β (12–20 Hz) and low γ (20–30 Hz) bands. Conversely, glutamatergic activation increased the power at less specific broad (1–150 Hz) bands. The cholinergic-induced alteration to specific power bands after LOC had opposite effects to that of propofol. These results suggested that the cholinergic system might act on more specific cortical neural circuits related to propofol anesthesia.
Highlights
General anesthesia is a reversible, anesthetic drug-induced state in which patients undergo an amalgamation of altered states of consciousness, analgesia, amnesia, and immobility (Brown et al, 2011)
These results showed that selective activation of cholinergic neurons in the basal forebrain (BF) delays the time to unconsciousness and promotes emergence from propofol anesthesia
We demonstrated that the selective activation of both cholinergic and glutamatergic neurons in the BF could reverse the hypnotic effect of propofol
Summary
General anesthesia is a reversible, anesthetic drug-induced state in which patients undergo an amalgamation of altered states of consciousness, analgesia, amnesia, and immobility (Brown et al, 2011). One of the biggest mysteries of modern medicine is how anesthetic drugs induce unconsciousness and how patients subsequently recover from general anesthesia (Kennedy and Norman, 2005). Different anesthetics induced altered specific oscillation band changes during the loss of consciousness (LOC) because of the discrepant molecular targets in the brain (Blain-Moraes et al, 2014, 2015). One of the GABAA receptor agonist anesthetics, exhibited specific activation of the delta band and theta-gamma coupling during the LOC and emergence, and is commonly used in clinical trials (Breshears et al, 2010). Due to the lack of current literature on the formation of propofol-induced
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