Although the precise neural correlates of consciousness have not yet been identified, there is one neurochemical marker that appears to track with our capacity to experience something: acetylcholine concentration in the cerebral cortex. Cortical acetylcholine concentration is high during wakefulness, decreases during slow-wave sleep, and increases again during rapid eye movement sleep, when we can have the conscious experience of dreaming. Based on the neuropharmacology of the particular anesthetic drug we might choose, the state of general anesthesia shows parallel changes. For example, the effects of the γ-aminobutyric acid–mediated (GABAergic) anesthetics propofol and sevoflurane are similar to slow-wave sleep and include low acetylcholine concentration, slower electroencephalographic frequency, and a low probability of experience.2,3  By contrast, the effects of the non-GABAergic anesthetics ketamine and nitrous oxide are similar to rapid eye movement sleep and...

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