Abstract
Although general anesthetics are routinely administered to surgical patients to induce loss of consciousness, the mechanisms underlying anesthetic-induced unconsciousness are not fully understood. In rats, we characterized changes in the extradural EEG and intracranial local field potentials (LFPs) within the prefrontal cortex (PFC), parietal cortex (PC), and central thalamus (CT) in response to progressively higher doses of the inhaled anesthetic sevoflurane. During induction with a low dose of sevoflurane, beta/low gamma (12–40 Hz) power increased in the frontal EEG and PFC, PC and CT LFPs, and PFC–CT and PFC–PFC LFP beta/low gamma coherence increased. Loss of movement (LOM) coincided with an abrupt decrease in beta/low gamma PFC–CT LFP coherence. Following LOM, cortically coherent slow-delta (0.1–4 Hz) oscillations were observed in the frontal EEG and PFC, PC and CT LFPs. At higher doses of sevoflurane sufficient to induce loss of the righting reflex, coherent slow-delta oscillations were dominant in the frontal EEG and PFC, PC and CT LFPs. Dynamics similar to those observed during induction were observed as animals emerged from sevoflurane anesthesia. We conclude that the rat is a useful animal model for sevoflurane-induced EEG oscillations in humans, and that coherent slow-delta oscillations are a correlate of sevoflurane-induced behavioral arrest and loss of righting in rats.
Highlights
General anesthesia is a reversible, drug-induced state characterized by unconsciousness, amnesia, analgesia, and immobility in the setting of hemodynamic stability (Brown et al, 2010)
Extradural EEG and intracranial local field potentials (LFPs) in the prefrontal cortex (PFC), parietal cortex (PC), and central thalamus (CT) were recorded in rats under sevoflurane anesthesia
Loss of movement (LOM) correlated with an abrupt decrease in PFC–CT LFP beta/low gamma coherence, and was followed by increased slow-delta power in PFC, PC, and CT LFPs and increased cortico-cortical slow-delta coherence
Summary
General anesthesia is a reversible, drug-induced state characterized by unconsciousness, amnesia, analgesia, and immobility in the setting of hemodynamic stability (Brown et al, 2010). The study of anesthetic mechanisms has focused primarily on characterizing the actions of anesthetic drugs at molecular targets in the brain and spinal cord (Rudolph and Antkowiak, 2004; Hemmings et al, 2005; Franks, 2006) This important work established that multiple molecular targets are involved in general anesthesia (Eger et al, 1997; Grasshoff et al, 2005). It remains unclear how anesthetics produce profound changes in neurophysiology at the systems level to induce unconsciousness (Franks, 2008; Brown et al, 2011). Anesthetic-induced oscillations may play a role in loss of consciousness (Lewis et al, 2012), their origins within the brain and precise relationship to unconsciousness are not known
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