Abstract
Introduction General anesthesia is known to be a drug-induces, reversible condition that includes specific behavioral and physiological traits, such as unconsciousness, amnesia, analgesia, and akinesia (Brown et al., 2010). Among those characteristic features, the underlying mechanisms of propofol-induces amnesia still remains unknown. Propofol is a commonly used anesthetic drug and is known to induce anesthetic state through enhancing inhibition at GABAA receptors. The hippocampal formation occupies a central position for generation of memory (Perouansky and Pearce, 2011). From an electrophysiological perspective, hippocampal formation is a central theta rhythm generator controlled by GABAergic hippocampal interneurons (Buzsaki, 2006). Taken together, we hypothesized that enhancement of inhibition at GABAA receptors induced by propofol influences on theta oscillations of hippocampal formation which leads to propofol-induced amnesia. To address this hypothesis, we investigated an electrocorticography (ECoG) signals obtained from mesial temporal lobe epilepsy patients (MTLE) with hippocampal sclerosis (HS). Methods We recruited five MTLE with HS. Because we are especially interested in the hippocampal theta oscillations, we only included the patients who had depth-electrodes over hippocampal formation. Two patients had the right HS and 3 patients had the left HS. ECoG signals were recorded during 3 different awaked states such as, resting-state, sleep state and word memory task. In addition, ECoG were recorded under general anesthesia with 3 different propofol concentrations of 5 μ g/ml, 4 μ g/ml and 3 μ g/ml. ECoG signals were epoched for 2 min. Bad channel removal, drift removal, re-referencing (common average reference), and low-pass filter of 100 Hz were applied. We evaluated relative theta power, theta/beta ratio, and cross-frequency phase-amplitude coupling analysis between theta (4–7 Hz) and beta (13–30 Hz) frequency band. Modulation index representing theta phase and beta amplitude coupling was derived. Results Hippocampal formation consistently showed the reduced relative theta power during propofol-induced state compared with those in the resting-state, sleep and memory task conditions. The theta/beta ratios of hippocampal formation during propofol-induced state and during memory task showed similar levels between them, but, lower than those during resting-state and sleep conditions. It is notable that the modulation index of theta phase and beta amplitude at hippocampal formation was higher during propofol-induced state than other conditions. Conclusion Our results suggest that this specific theta-beta coupling occurred at hippocampal formation during propofol-induced state could be a possible electrophysiological mechanism for explaining propofol-induced amnesia. Acknowledgements This study was funded by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (Grant No. 2015R1D1A1A02061486 ).
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