Fig. 1. Effects of sevoflurane and acetylcholine on action potential activity in neocortical slices. Sevoflurane data are depicted on the  left side of the figure, and corresponding data obtained from experiments with acetylcholine are shown on the  right side . (  A ) Original recordings are displayed in the absence (  upper panel ) and presence (  lower panel ) of 0.26 mm sevoflurane (corresponding to 0.75 MAC [1 MAC is defined to be the minimum alveolar concentration of an inhaled anesthetic required to suppress movement in response to noxious stimulation in 50% of subjects]) and 0.3 μm acetylcholine. Corresponding binned data are shown in  B and  C . Spikes were binned at 50-ms intervals. The depression of neuronal activity caused by 0.75 MAC sevoflurane arose as a decrease in the frequency of episodes of ongoing activity and a decrease in firing rates within these episodes. Although the episodes of ongoing activity were prolonged by the anesthetic, the overall time of neuronal silence was substantially lengthened (  C , left side ). Acetylcholine prolonged the duration of active states as observed with sevoflurane, but in contrast to the anesthetic, it increased average firing rates by elevating action potential activity within episodes of ongoing activity (  C , right side ). (  D ) Cumulative number of spikes over a recording period of 180 s. 

Fig. 1. Effects of sevoflurane and acetylcholine on action potential activity in neocortical slices. Sevoflurane data are depicted on the  left side of the figure, and corresponding data obtained from experiments with acetylcholine are shown on the  right side . (  A ) Original recordings are displayed in the absence (  upper panel ) and presence (  lower panel ) of 0.26 mm sevoflurane (corresponding to 0.75 MAC [1 MAC is defined to be the minimum alveolar concentration of an inhaled anesthetic required to suppress movement in response to noxious stimulation in 50% of subjects]) and 0.3 μm acetylcholine. Corresponding binned data are shown in  B and  C . Spikes were binned at 50-ms intervals. The depression of neuronal activity caused by 0.75 MAC sevoflurane arose as a decrease in the frequency of episodes of ongoing activity and a decrease in firing rates within these episodes. Although the episodes of ongoing activity were prolonged by the anesthetic, the overall time of neuronal silence was substantially lengthened (  C , left side ). Acetylcholine prolonged the duration of active states as observed with sevoflurane, but in contrast to the anesthetic, it increased average firing rates by elevating action potential activity within episodes of ongoing activity (  C , right side ). (  D ) Cumulative number of spikes over a recording period of 180 s. 

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