Fig. 10. Cholinergic activation of the cortical electroencephalogram during halothane anesthesia. (  A ) Electroencephalogram recorded from cat during wakefulness (WAKE), non–rapid eye movement (NREM) sleep, rapid eye movement (REM) sleep, and halothane anesthesia.  Left upper and lower traces illustrate the similarity in electroencephalogram between wakefulness and REM sleep.  Middle upper and lower traces show the similar bursts in the electroencephalogram recorded during NREM sleep and halothane anesthesia.  Right upper and lower traces show electroencephalographic recordings at a faster sweep speed to illustrate that waves in the 8- to 14-Hz frequency, referred to as  spindles , characterize the cortical electroencephalogram during NREM sleep and halothane anesthesia. Therefore, although NREM sleep and halothane anesthesia are different states of consciousness, both states exhibit similar electroencephalographic traits. This trait similarity suggests that an understanding of the neuronal mechanisms generating the electroencephalogram of NREM sleep can help to elucidate neuronal mechanisms regulating the electroencephalogram during anesthesia. (  B ) Microinjection of carbachol into the medial pontine reticular formation (mPRF) inhibits halothane-induced spindles in the electroencephalogram.  Inset illustrates microinjection site for delivery of the cholinergic agonist carbachol into the mPRF. The mPRF receives cholinergic input from the laterodorsal and pedunculopontine tegmental (LDT/PPT) nuclei.  Graph plots number of spindles in the electroencephalogram  versus end-tidal halothane measured from cat. The two functions show number of spindles in the electroencephalogram during halothane alone and after carbachol microinjection into the mPRF during halothane anesthesia. The key point is that the cortical electroencephalogram is activated by enhancing cholinergic input to the mPRF. During REM sleep and wakefulness, cholinergic output from the LDT/PPT is increased to suppress spindles in the electroencephalogram.  These preclinical studies suggest one mechanism potentially underlying the clinical finding  that physostigmine can reverse the loss of consciousness produced by propofol. From Keifer  et al. ;  used with permission. 

Fig. 10. Cholinergic activation of the cortical electroencephalogram during halothane anesthesia. (  A ) Electroencephalogram recorded from cat during wakefulness (WAKE), non–rapid eye movement (NREM) sleep, rapid eye movement (REM) sleep, and halothane anesthesia.  Left upper and lower traces illustrate the similarity in electroencephalogram between wakefulness and REM sleep.  Middle upper and lower traces show the similar bursts in the electroencephalogram recorded during NREM sleep and halothane anesthesia.  Right upper and lower traces show electroencephalographic recordings at a faster sweep speed to illustrate that waves in the 8- to 14-Hz frequency, referred to as  spindles , characterize the cortical electroencephalogram during NREM sleep and halothane anesthesia. Therefore, although NREM sleep and halothane anesthesia are different states of consciousness, both states exhibit similar electroencephalographic traits. This trait similarity suggests that an understanding of the neuronal mechanisms generating the electroencephalogram of NREM sleep can help to elucidate neuronal mechanisms regulating the electroencephalogram during anesthesia. (  B ) Microinjection of carbachol into the medial pontine reticular formation (mPRF) inhibits halothane-induced spindles in the electroencephalogram.  Inset illustrates microinjection site for delivery of the cholinergic agonist carbachol into the mPRF. The mPRF receives cholinergic input from the laterodorsal and pedunculopontine tegmental (LDT/PPT) nuclei.  Graph plots number of spindles in the electroencephalogram  versus end-tidal halothane measured from cat. The two functions show number of spindles in the electroencephalogram during halothane alone and after carbachol microinjection into the mPRF during halothane anesthesia. The key point is that the cortical electroencephalogram is activated by enhancing cholinergic input to the mPRF. During REM sleep and wakefulness, cholinergic output from the LDT/PPT is increased to suppress spindles in the electroencephalogram.  These preclinical studies suggest one mechanism potentially underlying the clinical finding  that physostigmine can reverse the loss of consciousness produced by propofol. From Keifer  et al. ;  used with permission. 

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