Neural Mechanisms of Sleep Apnea

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Under halothane anesthesia, the animal was decerebrated at the precollicular-postmammillary level. The glass-insulated tungsten microelectrode was inserted into the midpontine dorsal tegmentum (DTF). Tonic electrical stimulation was delivered to the DTF area, and the stimulus effects were confirmed. DTF stimulation evoked simultaneous suppression of postural tone and respiration. The another microelecrode was then inserted into the rostral pontine reticular formation, and was used for a recording function. DTF was stimulated at once per second, and the antidromically activated neurons were identified within the rostral pons. The antidromically activated neurons were located in the nucleus reticularis pontis oralis (PoO). Such neurons had little spontaneous discharges. A microinjection of carbachol, a cholinergic agonist, into the pontine reticular formation around or near the PoO resulted in the parallel suppression of postural tone and respiration, and the effects were very similar to those elicited by DTF stimulation. Hobson et al. reported that a carbachol injection into the PoO have led the animal to a REM sleep in chronic cats. We have already clarified that there exists a descending inhibitory pathway responsible for generalized motor suppression. The pathway originates from the neurons in the PoO and descends to the spinal cord via DTF area. All these findings lead us to suggest that the inhibitory system identified in this study may raise its activity during sleep, especially during REM sleep, and may result in the sleep apnea when the central chmosensitivity is damaged.