Development and assesment of the animal model for "sudden infant death syndrom".

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Based on our previous findings in decerebrated cats, we have proposed the hypothesis that dysfunction in the central chemosensitivity in the ventrolateral medulla induces "sleep apnea" and "sudden infant death" when the descending inhibitory system for the generalized suppression of postural muscle tone is activated during REM sleep.In this research project, we have tried to elucidate the rostral pontine neuronal mechanisms activated during REM sleep for the regulation of respiratory rhythm using brainstem-spinal cord preparations from neonatal rats. The results obtained from this study are summarized as follows :(1) Postnatal 0-to 3-day-old Wistar rats were anesthetized with ether, and the spinal cord was transected at the most caudal cervical cord. The rostral transection was done at the level of the rostral border of the pons.(2) The respiratory bursting discharges were recorded by a suction electrode from the fourth or fifth cervical ventral root containing the phrenic nerve.(3) A tungsten microelectrode was inserted into the ipsilateral or the contralateral pons to the recording sites for microstimulation. In order to identify the brainstem sites for the suppression of the respiratory discharges, the stimulation electrode was systematically moved within the pons, and the stimulus effects elicited were analyzed. However, we never induced the suppressive effects on respiration by stimulating the pons.(4) Loading of carbachol, an Ach agonist, to the perfusion solution resulted in the increase of the respiratory frequency. CO2 loading also increased the respiratory frequency.All the above results suggested the possibility that the chemical regulation mechanism for respiration originating from the central chemoreceptor is completed at this developmental stage, but the inhibitory system originating from the rostral pons is not yet fully developed.