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

基于我们以前在去脑猫中的发现，我们提出了这样的假设，即当在REM睡眠期间用于姿势肌张力的广泛抑制的下行抑制系统被激活时，延髓腹外侧区的中枢化学敏感性功能障碍引起“睡眠呼吸暂停”和“婴儿猝死”。我们已经尝试使用来自新生大鼠的脑干-脊髓制备物来阐明在REM睡眠期间激活的用于调节呼吸节律的脑桥嘴侧神经元机制。实验结果如下：（1）用乙醚麻醉出生后0 ~ 3日龄Wistar大鼠，在颈髓最尾侧切断脊髓。在脑桥的吻侧边缘水平进行吻侧横断。(2)在含膈神经的第四或第五颈前根用抽吸电极记录呼吸爆发放电。(3)将钨微电极插入同侧或对侧脑桥的记录部位进行微刺激。为了确定脑干部位的呼吸放电的抑制，刺激电极被系统地在脑桥内移动，并引发的刺激效果进行了分析。然而，我们从未通过刺激脑桥来诱导对呼吸的抑制作用。(4)在灌注液中加入乙酰胆碱激动剂卡巴胆碱可使呼吸频率增加。上述结果表明，在此发育阶段，起源于中枢化学感受器的呼吸化学调节机制已经完成，而起源于脑桥嘴侧的抑制系统尚未发育完全。

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.