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

基于我们之前对失觉猫的研究结果，我们提出了一个假设，即当快速眼动睡眠期间激活体位肌张力普遍抑制的下行抑制系统时，腹外侧髓质中枢化学敏感性的功能障碍会导致“睡眠呼吸暂停”和“婴儿猝死”。在本研究项目中，我们试图利用新生大鼠的脑干-脊髓制剂阐明快速眼动睡眠期间激活的桥侧吻侧神经元调节呼吸节律的机制。本研究结果总结如下：(1)出生后0 ~ 3日龄Wistar大鼠用乙醚麻醉，在最尾端颈髓处横切脊髓。在桥的吻侧边界处进行吻侧横切。(2)从含膈神经的第四或第五颈腹根用吸电极记录呼吸性爆裂性放电。(3)将钨微电极插入同侧或对侧脑桥至记录部位进行微刺激。为了确定抑制呼吸放电的脑干部位，在脑桥内系统地移动刺激电极，并分析所引起的刺激效应。然而，我们从未通过刺激脑桥诱导呼吸抑制作用。(4)灌注液中加入乙酰胆碱激动剂丙二醇导致呼吸频率增加。二氧化碳负荷也增加了呼吸频率。以上结果提示，中枢化学感受器对呼吸的化学调节机制可能在这一发育阶段已经完成，而源于桥喙侧的抑制系统尚未完全发育。

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.