Ramirez J M, Quellmalz U J, Wilken B
Department of Organismal Biology and Anatomy, The University of Chicago, Illinois 60637, USA.
J Neurophysiol. 1997 Jul;78(1):383-92. doi: 10.1152/jn.1997.78.1.383.
The transverse brain stem slice of mice containing the pre-Bötzinger complex (PBC), a region essential for respiratory rhythm generation in vitro, was used to study developmental changes of the response of the in vitro respiratory network to severe hypoxia (anoxia). This preparation generates, at different postnatal stages [postnatal day (P)0-22], spontaneous rhythmic activity in hypoglossal (XII) rootlets that are known to occur in synchrony with periodic bursts of neurons in the PBC. It is assumed that this rhythmic activity reflects respiratory rhythmic activity. At all examined stages anoxia led to a biphasic response: the frequency of rhythmic XII activity initially increased ("primary augmentation") and then decreased ("secondary depression"). In neonates (P0-7), anoxia did not significantly affect the amplitude of integrated XII bursts. Secondary depression never led to a cessation of rhythmic activity. In mice older than P7, augmentation was accompanied by a significant increase in the amplitude of XII bursts. A significant decrease of the amplitude of XII bursts occurred during secondary depression. This depression led always to cessation of rhythmic activity in XII rootlets. The anoxia-induced response of the respiratory rhythmic XII motor output is biphasic and changes during development in a similar way to the in vivo respiratory network. Whether this biphasic response is due to a biphasic response of the respiratory rhythm generator and/or to a biphasic modulation of the XII motor nucleus remains unresolved and needs further cellular analysis. We propose that the transverse slice is a useful model system for examination of the mechanisms underlying the hypoxic response.
使用包含前包钦格复合体（PBC）的小鼠脑桥横切片来研究体外呼吸网络对严重缺氧（无氧）反应的发育变化，PBC是体外呼吸节律产生所必需的区域。该制备物在不同的出生后阶段[出生后第（P）0 - 22天]，在舌下神经（XII）小根中产生自发节律性活动，已知该活动与PBC中神经元的周期性爆发同步发生。假定这种节律性活动反映呼吸节律性活动。在所有检查阶段，缺氧导致双相反应：节律性XII活动的频率最初增加（“初级增强”），然后降低（“次级抑制”）。在新生儿（P0 - 7）中，缺氧对整合的XII爆发的幅度没有显著影响。次级抑制从未导致节律性活动停止。在大于P7的小鼠中，增强伴随着XII爆发幅度的显著增加。在次级抑制期间，XII爆发的幅度显著降低。这种抑制总是导致XII小根中的节律性活动停止。缺氧诱导的呼吸节律性XII运动输出反应是双相的，并且在发育过程中的变化与体内呼吸网络类似。这种双相反应是由于呼吸节律发生器的双相反应和/或XII运动核的双相调节尚不清楚，需要进一步的细胞分析。我们提出，横切片是用于检查缺氧反应潜在机制的有用模型系统。
