Medullary Reticular Neurons Related to Hypoxic Respiratory Depression

我们进行了以下三个不同的实验。1.在去窦-主动脉神经支配、切断迷走神经、人工通气的猫上，研究了椎动脉内注射低氧或常氧盐水的呼吸效应。注射N_2饱和盐水（中枢低氧负荷）引起明显的呼吸抑制（膈神经活动减少），潜伏期短，在数秒内出现。在中丘水平去大脑后观察到类似的缺氧性呼吸抑制。因此，可以得出结论，负责缺氧性呼吸抑制的结构位于由椎-基底动脉供血的脑桥-延髓区.我们观察了上述缺氧性呼吸抑制过程中延髓网状神经元非时相性放电活动的变化。兴奋性单位和抑制性单位均被分离出来，且大多数位于延髓头端腹外侧区，对应于外侧巨细胞旁核.由于有研究表明中枢低氧负荷可抑制脑干5-羟色胺能神经系统，我们用多管微量移液器检测了延髓吸气神经元对5-羟色胺的反应性。本文研究的延髓吸气神经元根据放电模式的差异分为两个亚组。5-羟色胺可使放电模式递减的吸气神经元兴奋，而放电模式递增的吸气神经元则受到抑制。这些结果提示，供应上气道扩张肌的吸气运动前神经元可能对低氧性呼吸抑制更敏感。

We have performed the following three distinct experiments.1. Respiratory effect of intravertebral arterial injections of hypoxic or normoxic saline has been studied in sino-aortic denervated, vagotomized, artificially ventilated cats. Injections of N_2-saturated saline (a central hypoxic loading) evoked a clear respiratory depression (a decrease in phrenic nerve activity) with a short onset latency within a few seconds. Similar hypoxic respiratory depression was observed after decerebration at the mid-collicular level. Therefore, it was concluded that the structures responsible for the hypoxic respiratory depression were located within ponto-medullary regions supplied by the vertebral-basilar artery.2. We have examined changes in activity of medullary reticular neurons with non-phasic discharges during the forementioned hypoxic respiratory depression. Both excitatory and inhibitory units were isolated, and most of them were found in the rostral vetrolateral medulla, corresponding to the nuleus paragigantocellularis lateralis.3. Since it has been reported that brainstem serotonergic system was depressed during the central hypoxic loading, we have tested responsiveness of medullary inspiratory neurons to direct applications of serotonin, using a multi-barreled micropipette. The medullary inspiratory neurons examined herein were classified into two subgroups based upon the differences in firing patterns. The inspiratory neurons with decrementing firing pattern were excited by serotonin application, whereas the inspiratory neurons with augmenting firing pattern were inhibited. These results suggest a possibility that inspiratory premotor neurons supplying the dilator muscles of upper airway might be more sensitive to the hypoxic respiratory depression.