A carotid body-brainstem neural circuit mediates sighing in hypoxia

颈动脉体 孤束 缺氧(环境) 生物 脑干 神经科学 化学受体 内分泌学 外周化学感受器 髓质 内科学 血管球细胞 解剖 氧气 受体 化学 电生理学 医学 有机化学 生物化学
作者
Yilong Yao,Jingwen Chen,Xingyu Li,Zhou‐Feng Chen,Peng Li
出处
期刊:Current Biology [Elsevier BV]
卷期号:33 (5): 827-837.e4 被引量:4
标识
DOI:10.1016/j.cub.2023.01.019
摘要

Increased ventilation is a critical process that occurs when the body responds to a hypoxic environment. Sighs are long, deep breaths that prevent alveolar collapse, and their frequency is significantly increased by hypoxia. In this study, we first show that sighing is induced by hypoxia as a function of increased hypoxic severity and that hypoxia-induced sighing is capable of increasing the oxygen saturation in a mouse model. We next found that the gastrin-releasing peptide (Grp) expressing neurons in the nucleus of the solitary tract (NTS) are important in mediating hypoxia-induced sighing. Retrograde tracing from these Grp neurons reveals their direct afferent input from the petrosal ganglion neurons that innervate the carotid body, the major peripheral chemoreceptor that senses blood oxygen. Acute hypoxia preferentially activates these Grp neurons in the NTS. Photoactivation of these neurons through their projections in the inspiratory rhythm generator in the ventral medulla induces sighing, whereas genetic ablation or chemogenetic silencing of these neurons specifically diminishes the sighs, but not other respiratory responses, induced by hypoxia. Finally, the mice with reduced sighing in hypoxia exhibit an elevated heart-rate increase, which may compensate for maintaining the blood oxygen level. Therefore, we identified a neural circuit that connects the carotid body to the breathing control center in the ventral medulla with a specific function for hypoxia-induced sighing, which restores the oxygen level.
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