Neural Control of Breathing and CO2 Homeostasis.
Neural Control of Breathing and CO2 Homeostasis.
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DOI：
10.1016/j.neuron.2015.08.001
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发表时间：
2015-09-02
期刊：
影响因子：
16.2
通讯作者：
Bayliss DA
中科院分区：
文献类型：
--
作者：
Guyenet PG;Bayliss DA
最近的进展已经阐明了大脑如何检测CO2来调节呼吸（中枢呼吸化学感受）。这些机制进行审查，其意义是通过呼吸的CO2/pH稳态的一般情况下。在休息时，在外周和中枢部位启动的呼吸化学反射介导动脉PCO 2和pH的快速稳定。后斜方核，RTN;肾上腺素能）被PCO 2激活并刺激呼吸。RTN神经元通过内源性质子受体（ASK-2、GPR 4）、来自外周化学感受器的突触输入和来自星形胶质细胞的信号检测CO2。呼吸化学反射依赖于唤醒状态，而化学感受器刺激产生唤醒。当异常时，这些相互作用会导致睡眠呼吸障碍。在运动过程中，“中央命令”和运动肌肉的反射产生维持动脉PCO 2和pH所需的呼吸刺激，尽管代谢活动升高。神经回路的中枢命令和肌肉传入控制呼吸仍然难以捉摸，代表了一个肥沃的领域，为未来的调查。
Recent advances have clarified how the brain detects CO2 to regulate breathing (central respiratory chemoreception). These mechanisms are reviewed and their significance is presented in the general context of CO2/pH homeostasis through breathing. At rest, respiratory chemoreflexes initiated at peripheral and central sites mediate rapid stabilization of arterial PCO2 and pH. Specific brainstem neurons (e.g., retrotrapezoid nucleus, RTN; serotonergic) are activated by PCO2 and stimulate breathing. RTN neurons detect CO2 via intrinsic proton receptors (TASK-2, GPR4), synaptic input from peripheral chemoreceptors and signals from astrocytes. Respiratory chemoreflexes are arousal state-dependent whereas chemoreceptor stimulation produces arousal. When abnormal, these interactions lead to sleep-disordered breathing. During exercise, “central command” and reflexes from exercising muscles produce the breathing stimulation required to maintain arterial PCO2 and pH despite elevated metabolic activity. The neural circuits underlying central command and muscle afferent control of breathing remain elusive and represent a fertile area for future investigation.