Long term facilitation of phrenic motor output
Long term facilitation of phrenic motor output
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DOI：
10.1016/s0034-5687(00)00124-9
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发表时间：
2000-07-01
期刊：
影响因子：
--
通讯作者：
Mitchell, GS
中科院分区：
文献类型：
--
作者：
Fuller, DD;Bach, KB;Mitchell, GS
间歇性缺氧或电刺激颈动脉化学传入神经元可引起呼吸运动输出的持续、依赖于降钙素的增强，称为长时程易化（LTF）。本文的主要目的是提供一个最新的文献综述有关LTF，调查选定的变量对LTF的影响，通过荟萃分析的大数据集从LTF实验麻醉大鼠，并提出一个更新的LTF的机制。LTF已经在麻醉和清醒的实验制剂中得到证实，并且可以在睡眠期间在一些人类受试者中诱发。LTF的机制需要间歇性的化学传入刺激，而不是由持续缺氧的累积时间引起的。在麻醉大鼠的63个实验中，对间歇性缺氧后膈神经反应的荟萃分析（由四名研究人员在几年的时间内进行）表明，膈LTF幅度与缺氧和高碳酸血症期间的峰值膈反应相关，但与间歇性暴露期间的缺氧水平无关。潜在的机制，这些关系进行了讨论，目前可用的数据合成到一个更新的机制模型LTF。在这个模型中，我们提出，LTF主要是从间歇性激活膈运动神经元上的多巴胺能受体，激活细胞内激酶，从而磷酸化和增强离子电流与谷氨酸受体介导的呼吸驱动。(C)2000 Elsevier Science B.V.保留所有权利。
Episodic hypoxia or electrical stimulation of carotid chemoafferent neurons elicits a sustained, serotonin-dependent augmentation of respiratory motor output known as long term facilitation (LTF). The primary objectives of this paper are to provide an updated review of the literature pertaining to LTF, to investigate the influence of selected variables on LTF via meta-analysis of a large data set from LTF experiments on anesthetized rats, and to propose an updated mechanism of LTF. LTF has been demonstrated in anesthetized and awake experimental preparations, and can be evoked in some human subjects during sleep. The mechanism underlying LTF requires episodic chemoafferent stimulation, and is not elicited by similar cumulative durations of sustained hypoxia. Meta-analysis of phrenic nerve responses following episodic hypoxia in 63 experiments on anesthetized rats (conducted by four investigators over a period of several years) indicates that phrenic LTF magnitude correlates with peak phrenic responses during hypoxia and hypercapnia, but not with the level of hypoxia during episodic exposures. Potential mechanisms underlying these relationships are discussed, and currently available data are synthesized into an updated mechanistic model of LTF. In this model, we propose that LTF arises predominantly from episodic activation of serotonergic receptors on phrenic motoneurons, activating intracellular kinases and, thus, phosphorylating and potentiating ionic currents associated with the glutamate receptors that mediate respiratory drive. (C) 2000 Elsevier Science B.V. All rights reserved.