Hypoxic augmentation of neuronal nicotinic acetylcholine receptors and carotid body function.
Hypoxic augmentation of neuronal nicotinic acetylcholine receptors and carotid body function.
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缺氧增强神经元烟碱乙酰胆碱受体和颈动脉体功能。
DOI：
10.1007/978-1-4419-9280-2_35
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发表时间：
2003
影响因子：
--
通讯作者：
Hirasawa,Serabi
中科院分区：
文献类型：
--
作者：
Shirahata,Machiko;Higashi,Tomoko;Mendoza,JeffreyA;Hirasawa,Serabi
一般认为神经递质参与了颈动脉体的缺氧化学传递。神经递质从血管球细胞（一种假定的化学感受器细胞）的释放似乎是由钙内流和随后的细胞内钙（[Ca 2 +]i）增加触发的。一些报道表明，L型和一些其他类型的电压门控钙通道负责从血管球细胞释放神经递质。由于这些通道通过细胞膜的去极化而激活，因此血管球细胞的缺氧去极化机制一直是研究的主要焦点（Shirahata和Sham，1999）。
It is generally accepted that neurotransmitters are involved in hypoxic chemotransmission of the carotid body. The release of neurotransmitters from the glomus cell, a putative chemoreceptor cell, appears to be triggered by an influx of calcium and subsequent increase in intracellular calcium ([Ca2+]i). Several reports indicate that L-type and some other types of voltage-gated calcium channels are responsible for neurotranmitter release from glomus cells. Since these channels are activated by depolarization of the cell membrane, mechanisms of hypoxic depolarization of glomus cells has been a major focus of investigation (Shirahata and Sham, 1999).