Hypoxic modulation of the cholinergic system in the cat carotid glomus cell.

Hypoxic modulation of the cholinergic system in the cat carotid glomus cell.
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猫颈动脉球细胞中胆碱能系统的缺氧调节。

DOI:
10.1007/0-387-31311-7_43
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发表时间:
2006
影响因子:
--
通讯作者:
Shirahata,Machiko
Shirahata,Machiko
中科院分区:
医学4区
文献类型:
--
作者:
Mendoza,JeffreyA;Chang,Irene;Shirahata,Machiko

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颈动脉体是动脉缺氧的主要感觉器官。化学感觉球细胞在颈动脉体释放神经递质,包括乙酰胆碱,响应缺氧。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。几个报道表明,L型和一些其它类型的电压门控钙通道负责从血管球细胞释放神经递质(Gonzalez等人,1994年)。这些通道被细胞膜的去极化激活。然而,血管球细胞中去极化的速度和程度可能不足以在轻度缺氧时激活电压门控Ca2+通道(Chou等人,1998),其中来自颈动脉体的传入神经活动开始增加。这种差异导致我们寻找其他机制,提高[Ca2+]i,然后释放神经递质。
AbstractThe carotid body is a primary sensory organ for arterial hypoxia. Chemosensory glomus cells in the carotid body release neurotransmitters, including ACh, in response to hypoxia. 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 (Gonzalez et al., 1994). These channels are activated by depolarization of the cell membrane. However, the speed and the degree of depolarization in glomus cells may not be sufficient to activate voltage-gated Ca2+channels at mild hypoxia (Chou et al., 1998), where afferent neural activity from the carotid body starts increasing. This discrepancy led us to search for other mechanisms which elevate [Ca2+]i followed by neurotransmitter release.
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