Inhibition of Ca2+ channels and adrenal catecholamine release by G protein coupled receptors.
Inhibition of Ca2+ channels and adrenal catecholamine release by G protein coupled receptors.
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DOI：
10.1007/s10571-010-9596-7
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发表时间：
2010-11
影响因子：
4
通讯作者：
Currie, Kevin P. M.
中科院分区：
文献类型：
--
作者：
Currie, Kevin P. M.
肾上腺嗜铬细胞释放的儿茶酚胺和其他递质在“战斗或逃跑”反应中发挥核心作用，并对心血管、内分泌、免疫和神经系统功能产生深远影响。因此，嗜铬细胞胞吐作用的精确调节是维持正常生理功能和对急性应激的适当反应的关键。嗜铬细胞表达许多不同的 G 蛋白偶联受体 (GPCR)，这些受体感知局部环境并协调递质释放的精确控制。儿茶酚胺释放的主要触发因素是 Ca2+ 通过电压门控 Ca2+ 通道进入，因此这些通道受到 GPCR 的复杂调节是有道理的。特别是 G 蛋白 βγ 异二聚体 (Gβγ) 结合并抑制 Ca2+ 通道。在这里，我回顾了 GPCR 抑制嗜铬细胞中 Ca2+ 通道的机制，以及细胞环境如何改变这种机制。这与嗜铬细胞中 Ca2+ 进入和递质释放的有效自分泌抑制有关。最近的数据表明 Gβγ 对胞吐机制有一个额外的抑制靶点，以及它如何微调神经内分泌分泌。
Catecholamines and other transmitters released from adrenal chromaffin cells play central roles in the “fight-or-flight” response and exert profound effects on cardiovascular, endocrine, immune, and nervous system function. As such, precise regulation of chromaffin cell exocytosis is key to maintaining normal physiological function and appropriate responsiveness to acute stress. Chromaffin cells express a number of different G protein coupled receptors (GPCRs) that sense the local environment and orchestrate this precise control of transmitter release. The primary trigger for catecholamine release is Ca2+ entry through voltage-gated Ca2+ channels, so it makes sense that these channels are subject to complex regulation by GPCRs. In particular G protein βγ heterodimers (Gβγ) bind to and inhibit Ca2+ channels. Here I review the mechanisms by which GPCRs inhibit Ca2+ channels in chromaffin cells and how this might be altered by cellular context. This is related to the potent autocrine inhibition of Ca2+ entry and transmitter release seen in chromaffin cells. Recent data that implicate an additional inhibitory target of Gβγ on the exocytotic machinery and how this might fine tune neuroendocrine secretion are also discussed.
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