Department of Neurobiology, Institute of Life Sciences, Hebrew University, Jerusalem, Israel.
J Cell Biol. 2011 Jan 10;192(1):137-51. doi: 10.1083/jcb.201007053. Epub 2011 Jan 3.
Reliable neuronal communication depends on accurate temporal correlation between the action potential and neurotransmitter release. Although a requirement for Ca(2+) in neurotransmitter release is amply documented, recent studies have shown that voltage-sensitive G protein-coupled receptors (GPCRs) are also involved in this process. However, how slow-acting GPCRs control fast neurotransmitter release is an unsolved question. Here we examine whether the recently discovered fast depolarization-induced charge movement in the M(2)-muscarinic receptor (M(2)R) is responsible for M(2)R-mediated control of acetylcholine release. We show that inhibition of the M(2)R charge movement in Xenopus oocytes correlated well with inhibition of acetylcholine release at the mouse neuromuscular junction. Our results suggest that, in addition to Ca(2+) influx, charge movement in GPCRs is also necessary for release control.
可靠的神经元通讯依赖于动作电位和神经递质释放之间的精确时间相关。尽管钙（Ca(2+)）在神经递质释放中的作用已经得到充分证明，但最近的研究表明，电压敏感性 G 蛋白偶联受体（GPCRs）也参与了这一过程。然而，慢作用 GPCR 如何控制快速神经递质释放仍是一个悬而未决的问题。在这里，我们研究了最近发现的 M2-毒蕈碱受体（M2R）中的快速去极化诱导的电荷移动是否负责 M2R 介导的乙酰胆碱释放的控制。我们发现，在爪蟾卵母细胞中抑制 M2R 电荷移动与在小鼠神经肌肉接头处抑制乙酰胆碱释放密切相关。我们的结果表明，除了 Ca(2+)内流之外，GPCR 中的电荷移动对于释放控制也是必要的。
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