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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Na+/Cl- dipole couples agonist binding to kainate receptor activation.
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Na+/Cl- dipole couples agonist binding to kainate receptor activation.

机译：Na + / Cl-偶极子结合激动剂与红藻氨酸受体激活。

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摘要

Kainate-selective ionotropic glutamate receptors (GluRs) require external Na+ and Cl- as well as the neurotransmitter L-glutamate for activation. Although, external anions and cations apparently coactivate kainate receptors (KARs) in an identical manner, it has yet to be established how ions of opposite charge achieve this. An additional complication is that KARs are subject to other forms of cation modulation via extracellular acidification (i.e., protons) and divalent ions. Consequently, other cation species may compete with Na+ to regulate the time KARs remain in the open state. Here we designed experiments to unravel how external ions regulate GluR6 KARs. We show that GluR6 kinetics are unaffected by alterations in physiological pH but that divalent and alkali metal ions compete to determine the time course of KAR channel activity. Additionally, Na+ and Cl- ions coactivate GluR6 receptors by establishing a dipole, accounting for their common effect on KARs. Using charged amino acids as tethered ions, we further demonstrate that the docking order is fixed with cations binding first, followed by anions. Together, our findings identify the dipole as a novel gating feature that couples neurotransmitter binding to KAR activation.
机译：海藻酸盐选择性离子型谷氨酸受体（GluRs）需要外部Na +和Cl-以及神经递质L-谷氨酸来激活。尽管外部阴离子和阳离子显然以相同的方式共活化红藻氨酸受体（KARs），但尚需确定带相反电荷的离子如何实现此目的。另一复杂情况是，KAR通过细胞外酸化（即质子）和二价离子经受其他形式的阳离子调节。因此，其他阳离子可能会与Na +竞争，以调节KAR保持开放状态的时间。在这里，我们设计了一些实验来阐明外部离子如何调节GluR6 KAR。我们表明，GluR6动力学不受生理pH值变化的影响，但是二价和碱金属离子竞争确定KAR通道活性的时间过程。此外，Na +和Cl-离子通过建立偶极子来共激活GluR6受体，这说明它们对KAR的共同作用。使用带电荷的氨基酸作为束缚离子，我们进一步证明了对接顺序是固定的，首先结合阳离子，然后是阴离子。在一起，我们的研究结果确定偶极子是一种新型的门控功能，它将神经递质结合到KAR激活上。

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