Kv2.1 and silent Kv subunits underlie the delayed rectifier K+ current in cultured small mouse DRG neurons
Kv2.1 and silent Kv subunits underlie the delayed rectifier K+ current in cultured small mouse DRG neurons
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DOI：
10.1152/ajpcell.00088.2009
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发表时间：
2009-06-01
影响因子：
5.5
通讯作者：
Snyders, Dirk J.
中科院分区：
文献类型：
--
作者：
Bocksteins, Elke;Raes, Adam L.;Snyders, Dirk J.
bockstein E, Raes AL, Van de Vijver G, Bruyns T, Van Bogaert PP, Snyders DJ。K(v)2.1和沉默K-v亚基是培养的小鼠DRG神经元延迟整流K+电流的基础。[J] .中国生物医学工程学报，2009,31(6):871 - 878。首次发表于2009年4月8日；doi: 10.1152 / ajpcell.00088.2009。沉默电压门控K+ (K-v)亚基与Kv2亚基相互作用，主要调节这些异四聚体通道失活的电压依赖性。K(v)2和沉默K-v亚基都在哺乳动物神经系统中表达，但对它们在感觉神经元中的表达和功能知之甚少。本研究报道了小鼠背根神经节（DRG）中存在K(v)2.1、K(v)2.2和沉默亚基K(v)6.1、K(v)8.1、K(v)9.1、K(v)9.2和K(v)9.3 mRNA。免疫细胞化学证实了K(v)2蛋白的表达。x和K(v)9。x亚单位在培养的小DRG神经元。为了研究K(v)2和沉默K-v亚基是否在这些神经元中延迟的整流K+电流（I-K）的基础上，通过细胞外应用rStromatoxin-1 （ScTx）或细胞内应用K(v)2抗体分离K(v)2介导的电流。ScTx-和抗k (v)2.1敏感电流在失活的电压依赖性上显示出两个分量。这两种成分加起来约占I-K的三分之二。与异种表达系统的结果比较表明，一个组分反映同四聚体K(v)2.1通道，而另一个组分代表异四聚体K(v)2.1/沉默K-v通道。这些观察结果支持沉默的K-v亚基在小DRG神经元中的生理作用。
Bocksteins E, Raes AL, Van de Vijver G, Bruyns T, Van Bogaert PP, Snyders DJ. K(v)2.1 and silent K-v subunits underlie the delayed rectifier K+ current in cultured small mouse DRG neurons. Am J Physiol Cell Physiol 296: C1271-C1278, 2009. First published April 8, 2009; doi:10.1152/ajpcell.00088.2009. -Silent voltage-gated K+ (K-v) subunits interact with Kv2 subunits and primarily modulate the voltage dependence of inactivation of these heterotetrameric channels. Both K(v)2 and silent K-v subunits are expressed in the mammalian nervous system, but little is known about their expression and function in sensory neurons. This study reports the presence of K(v)2.1, K(v)2.2, and silent subunit K(v)6.1, K(v)8.1, K(v)9.1, K(v)9.2, and K(v)9.3 mRNA in mouse dorsal root ganglia (DRG). Immunocytochemistry confirmed the protein expression of K(v)2.x and K(v)9.x subunits in cultured small DRG neurons. To investigate if K(v)2 and silent K-v subunits are underlying the delayed rectifier K+ current (I-K) in these neurons, K(v)2-mediated currents were isolated by the extracellular application of rStromatoxin-1 (ScTx) or by the intracellular application of K(v)2 antibodies. Both ScTx- and anti-K(v)2.1-sensitive currents displayed two components in their voltage dependence of inactivation. Together, both components accounted for approximately two-thirds of I-K. A comparison with results obtained in heterologous expression systems suggests that one component reflects homotetrameric K(v)2.1 channels, whereas the other component represents heterotetrameric K(v)2.1/silent K-v channels. These observations support a physiological role for silent K-v subunits in small DRG neurons.