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首页> 外文期刊>American Journal of Physiology >Kv1.1 and Kv1.3 channels contribute to the delayed-rectifying K+ conductance in rat choroid plexus epithelial cells.
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Kv1.1 and Kv1.3 channels contribute to the delayed-rectifying K+ conductance in rat choroid plexus epithelial cells.

机译：Kv1.1和Kv1.3通道有助于大鼠脉络丛上皮细胞的K +电导的延迟整流。

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摘要

The choroid plexuses secrete, and maintain the composition of, the cerebrospinal fluid. K+ channels play an important role in these processes. In this study the molecular identity and properties of the delayed-rectifying K+ (Kv) conductance in rat choroid plexus epithelial cells were investigated. Whole cell K+ currents were significantly reduced by 10 nM dendrotoxin-K and 1 nM margatoxin, which are specific inhibitors of Kv1.1 and Kv1.3 channels, respectively. A combination of dendrotoxin-K and margatoxin caused a depolarization of the membrane potential in current-clamp experiments. Western blot analysis indicated the presence of Kv1.1 and Kv1.3 proteins in the choroid plexus. Furthermore, the Kv1.3 and Kv1.1 proteins appear to be expressed in the apical membrane of the epithelial cells in immunocytochemical studies. The Kv conductance was inhibited by 1 microM serotonin (5-HT), with maximum inhibition to 48% of control occurring in 8 min (P < 0.05 by Student's t-test for paired data). Channel inhibition by 5-HT was prevented by the 5-HT2C antagonist mesulergine (300 nM). It was also attenuated in the presence of calphostin C (a protein kinase C inhibitor). The conductance was partially inhibited by 1,2-dioctanoyl-sn-glycerol and phorbol 12-myristate 13-acetate, both of which activate protein kinase C. These data suggest that 5-HT acts at 5-HT2C receptors to activate protein kinase C, which inhibits the Kv channels. In conclusion, Kv1.1 and Kv1.3 channels make a significant contribution to K+ efflux at the apical membrane of the choroid plexus.
机译：脉络膜丛分泌并维持脑脊液的成分。 K +通道在这些过程中起着重要作用。在这项研究中，研究了大鼠脉络丛神经上皮细胞中延迟整流K +（Kv）电导的分子身份和特性。全细胞K +电流显着降低了10nM树突毒素K和1nM玛格毒素，它们分别是Kv1.1和Kv1.3通道的特异性抑制剂。在电流钳实验中，树突毒素-K和玛格毒素的组合引起膜电位的去极化。 Western印迹分析表明脉络丛中存在Kv1.1和Kv1.3蛋白。此外，在免疫细胞化学研究中，Kv1.3和Kv1.1蛋白似乎在上皮细胞的顶膜中表达。 Kv电导被1 microM血清素（5-HT）抑制，在8分钟内最大程度地抑制了48％的对照（通过配对数据的Student t检验，P <0.05）。 5-HT2C拮抗剂美素麦角碱（300 nM）阻止了5-HT的通道抑制作用。在钙磷蛋白C（一种蛋白激酶C抑制剂）的存在下，它也被减弱。电导被1,2-二辛酰基-sn-甘油和佛波醇12-肉豆蔻酸酯13-乙酸酯部分抑制，它们均激活蛋白激酶C。这些数据表明5-HT作用于5-HT2C受体以激活蛋白激酶C。 ，这会抑制Kv频道。总之，Kv1.1和Kv1.3通道对脉络丛根尖膜的K +外排起重要作用。

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