Kv7.2 regulates the function of peripheral sensory neurons.

Kv7.2 regulates the function of peripheral sensory neurons.
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KV7.2调节周围感觉神经元的功能。

DOI:
10.1002/cne.23595
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发表时间:
2014-10-01
影响因子:
2.5
通讯作者:
Scherer, Steven S.
Scherer, Steven S.
中科院分区:
医学3区
文献类型:
--
作者:
King, Chih H.;Lancaster, Eric;Salomon, Daniela;Peles, Elior;Scherer, Steven S.

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电压门控K+通道的Kv 7(KCNQ)家族调节细胞兴奋性。Kv7.2的功能作用由于缺乏可行的Kcnq 2无效动物模型而受到阻碍。在这项研究中,我们使用Cre-Lox系统产生了纯合的Kcnq 2-null感觉神经元;在这些小鼠中,Kv7.2表达在外周感觉神经元中不存在,而节点(包括Kv7.3),paranodes和parantaparanodes的其他分子组分的表达没有改变。条件性Kcnq 2缺失动物表现出正常的运动性能,但具有增加的热痛觉过敏和机械异常性疼痛。全细胞膜片钳记录技术表明,Kcnq 2-null感觉神经元具有增强的兴奋性和降低的锋电位频率适应性。总之,我们的研究结果表明,Kv7.2活性的损失增加了初级感觉神经元的兴奋性。
The Kv7 (KCNQ) family of voltage-gated K+ channels regulates cellular excitability. The functional role of Kv7.2 has been hampered by the lack of a viable Kcnq2-null animal model. In this study, we generated homozygous Kcnq2-null sensory neurons using the Cre-Lox system; in these mice, Kv7.2 expression is absent in the peripheral sensory neurons, whereas the expression of other molecular components of nodes (including Kv7.3), paranodes, and juxtaparanodes is not altered. The conditional Kcnq2-null animals exhibit normal motor performance, but have increased thermal hyperalgesia and mechanical allodynia. Whole cell patch recording technique demonstrates that Kcnq2-null sensory neurons have increased excitability and reduced spike frequency adaptation. Taken together, our results suggest that the loss of Kv7.2 activity increases the excitability of primary sensory neurons.
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