The voltage-gated sodium channel Nav1.9 is required for inflammation-based urinary bladder dysfunction
The voltage-gated sodium channel Nav1.9 is required for inflammation-based urinary bladder dysfunction
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DOI：
10.1016/j.neulet.2008.12.051
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发表时间：
2009-03-06
影响因子：
2.5
通讯作者：
Thorneloe, Kevin S.
中科院分区：
文献类型：
--
作者：
Ritter, Amy M.;Martin, William J.;Thorneloe, Kevin S.
河豚毒素（TFX）抗性钠通道发现于小直径的初级感觉神经元中，并且被认为在维持炎性疼痛中是重要的。在这里，我们检查了Nav1.9电压门控钠通道敲除（KO）小鼠的膀胱尿动力学，以及Nav1.9对炎症性膀胱功能障碍发展的贡献。基础尿动力学在野生型（WT）小鼠和缺乏Nav1.9的小鼠之间没有差异。Nav1.9 KO小鼠盆腔传入神经的外周神经记录显示对囊内应用的前列腺素E2（PGE2）缺乏敏感性。与此一致，体内环磷酰胺治疗（与PGE2产生的增强相关）引起WT而非Nav1.9 KO小鼠膀胱容量的降低。我们的结论是Nav1.9钠通道提供了一个重要的联系炎症过程和尿动力学特性的变化，发生在膀胱炎症。(C)2009爱思唯尔爱尔兰有限公司保留所有权利。
Tetrodotoxin (TFX)-resistant sodium channels are found in small diameter primary sensory neurons and are thought to be important in the maintenance of inflammatory pain. Here we examined bladder urodynamics of Nav1.9 voltage-gated sodium channel knock out (KO) mice, and the contribution of Nav1.9 to the development of inflammation-based bladder dysfunction. Basal urodynamics were not different between wildtype (WT) mice and those lacking Nav1.9. Peripheral nerve recordings from pelvic afferents in Nav1.9 KO mice revealed a lack of sensitization to intravesicularly applied prostaglandin E2 (PGE2). Consistent with this, cyclophosphamide treatment in vivo, which is associated with an enhancement of PGE2 production, evoked a reduction in bladder capacity of WT, but not Nav1.9 KO mice. We conclude that the Nav1.9 sodium channel provides an important link between inflammatory processes and changes in urodynamic properties that occur during urinary bladder inflammation. (C) 2009 Elsevier Ireland Ltd. All rights reserved.