Does chloride channel accessory 3 have a role in arthritis pain? A study on murine antigen-induced arthritis
Does chloride channel accessory 3 have a role in arthritis pain? A study on murine antigen-induced arthritis
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氯离子通道附件 3 对关节炎疼痛有作用吗？
DOI：
10.1016/j.neulet.2014.05.051
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发表时间：
2014
影响因子：
2.5
通讯作者：
Schaible HG
中科院分区：
文献类型：
--
作者：
Ebbinghaus M;Gajda M;Holtzman MJ;Schulz S;Schaible HG
钙激活的氯离子通道（CaCCs）被认为可以调节神经元的兴奋性，近年来，DRG神经元中的氯离子（Cl−）调节在疼痛研究中受到了广泛关注。此外，一个CLCA蛋白家族修饰了CaCCs的活性。在急性抗原诱导关节炎（AIA）中，小鼠背根神经节（DRG）神经元中氯离子通道附件3 （mClca3）显著上调。因此，我们检验了mcca3参与关节炎疼痛感知的假设。在mClca3敲除小鼠和野生型对照小鼠中，诱导AIA，并评估炎症和疼痛的测量。在AIA的极急性期，mcca3敲除小鼠的关节肿胀减轻。这种效应在AIA过程中消失。我们无法显示两组小鼠在机械痛觉过敏方面的显著差异，无论是在急性期还是在慢性期（AIA的21天）。在AIA的前3天，野生型和mcca3敲除小鼠的热痛觉过敏实验也没有显示出差异。此外，尼氟酸（CaCCs的拮抗剂）在AIA期间对痛觉过敏没有显著影响。因此，我们无法提供证据证明CaCCs，特别是mcca3在关节炎或炎症诱发的痛觉过敏的表达中的作用。
Calcium-activated chloride channels (CaCCs) are thought to regulate neuronal excitability, and recently chloride (Cl−) regulation in DRG neurons has attracted much attention in pain research. Furthermore, the activity of CaCCs is modified by a family of CLCA proteins. In acute antigen-induced arthritis (AIA), a remarkable up-regulation of the murine chloride channel accessory 3 (mClca3) was shown in dorsal root ganglion (DRG) neurons. Therefore we tested the hypothesis that mClca3 is involved in arthritic pain perception. In mClca3 knock-out mice and wild-type control mice, AIA was induced and measures of inflammation and pain were assessed. In the very acute phase of AIA, joint swelling was reduced in mClca3 knock-out mice. This effect disappeared during the course of AIA. We could not show significant differences in mechanical hyperalgesia between both groups of mice, neither at the acute nor at the chronic stage (21 days of AIA). Additional experiments on thermal hyperalgesia in wild-type and mClca3 knock-out mice in the first 3 days of AIA did not show a difference either. In addition, niflumic acid, an antagonist at CaCCs, did not significantly influence hyperalgesia during AIA. Thus, we were not able to provide evidence for a role of CaCCs, and in particular of mClca3, on the expression of arthritis or inflammation-evoked hyperalgesia.
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影响因子：
4.9
作者：
Imhof AK;Glück L;Gajda M;Bräuer R;Schaible HG;Schulz S
通讯作者：
Schulz S
影响因子：
--
作者：
Richter, Frank;Natura, Gabriel;Schaible, Hans-Georg
通讯作者：
Schaible, Hans-Georg
影响因子：
7.4
作者：
Boettger, Michael K.;Weber, Konstanze;Schaible, Hans-Georg
通讯作者：
Schaible, Hans-Georg
影响因子：
--
作者：
Imhof, Anne-Katja;Glueck, Laura;Schulz, Stefan
通讯作者：
Schulz, Stefan