OBJECTIVE To evaluate the role of K+ channels in pain following gouty arthritis. METHODS The model of acute gouty arthritis was induced by monosodium urate (MSU) in mice. The swelling degree was determined by measuring the circumference of the ankle joint. Mechanical hyperalgesia was detected by von Frey filaments. Two types of K+ currents, A-type currents (IA) and delayed rectifier currents (IK), were recorded in dorsal root ganglion (DRG) neurons using patch-clamp techniques. RESULTS The swelling degree reached its maximum at 10 h and the minimum pain threshold was maintained between 8 and 48 h after MSU treatment in mice. The amplitudes of IA and IK in DRG neurons were moderately increased on day 1 after MSU treatment, and then, they were gradually decreased with times and reached their minimums on day 4 (for IA) or 5 (for IK). Compared with control group, the activation curve of IA was significantly shifted to more positive potential and the recovery time of IA from inactivation was markedly prolonged, but inactivation and frequency dependence of IA appeared unaffected in MSU-treated group. Additionally, no change was observed in the activation curve of IK after MSU treatment. The excitability was significantly higher in the MSU group than in the control group. CONCLUSIONS MSU-induced gout pain may be related to the hyperexcitability of DRG neurons elicited by decreasing K+ currents.

中文翻译：

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尿酸一钠诱发小鼠痛风性关节炎中电压门控钾电流的特征。

目的评估痛风性关节炎后K +通道在疼痛中的作用。方法采用尿酸钠（MSU）诱导小鼠急性痛风性关节炎模型。通过测量踝关节的周长来确定肿胀程度。von Frey细丝检测出机械性痛觉过敏。使用膜片钳技术在背根神经节（DRG）神经元中记录了两种类型的K +电流，即A型电流（IA）和延迟整流器电流（IK）。结果小鼠MSU治疗后10h肿胀程度达到最大，最小疼痛阈值维持在8至48h之间。MSU治疗后第1天，DRG神经元的IA和IK振幅适度增加，然后随时间逐渐降低，并在第4天（IA）或第5天（IK）达到最小值。与对照组相比，IA的活化曲线明显向正电位移动，IA从失活的恢复时间明显延长，但MSU治疗组IA的失活和频率依赖性似乎不受影响。此外，在MSU处理后，IK的激活曲线未见变化。MSU组的兴奋性显着高于对照组。结论MSU引起的痛风痛可能与K +电流降低引起的DRG神经元的过度兴奋有关。MSU处理后，IK的激活曲线未见变化。MSU组的兴奋性显着高于对照组。结论MSU引起的痛风痛可能与K +电流降低引起的DRG神经元的过度兴奋有关。MSU处理后，IK的激活曲线未见变化。MSU组的兴奋性显着高于对照组。结论MSU引起的痛风痛可能与K +电流降低引起的DRG神经元的过度兴奋有关。