Acid-sensing ion channels (ASICs) in dorsal root ganglion (DRG) neurons play an important role in inflammatory pain. The objective of this study is to observe the regulatory role of ASICs in monosodium urate (MSU) crystal-induced gout pain and explore the basis for ASICs in DRG neurons as a target for gout pain treatment. The gout arthritis model was induced by injecting MSU crystals into the ankle joint of mice. The circumference of the ankle joint was used to evaluate the degree of swelling; the von Frey filaments were used to determine the withdrawal threshold of the paw. ASIC currents and action potentials (APs) were recorded by patch clamp technique in DRG neurons. The results displayed that injecting MSU crystals caused ankle edema and mechanical hyperalgesia of the paw, which was relieved after amiloride treatment. The ASIC currents in DRG neurons were increased to a peak on the second day after injecting MSU crystals, which were decreased after amiloride treatment. MSU treatment increased the current density of ASICs in different diameter DRG cells. MSU treatment does not change the characteristics of AP. The results suggest that ASICs in DRG neurons participate in MSU crystal-induced gout pain.

背根神经节 (DRG) 神经元中的酸敏感离子通道 (ASIC) 在炎性疼痛中发挥重要作用。本研究的目的是观察ASIC在尿酸钠（MSU）晶体诱发的痛风疼痛中的调节作用，并探讨DRG神经元中的ASIC作为痛风疼痛治疗靶点的基础。通过将MSU晶体注射到小鼠的踝关节中来诱导痛风关节炎模型。以踝关节周长来评估肿胀程度；冯弗雷细丝用于确定爪子的缩回阈值。通过膜片钳技术记录 DRG 神经元中的 ASIC 电流和动作电位 (AP)。结果显示，注射MSU晶体引起踝关节水肿和足爪机械性痛觉过敏，经阿米洛利治疗后缓解。注射MSU晶体后的第二天，DRG神经元中的ASIC电流增加至峰值，而阿米洛利治疗后则下降。 MSU 处理增加了不同直径 DRG 细胞中 ASIC 的电流密度。 MSU治疗不会改变AP的特征。结果表明，DRG 神经元中的 ASIC 参与了 MSU 晶体诱发的痛风疼痛。