Serum of Isaacs' syndrome suppresses potassium channels in PC‐12 cell lines
Serum of Isaacs' syndrome suppresses potassium channels in PC‐12 cell lines
复制标题
艾萨克斯综合征血清抑制 PC-12 细胞系中的钾通道
作者：
Y. Sonoda;K. Arimura;A. Kurono;M. Suehara;M. Kameyama;Seiichi Minato;Akito Hayashi;M. Osame
免疫球蛋白阻断神经末梢的K+通道是Isaacs综合征的推测病理机制。我们使用膜片钳技术（全细胞钳），采用克隆细胞系PC-12研究了2例艾萨克斯综合征患者血清对K+电流的影响。向灌注液中加入患者血清对P-12细胞的K+电流几乎没有影响。相比之下，与对照血清值相比，当细胞用2%血清培养3-6天时，K+电流降低25-80%。K+电流的抑制似乎是随着培养时间的推移而逐渐发展的。我们的研究结果表明，Isaacs综合征的病理机制是通过血清中的体液因子抑制K+通道，随后诱导神经过度兴奋。John Wiley & Sons，Inc.
Blockage of K+ channels in nerve terminals by immunoglobulin is the speculated pathomechanism of Isaacs' syndrom. Using patch‐clamp technique (whole‐cell clamp), we investigated the effects on K+ current of serum taken from 2 patients with Isaacs' syndrom employing the clonal cell line PC‐12. The addition of a patient's serum to the perfusion solution had little effect on the K+ current of P‐12 cells. In contrast, K+ current was reduced by 25–80% when cells were cultured for 3–6 days with 2% serum as compared to control serum values. Supperession of the K+ current appears to develop gradually over the period of culture. Our results suggest that the pathomechanism of Isaacs' syndrome is caused by K+ channel suppression via a humoral factor(s) in the serum, which subsequently induces nerve hyperexcitability. © 1996 John Wiley & Sons, Inc.