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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Inhibition of K+ outward currents by linopirdine in the cochlear outer hair cells of circling mice within the first postnatal week
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Inhibition of K+ outward currents by linopirdine in the cochlear outer hair cells of circling mice within the first postnatal week

机译：产后第一个星期内利尼平对循环小鼠耳蜗外毛细胞中K +外向电流的抑制作用

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Inhibition of K+ outward currents by linopirdine in the outer hair cells (OHCs) of circling mice (homozygous ( cir / cir ) mice), an animal model for human deafness (DFNB6 type), was investigated using a whole cell patch clamp technique. Littermate heterozygous (+/ cir ) and ICR mice of the same age (postnatal day (P) 0 –P6) were used as controls. Voltage steps from –100 mV to 40 mV elicited small inward currents (–100 mV~–70 mV) and slow rising K+ outward currents (–60 mV ~40 mV) which activated near –50 mV in all OHCs tested. Linopirdine, a known blocker of K+ currents activated at negative potentials ( I K,n), did cause inhibition at varying degree (severe, moderate, mild) in K+ outward currents of heterozygous (+/ cir ) or homozygous ( cir / cir ) mice OHCs in the concentration range between 1 and 100 μM, while it was apparent only in one ICR mice OHC out of nine OHCs at 100 μM. Although the half inhibition concentrations in heterozygous (+/ cir ) or homozygous ( cir / cir ) mice OHCs were close to those reported in I K,n, biophysical and pharmacological properties of K+ outward currents, such as the activation close to –50 mV, small inward currents evoked by hyperpolarizing steps and TEA sensitivity, were not in line with I K,n reported in other tissues. Our results show that the delayed rectifier type K+ outward currents, which are not similar to I K,n with respect to biophysical and pharmacological properties, are inhibited by linopirdine in the developing (P0~P6) homozygous ( cir / cir ) or heterozygous (+/ cir ) mice OHCs.
机译：研究了利诺吡丁对盘旋小鼠（纯合子（cir / cir）小鼠）（人耳聋的动物模型（DFNB6型））的外毛细胞（OHC）对K + 外向电流的抑制作用。全细胞膜片钳技术。相同年龄（产后天数（P）0 –P6）的同伴杂合子（+ / cir）和ICR小鼠用作对照。从–100 mV到40 mV的电压阶跃会引起较小的内向电流（–100 mV〜–70 mV）和缓慢上升的K + 外向电流（–60 mV〜40 mV），该电流在–50 mV附近激活在所有测试的OHC中。 Linopirdine是一种已知的负电势（I K，n ）激活的K + 电流阻滞剂，确实在不同程度上（严重，中度，轻度）引起了K <在1至100μM浓度范围内的杂合（+ / cir）或纯合（cir / cir）小鼠OHC的sup> + 向外电流，而在9个OHC中，只有一只ICR小鼠OHC出现在100微米尽管杂合子（+ / cir）或纯合子（cir / cir）小鼠中的半数抑制浓度与I K，n ，K + < / sup>外向电流，例如接近–50 mV的激活，超极化步骤和TEA敏感性引起的小向内电流，与其他组织中报道的I K，n 不符。我们的结果表明，在生物物理和药理特性方面，与I K，n 不相似的延迟整流器K + 向外流受到了尼古丁碱的抑制。发育（P0〜P6）纯合子（cir / cir）或杂合（+ / cir）小鼠OHC。

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