中文摘要：

目的探讨急性缺氧对大鼠耳蜗螺旋神经节细胞（spiralganglioncell，SGC）外向钾通道电流的影响。方法分离并酶解出生1～3dSprague Dawley（SD）大鼠SGC，37℃培养8h获得贴壁牢固的原代细胞，在室温条件下（22～25℃）通过多管灌流给药系统持续给予无糖低氧灌流液（20％CO2和80％N2混合气体充分饱和，pH值6．5）5～15min，采用全细胞膜片钳技术记录SGC胞膜外向电流，并观察K＋通道阻断剂四乙胺（tetraethylammonium，TEA）和四氨基吡啶（4-AP）对电流的影响。结果乳鼠SGC激活的外向电流具有电压门控外向整流特性，主要包括对TEA敏感的大电导钙激活钾电流（BKCa）和对4-AP敏感的电压门控钾离子通道电流（Kv）。当钳制电压在-60mV时，急性缺氧能电压依赖性地增强SGC的外向电流，以增强0±60mV电压区间的激活电流为主，＋60mV时激活的电流幅度从（1160．0±129．1）pA增加到（2428．0±239．3）pA，差异具有统计学意义（n=9，P〈0．01）。预灌流TEA（1mmol／L）后，缺氧对SGC外向电流的增强作用明显减小，＋60mV激活电压时，TEA＋缺氧组与缺氧组相比，外向电流幅度从（2070．8±115．7）pA降低到（1062．6±30．9）pA，差异具有统计学意义（n=6，P〈0．05）。而预灌流4-AP（1mmol／L）后，缺氧对SGC外向电流的增强作用无明显改变（n=6，P〉0．05）。结论急性缺氧可能通过增强大鼠SGC的BK。引起K’外流，使细胞膜电位超极化，细胞兴奋性降低，影响SGC的兴奋传导功能。

英文摘要：

Objective The present study was to investigate the effects of acute hypoxia on the eleetrophysiological properties and outward current of spiral ganglion cell （SGC）. Methods SGC of newborn＇s Spragne Dawley （SD） rats were isolated and digested, primary cultured neurons for 8 h . By perfusion with physical saline solution containing no glucose and low oxygen, SGNs model of acute hypoxia was established. The whole-cell patch clamp recording was used to clarify the effect of hypoxia on the outward currents of SGC. Results The outward current of SGC showed characteristics of outward rectification, which contained two major components, one sensitive to the big conductance Ca2＋ -activated K ＋ channels （BKca） which blocked by TEA, and the other could be suppressed by the Kv channel blocker 4-AP. When holding at -60 mV, acute hypoxia increased the outward current of SGC in a voltagedependent manner, which mainly increased the amplitude of the current activated by the votage ranged from 0 mV to ＋ 60 mV, and increased the amplitude of outward current from （ 1 160. 0 ± 129. 1 ） pA to （2 428±239. 3） pA（n =9,P 〈0. 01 ） at holding potential of -60mV. By perfusion with the Potassium channel blocker TEA or 4-AP, the former could significantly reduced the increasing of outward currents induced by hypoxia on the SGC, the latter had no significant effect on the outward current increased by the hypoxia.Conclusions These results suggest that acute hypoxia causes neuron hyperpolarization possibly by activating big conductance BKca of the SGC. When the BKca channels are activated, K ＋ eflluxes increase, which induces cell membrane hyperpolarization , and decreases cell excitability, which may affect the conducting function of SGC.