大电导钙激活钾通道参与缺氧致前庭内侧核神经元兴奋性异常

Large Calcium-Activated Potassium Channels Contribute to Neuronal Abnormal Firing in the Medial Vestibular Nucleus Following Hypoxia

吴曙辉;刘丹;阎勇;石光明;

1:上海市宝山区中西医结合医院耳鼻喉科

2:湖北省黄石市中心医院耳鼻喉科(湖北理工学院附属医院)

摘要
目的探讨大电导钙激活钾通道(large conductance calcium-activated potassium channels,BKCa)对缺氧致前庭内侧核神经元兴奋性异常的作用及可能机制。方法选用69周龄C57BL/6小鼠6只,随机分为常氧组(吸入常氧,21%O_2/5%CO_21h)和缺氧组(吸入低氧,5%O_2/5%CO_21h),每组3只,缺氧组制备前庭内侧核神经元缺氧损伤模型后,与常氧组小鼠均断头处死取脑,冠状切取脑片,并将缺氧组小鼠的脑片随机分为无NS1619(特异性BKCa诱导剂)预处理组9张脑片,NS1619预处理组8张脑片。用膜片钳技术检测小鼠脑片前庭内侧核神经元兴奋性的变化及BKCa通道电流幅值的变化;免疫组化检测小鼠前庭内侧核(medial vestibular nuclei,MVN)BKCa通道α亚单位的表达。结果 NS1619预处理能显著性延缓缺氧致MVN神经元动作电位频率增加至峰值的达峰时间(P<0.05)、降低缺氧3min后MVN神经元动作电位频率增加幅值(P<0.05),降低缺氧10min后MVN神经元静息膜电位去极化幅值(P<0.05)。缺氧可导致MVN中BKCa通道α亚单位阳性细胞数明显降低(P<0.01)。结论急性缺氧损伤后,前庭内侧核神经元兴奋性增加,BKCa通道的减少参与缺氧致前庭内侧核神经元兴奋性异常。
关键词
钙激活钾通道;缺氧;全细胞记录;前庭内侧核神经元
基金项目(Foundation):
上海市宝山区科学技术委员会基金项目(12-E-22);; 上海市宝山区卫生青年医学人才培养计划(bswsyq-2015-A11)联合资助
作者
吴曙辉;刘丹;阎勇;石光明;
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