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

发布时间：2018-10-08 09:09

【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6~9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(P0.05)、降低缺氧3min后MVN神经元动作电位频率增加幅值(P0.05),降低缺氧10min后MVN神经元静息膜电位去极化幅值(P0.05)。缺氧可导致MVN中BKCa通道α亚单位阳性细胞数明显降低(P0.01)。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。
[Abstract]:Objective to investigate the effect and possible mechanism of large conductance calcium activated potassium channel (large conductance calcium-activated potassium channels,BKCa) on hypoxia-induced excitability of medial vestibular nucleus neurons. Methods six C57BL/6 mice aged from 6 to 9 weeks old were randomly divided into two groups: normoxic group (inhalation of normoxic 2 / 5 COD for 21 h) and hypoxia group (inhaling hypoxia 5 / 5 CO5 / 5 CO21 h). Three rats in each group were subjected to hypoxia injury model of medial vestibular nucleus neurons in hypoxia group, and the mice in normoxic group were killed by decapitation. The brain slices of hypoxic mice were randomly divided into 9 brain slices pretreated with no NS1619 (specific BKCa inducer) and 8 brain slices in NS1619 preconditioning group. The changes of neuronal excitability and the amplitude of BKCa channel current in the medial vestibular nucleus of mice were detected by patch clamp technique, and the expression of BKCa channel 伪 subunit in the (medial vestibular nuclei,MVN of the medial vestibular nucleus was detected by immunohistochemistry. Results NS1619 pretreatment could significantly delay the peak time of action potential frequency of MVN neurons induced by hypoxia (P0.05), decrease the amplitude of action potential frequency of MVN neurons after hypoxia 3min (P0.05), and decrease the resting time of MVN neurons after anoxic 10min (P0.05). Membrane potential depolarization amplitude (P0.05). Hypoxia reduced the number of BKCa channel 伪-subunit positive cells in MVN (P0.01). Conclusion after acute hypoxia injury, the increased excitability of neurons in the medial vestibular nucleus and the decrease of the BK Ca channel are involved in the abnormal excitability of the neurons in the medial vestibular nucleus induced by hypoxia.
【作者单位】：上海市宝山区中西医结合医院耳鼻喉科;湖北省黄石市中心医院耳鼻喉科(湖北理工学院附属医院);
【基金】：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
【分类号】：R741

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