缺氧调控耳蜗听神经元电压门控性钾通道的表达

Hypoxia regulates expression of voltage-gated potassium channels in cochlear auditory neurons

目的 研究缺氧后大鼠螺旋神经节神经元电压门控性钾通道(Kv)亚单位表达的特点。方法 取出生3~5 d SD大鼠,断头后分离并原代培养螺旋神经节神经元。将载有螺旋神经节神经元的培养皿分为对照组及实验组(无氧处理24 h),随后提取总RNA,通过实时荧光定量聚合酶链反应(qPCR),检测caspase-3,Kv1.1、Kv1.2和Kv3.1α亚单位mRNA表达的特点。结果 无氧处理24 h后,大鼠螺旋神经节神经元caspase-3 mRNA表达增加;同时,Kv1.1、Kv1.2和Kv3.1α亚单位mRNA在该神经元的表达也上调,与对照组相比,分别增加3.71、3.59、4.33倍。结论 严重缺氧可显著上调初级听神经节神经元Kv mRNA的表达,这可能是缺氧影响听力的机制之一。

Objective To study the characteristics of voltage gated potassium channel(Kv) subunit expression in rat spiral ganglion neurons(SGNs) after hypoxia.Methods SGNs were isolated and cultured in SD rats on 3-5 d after decapitated.The rats were divided into the control group and experiment group(anoxic treatment for 24 h),and then total RNA was extracted.The real-time fluorescence quantitative polymerase chain reaction(qPCR) was used to detect the mRNA expression characteristics of caspase-3,Kv1.1,Kv1.2 and Kv3.1α subunits.Results After anoxic treatment for 24 h, caspase-3 mRNA expression in rat spiral ganglion neurons was increased;meanwhile the expressions of Kv1.1,Kv1.2 and Kv3.1α mRNA in these neurons were also up-regulated, compared with the control group, which were increased by 3.71,3.59,4.33 times respectively.Conclusion Severe hypoxia can significantly up-regulate the expression of voltage gated potassium channel Kv mRNA in primary auditory ganglion neurons, which may be one of the mechanism of anoxia affecting hearing.