大鼠食道扩张内脏痛模型的建立及酸敏感离子通道3的功能变化及意义  

Establishment of Rat Esophageal Dilatation Visceral Pain Model and Significance of Functional Changes of Acid-Sensitive Ion Channel

作　　者：牛小平[1] 刘少锋[1] 王运东[1] 

机构地区：[1]皖南医学院附属弋矶山医院消化内科,安徽省芜湖市241001

出　　处：《医学理论与实践》2017年第23期3449-3451,3459,共4页The Journal of Medical Theory and Practice

基　　金：皖南医学院弋矶山医院引进人才基金项目(YR201206);皖南医学院重点培育基金项目(WK2014ZF09)

摘　　要：目的:通过建立大鼠食道扩张(Esophageal distensions,ED)内脏痛动物模型并研究其脊髓背根神经元(DRG)中酸敏感性离子通道3(ASIC3)的表达及功能的改变,探讨ASIC3参与ED内脏痛模型中DRG神经元高敏感性发生的可能机制。方法:50只SD大鼠随机分成2组:ED动物模型组30只,对照组20只;免疫荧光检测DRG神经元ASIC3的表达,膜片钳分析技术记录ED刺激后DRG神经元兴奋性改变及ASIC3电流变化,并与对照组比较。结果:免疫荧光检测发现,ASIC3在DRG细胞中表达定位于细胞膜及细胞质;在给予大鼠1h的重复ED刺激之后,相应节段的DRG神经元受到去极化刺激时产生的动作电位数量明显增多,且ED大鼠ASIC3通道离子电流也明显增加。结论:食道球囊扩张可成功建立食道内脏痛动物模型,DRG神经元中ASIC3表达与功能的改变可能是导致GERD食管内脏高敏感发生的原因之一。Objective：To establish the visceral pain model of esophageal distension（ED）in rats and study the changes of ASIC3 expression and function in the dorsal root ganglion（DRG）,and to explore possible mechanism of ASIC3 in the DRG neurons in ED visceral pain model.Methods：Animal model of visceral pain was established by esophageal distension（ED）.Fifty SD rats were randomly divided into two groups：30 rats in the ED group and 20 rats in the control group.Location and expression of ASIC3 in DRG neurons were detected by immunofluorescence assay.The action potential and current of ASIC3 in DRG neurons were recorded by cell patch-clamp technique.Results：Immunohistochemistry results showed that ASIC3 mainly expressed on the cell membranes and in the cytoplasm.We found that both the number of action potentials and the currents of ASIC3 ion channels are significantly increased in ED group compared to control group.Conclusion：Animal model of esophageal visceral pain can be successfully induced by Balloon dilatation.The changes of ASIC3 expression and function in DRG neurons may be one of the important mechanisms for GERD esophageal visceral hypersensitivity.

关 键 词：酸敏感性离子通道3 脊髓背根神经元 球囊扩张 内脏高敏 

分 类 号：R-33[医药卫生]