瞬时感受器电位阳离子通道V2活动促进损伤轴突再生的体外研究  

Transient receptor potential cation channel subfamily V member 2 promote the regeneration of injured axons in vitro

作　　者：郑联合[1,2] 王育才[1,2] 张云飞[1,2] 张永远[1,2] 

机构地区：[1]第四军医大学 [2]第四军医大学唐都医院骨科,西安710038

出　　处：《神经解剖学杂志》2014年第2期201-205,共5页Chinese Journal of Neuroanatomy

基　　金：国家自然科学基金(30872597);陕西省科学技术研究发展项目(S2012KW313)

摘　　要：目的:在体外探讨瞬时感受器电位阳离子通道V2(TRPV2)的活动对损伤神经元轴突再生的作用。方法:原代培养小鼠胚胎背根节神经元,制备划伤模型。用全细胞膜片钳记录损伤神经元的自发放电活动。实时定量PCR和免疫细胞化学观察神经元损伤后TRPV2的表达。免疫细胞化学法观察TRPV2的激动剂Cannabidiol及siRNA对体外神经元轴突生长的作用。结果:划伤后,神经元自发性放电增加;神经元突起的TRPV2表达增加。10μmol/L TRPV2激动剂Cannabidiol可显著促进神经元存活和突起生长。针对TRPV2的siRNA可显著抑制突起生长。结论:在体外,神经元损伤可诱导TRPV2表达升高,后者参与损伤神经元的轴突再生。Objective： To assess the roles of transient receptor potential cation channel subfamily V member 2 （TRPV2） in the regeneration of injured axons in vitro. Methods： Primary culuture of dorsal root ganglion （DRG） neu- rons were performed and scraped. Spontaneous electronic activity of neurons was recorded by whole-cell patch clamp. The expression of TRPV2 was examined post neuronal injury by real-time RT-PCR and immunocytochemistry. Effects of can- nabidiol, the agonist of TRPV2 and siRNA of TRPV2 on the regeneration of axons were observed by immunocytochemis- try. Results： Neuron injury resulted in an increase of spontaneous firing. The expression of TRP^2 increased quickly af- ter injury and mainly distributed in of neurites. 10 Ixmol/L cannabidiol significantly promoted the survival and neurite growth of injured neurons. Furthermore, silencing the expression of TRPV2 significantly inhibited the growth of neurites. Conclusion： Expresson of TRPV2 was upregulated due to neuronal injury, which played an important role in the regener- ation of axons in vitro.

关 键 词：TRPV2 轴突损伤 再生 细胞培养 小鼠 

分 类 号：R651.2[医药卫生—外科学]