Up-Regulation of Akt and Nav1.8 in BmK I-Induced Pain  

作　　者：Guokun Zhou Yunlu Jiao You Zhou Shichao Qin Jie Tao Feng Jiang Zhi-Yong Tan Yong-Hua Ji 

机构地区：[1]Lab of Neuropharmacology and Neurotoxicology, Shanghai University, Shanghai 200444, China [2]Xinhua Translational Institute for Cancer Pain, Shanghai 202150, China [3]Department of Pharmacology and Toxicology and Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA

出　　处：《Neuroscience Bulletin》2018年第3期539-542,共4页神经科学通报（英文版）

基　　金：supported by grants from the National Natural Science Foundation of China (31571032, 31771191, and 81402903);supported by an Indiana Spinal Cord and Brain Injury Research Fund grant (ISCBIRF2017)

摘　　要：Dear Editor,As the key contributor to the rising phase of action potentials in dorsal root ganglion（DRG）neurons,voltagegated sodium channels（VGSCs）are important in physiological and pathological pain conditions.For instance,abnormal expression of VGSCs in DRG neurons is theDear Editor,As the key contributor to the rising phase of action potentials in dorsal root ganglion（DRG）neurons,voltagegated sodium channels（VGSCs）are important in physiological and pathological pain conditions.For instance,abnormal expression of VGSCs in DRG neurons is the

关 键 词：Akt In Up-Regulation of Akt and Nav1.8 in BmK I-Induced Pain 

分 类 号：R402[医药卫生—临床医学]