单位：[1]Department of Anesthesiology, China-Japan Friendship Hospital, Beijing,[2]Jiangsu Province Key Laboratory of Anesthesiology, School of Anesthesiology, Xuzhou Medical University, Xuzhou, Jiangsu[3]Institute of Neuroscience, State Key Laboratory of Neuroscience, CAS Center for Excellence in Brain Science & Intelligence Technology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China
Insulin-like growth factor-1 (IGF-1) is a neurotrophic factor and plays important roles in the nervous system. Increasing evidence supports that IGF-1 contributes to pain hypersensitivity through its insulin-like growth factor-1 receptor (IGF-1R) by activating IGF-1R/Akt or MAPK signaling pathways, whereas T-type Ca(v)3.2 channel can facilitate and amplify pain signals originating from the sensory periphery. A recent study showed that activated IGF-1R can increase T-type Ca(v)3.2 channel currents and further activate the G protein-dependent PKC alpha pathway to contribute to inflammatory pain sensitivity. However, the colocalization of IGF-1R and Ca(v)3.2 in mouse dorsal root ganglion (DRG) under chronic inflammatory pain conditions remains elusive. In this study, we investigated changes in the expression of IGF-1R and the Ca(v)3.2 channel, and their colocalization in mouse DRGs in chronic inflammatory pain condition (induced by complete Freund's adjuvant intraplanter injection) using real-time RT-PCR and immunohistochemistry approaches to confirm that Ca(v)3.2 channel can mediate pain facilitation following IGF-1/IGF-1R signaling. We found that IGF-1R was expressed extensively in DRG neurons including small-, medium-, and large-sized neurons, whereas Ca(v)3.2 channel was expressed exclusively in small-sized DRG neurons of naive mice. Expression of Ca(v)3.2, but not IGF-1R, and colocalization of Ca(v)3.2 and IGF-1R were increased in lumbar (L)4-L6 primary sensory neurons in DRGs of mice in chronic inflammatory pain. Moreover, the increased colocalization of IGF-1R and Ca(v)3.2 is exclusively localized in small-and medium-sized primary sensory neurons. Our findings provided morphological evidence that T-type Ca(v)3.2 channel, at least partially, mediates the pain facilitation of IGF-1/IGF-1R signaling in chronic inflammatory pain condition. Copyright (C) 2016 Wolters Kluwer Health, Inc. All rights reserved.
基金：
research projects of the hospital of China-Japan Friendship Hospital [2015-1-QN-18]; National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [31371122, 81322015, 30870832]; Strategic Priority Research Program of the Chinese Academy of SciencesChinese Academy of Sciences [XDB02010000]
第一作者单位：[1]Department of Anesthesiology, China-Japan Friendship Hospital, Beijing,[2]Jiangsu Province Key Laboratory of Anesthesiology, School of Anesthesiology, Xuzhou Medical University, Xuzhou, Jiangsu
共同第一作者：
通讯作者：
通讯机构：[2]Jiangsu Province Key Laboratory of Anesthesiology, School of Anesthesiology, Xuzhou Medical University, Xuzhou, Jiangsu[*1]Department of Anesthesiology, Xuzhou Medical University, D439, 209 Tongshan Road, Xuzhou, Jiangsu 221004, China
推荐引用方式(GB/T 7714)：
Lin SiFang,Yu XiaoLu,Wang Bing,et al.Colocalization of insulin-like growth factor-1 receptor and T type Ca(v)3.2 channel in dorsal root ganglia in chronic inflammatory pain mouse model[J].NEUROREPORT.2016,27(10):737-743.doi:10.1097/WNR.0000000000000607.
APA：
Lin, SiFang,Yu, XiaoLu,Wang, Bing,Zhang, YaJun,Sun, YanGang&Liu, XingJun.(2016).Colocalization of insulin-like growth factor-1 receptor and T type Ca(v)3.2 channel in dorsal root ganglia in chronic inflammatory pain mouse model.NEUROREPORT,27,(10)
MLA：
Lin, SiFang,et al."Colocalization of insulin-like growth factor-1 receptor and T type Ca(v)3.2 channel in dorsal root ganglia in chronic inflammatory pain mouse model".NEUROREPORT 27..10(2016):737-743
