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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
文献类型：期刊论文
| 作者 | Lin, SF; Yu, XL; Wang, B; Zhang, YJ; Sun, YG; Liu, XJ |
| 刊名 | NEUROREPORT
 |
| 出版日期 | 2016 |
| 卷号 | 27期号:10页码:737-743 |
| 关键词 | GATED CALCIUM-CHANNELS DIABETIC-NEUROPATHY SENSORY NEURONS TRK EXPRESSION DRG NEURONS IGF-I TRPV1 SENSITIZATION INHIBITION VITRO |
| 通讯作者 | Liu, XJ (reprint author), Xuzhou Med Univ, Dept Anesthesiol, D439,209 Tongshan Rd, Xuzhou 221004, Jiangsu, Peoples R China.,edvin201@163.com |
| 英文摘要 | 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. |
| WOS标题词 | Neurosciences & Neurology |
| 学科主题 | Neurosciences |
| 语种 | 英语 |
| WOS记录号 | WOS:000379445800004 |
| 源URL | [http://ir.sibs.ac.cn/handle/331001/4013]  |
| 专题 | 上海神经科学研究所_神经所(总) |
| 推荐引用方式 GB/T 7714 | Lin, SF,Yu, XL,Wang, B,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. |
| APA | Lin, SF,Yu, XL,Wang, B,Zhang, YJ,Sun, YG,&Liu, XJ.(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),737-743. |
| MLA | Lin, SF,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. |
入库方式： OAI收割
来源：上海神经科学研究所
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