期刊
EUROPEAN JOURNAL OF PAIN
卷 13, 期 4, 页码 380-386出版社
WILEY
DOI: 10.1016/j.ejpain.2008.05.008
关键词
Inflammatory pain; Opiates; Endomorphin-2; Gene therapy; Herpes simplex virus
资金
- NIDA NIH HHS [R03 DA020078-01, R03 DA020078] Funding Source: Medline
- NIDDK NIH HHS [P01 DK044935, P01 DK044935-130001] Funding Source: Medline
- NINDS NIH HHS [R01 NS038850-08A2, R01 NS038850, R01 NS066792] Funding Source: Medline
We examined the analgesic properties of endomorphin-2 expressed in DRG neurons transduced with a non-replicating herpes simplex virus (HSV)-based vector containing a synthetic endomorphin-2 gene construct. HSV-mediated endomorphin-2 expression reduced nocisponsive behaviors in response to mechanical and thermal stimuli after injection of complete Freund's adjuvant (CFA) into the paw, and reduced peripheral inflammation measured by paw swelling after injection of CFA. The analgesic effect of the vector was blocked by either intraperitoneal or intrathecal administration of naloxone methiodide, blocking peripheral and central p opioid receptors, respectively. Endomorphin-2 vector injection also reduced spontaneous pain-related behaviors in the delayed phase of the formalin test and in both CFA and formalin models suppressed spinal c-fos expression. The magnitude of the vector-mediated analgesic effect on the delayed phase of the formalin test was similar in naive animals and in animals with opiate tolerance induced by twice daily treatment with morphine, suggesting that there was no cross-tolerance between vector-mediated endomorphin-2 and morphine. These results suggest that transgene-mediated expression of endomorphin-2 in transduced DRG neurons in vivo acts both peripherally and centrally through mu opioid receptors to reduce pain perception. (c) 2005 European Federation of Chapters of the International Association for the Study of Pain. Published by Elsevier Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据