Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2015, Article ID 265056, 11 pages
http://dx.doi.org/10.1155/2015/265056
Research Article

Sigma-1 Receptor Antagonist BD1047 Reduces Mechanical Allodynia in a Rat Model of Bone Cancer Pain through the Inhibition of Spinal NR1 Phosphorylation and Microglia Activation

1Department of Anesthesiology, Xuzhou Cancer Hospital, Affiliated Xuzhou Hospital, Jiangsu University, Xuzhou 221005, China
2Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical College, Xuzhou 221002, China
3Jiangsu Province Key Laboratory of Anesthesia and Analgesia Application Technology, Xuzhou 221002, China
4Department of Anesthesiology, Xuzhou Children’s Hospital, Xuzhou 221006, China
5Department of Anesthesiology, Affiliated Hospital, Xuzhou Medical College, Xuzhou 221006, China
6Department of Oncology, Affiliated Hospital, Xuzhou Medical College, Xuzhou 221006, China
7Department of Pain, Affiliated Hospital, Xuzhou Medical College, Xuzhou 221006, China
8Department of Anesthesiology, Xuzhou Maternity and Child Health Hospital, Xuzhou 221009, China

Received 23 July 2015; Accepted 5 November 2015

Academic Editor: Robert LaMotte

Copyright © 2015 Shanshan Zhu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Previous studies have demonstrated that sigma-1 receptor plays important roles in the induction phase of rodent neuropathic pain; however, whether it is involved in bone cancer pain (BCP) and the underlying mechanisms remain elusive. The aim of this study was to examine the potential role of the spinal sigma-1 receptor in the development of bone cancer pain. Walker 256 mammary gland carcinoma cells were implanted into the intramedullary space of the right tibia of Sprague-Dawley rats to induce ongoing bone cancer-related pain behaviors; our findings indicated that, on days 7, 10, 14, and 21 after operation, the expression of sigma-1 receptor in the spinal cord was higher in BCP rats compared to the sham rats. Furthermore, intrathecal injection of 120 nmol of sigma-1 receptor antagonist BD1047 on days 5, 6, and 7 after operation attenuated mechanical allodynia as well as the associated induction of c-Fos and activation of microglial cells, NR1, and the subsequent Ca2+-dependent signals of BCP rats. These results suggest that sigma-1 receptor is involved in the development of bone cancer pain and that targeting sigma-1 receptor may be a new strategy for the treatment of bone cancer pain.