Expression of the sodium channel transcripts Nav1.8 and Nav1.9 in injured dorsal root ganglion neurons of interferon-γ or interferon-γ receptor deficient mice

被引：3

作者：

Eriksson, J

Fried, K

机构：

[1] Karolinska Inst, Ctr Oral Biol, Novum, S-14104 Huddinge, Sweden

[2] Karolinska Inst, Dept Neurosci, S-17177 Stockholm, Sweden

来源：

NEUROSCIENCE LETTERS | 2003年 / 338卷 / 03期

关键词：

sodium channel; Na(v)1.8; Na(v)1.9; interferon-gamma; nerve injury; dorsal root ganglion; in situ hybridization; pain;

D O I：

10.1016/S0304-3940(02)01407-6

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Changes in the dorsal root ganglion (DRG) expression of the sodium channels Na(v)1.8 and Na(v)1.9 may contribute to injury-induced hyperexcitability and pain. Interferon (IFN)-gamma receptor - /- mice display a reduced pain-related behavior after nerve injury as compared to wild-type mice (NeuroReport 8 (1997) 1311). To elucidate a possible role for IFN-gamma in the regulation of sodium channels, we have studied the DRG mRNA expression of Na(v)1.8/Na(v)1.9 in IFN-gamma or IFN-gamma receptor-deficient mice. In both types of mice, nerve damage induced a downregulation of Na(v)1.8 as well as Na(v)1.9. The magnitude of this reduction was similar to that observed in wild-type animals. These results indicate that the downregulation of Na(v)1.8/Na(v)1.9 in damaged DRG neurons is not influenced by IFN-gamma. Thus, the reduced pain-related behavior of nerve-injured IFN-gamma receptor null mice is not due to differential changes in the regulation of Na(v)1.8/Na(v)1.9 mRNA. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：242 / 246

页数：5

共 20 条

[1] The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways [J].