Expression of the sodium channel transcripts Na(v)1.8 and Na(v)1.9 in injured dorsal root ganglion neurons of interferon-gamma or interferon-gamma receptor deficient mice.
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.
Eriksson
Jonas
J
Center for Oral Biology, Novum, Karolinska Institutet, PO Box 4064, S-141 04, Huddinge, Sweden.
Fried
Kaj
K
D000818:Animals; D019771:Axotomy; D015536:Down-Regulation; D005727:Ganglia, Spinal / Q000293:injuries / Q000378:metabolism*; D017403:In Situ Hybridization; D051379:Mice; D018345:Mice, Knockout; D062558:NAV1.9 Voltage-Gated Sodium Channel; D009474:Neurons / Q000378:metabolism*; D009479:Neuropeptides / Q000096:biosynthesis*; D012333:RNA, Messenger / Q000032:analysis; D017471:Receptors, Interferon / Q000172:deficiency* / Q000378:metabolism*; D012584:Sciatic Nerve / Q000502:physiology; D015222:Sodium Channels / Q000096:biosynthesis*; D000096743:Interferon gamma Receptor
D062558:NAV1.9 Voltage-Gated Sodium Channel; D009479:Neuropeptides; D012333:RNA, Messenger; D017471:Receptors, Interferon; D015222:Sodium Channels; D000096743:Interferon gamma Receptor; C491885:Scn11a protein, mouse