Increase of Sodium Channels (Nav 1.8 and Nav 1.9) in Rat Dorsal Root Ganglion Neurons Exposed to Autologous Nucleus Pulposus
Kazuyuki Watanabe1, 2, Karin Larsson1, Björn Rydevik1, Shin-ichi Konno2, Claes Nordborg3, Kjell Olmarker*, 4
Identifiers and Pagination:Year: 2014
First Page: 69
Last Page: 73
Publisher Id: TOORTHJ-8-69
Article History:Received Date: 5/2/2014
Revision Received Date: 12/3/2014
Acceptance Date: 29/3/2014
Electronic publication date: 4/4/2014
Collection year: 2014
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/) which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.
It has been assumed that nucleus pulposus-induced activation of the dorsal root ganglion (DRG) may be related to an activation of sodium channels in the DRG neurons. In this study we assessed the expression of Nav 1.8 and Nav 1.9 following disc puncture.
Thirty female Sprague-Dawley rats were used. The L4/L5 disc was punctured by a needle (n=12) and compared to a sham group without disc puncture (n=12) and a naive group (n=6). At day 1 and 7, sections of the left L4 DRG were immunostained with anti-Nav 1.8 and Nav 1.9 antibodies.
At day 1 after surgery, both Nav 1.8-IR neurons and Nav 1.9-IR neurons were significantly increased in the disc puncture group compared to the sham and naive groups (p<0.05), but not at day 7.
The findings in the present study demonstrate a neuronal mechanism that may be of importance in the pathophysiology of sciatic pain in disc herniation.