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Increased Expression of Sodium Channel Subunit Nav1.1 in the Injured Dorsal Root Ganglion After Peripheral Nerve Injury
Author(s) -
Wang Wei,
Atianjoh Fidelis,
Gauda Estelle B.,
Yaster Myron,
Li Yunqing,
Tao YuanXiang
Publication year - 2011
Publication title -
the anatomical record: advances in integrative anatomy and evolutionary biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.21437
Subject(s) - dorsal root ganglion , medicine , neuropathic pain , peripheral nerve injury , axotomy , sodium channel , nerve injury , sciatic nerve , lumbar , atf3 , ligation , anesthesia , immunohistochemistry , sciatic nerve injury , anatomy , dorsum , sodium , central nervous system , chemistry , gene expression , biochemistry , promoter , organic chemistry , gene
The mechanisms underlying neuropathic pain induction are very complex but might involve abnormal spontaneous activity in the sensory dorsal root ganglion (DRG). Voltage‐gated sodium channels in the DRG are essential for the genesis of abnormal spontaneous neuronal activity. In this study, we examined the changes in expression of the voltage‐gated sodium channel Nav1.1 in the DRG after peripheral nerve injury. Western blot analysis showed that the level of Nav1.1 protein in the ipsilateral L5 DRG was significantly increased on Days 3 and 7 after fifth lumbar spinal nerve ligation. Immunohistochemical study further confirmed a marked increase in the percentage of Nav1.1‐positive cells in the ipsilateral DRG on Day 3 after fifth lumbar spinal nerve ligation. Similarly, on Day 7 after sciatic nerve axotomy, the amount of Nav1.1 protein and the percentage of Nav1.1‐positive cells in the ipsilateral L5 DRG were also significantly increased. Our results suggest that an early increase in DRG Nav1.1 expression after peripheral nerve injury might be involved in the induction of neuropathic pain. Anat Rec, 2011. © 2011 Wiley‐Liss, Inc.