Multiple voltage-gated sodium channels are the primary mediators of cell excitability. They are multimers that consist of the pore-forming α subunit and auxiliary β subunits. Although ion permeability and voltage sensing are primarily determined by the α subunit, β subunits are important modulators of sodium channel function. The purpose of this study was to assess the effect of axotomy on the expression of β subunits (β 1 , β 2 and β 3 ) and coexpression of Na v 1.3 and β 3 subunits in the dorsal root ganglion (DRG). We used sciatic nerve transection models or spared nerve injury (SNI) models in the rat. In reverse transcriptase-polymerase chain reaction analysis, there were no significant differences between contralateral and ipsilateral DRGs of β 1 and β 2 mRNA 3 days after axotomy. β 3 mRNA expression in ipsilateral DRGs increased significantly compared with contralateral DRGs 3 days after axotomy. In in situ hybridization histochemistry, β 1 mRNA was predominantly expressed in medium- to large-size neurons, whereas β 2 mRNA was expressed in small- to large-size neurons. There were no significant differences in β 1 and β 2 mRNA between contralateral and ipsilateral DRGs 3 days after axotomy. In contrast, β 3 mRNA was mainly expressed in small neurons and occasionally in medium- to large-size neurons, and β 3 mRNA expression in small c-type neurons in ipsilateral DRGs was increased significantly compared with contralateral DRGs. We examined β 3 mRNA expression with one of α subunits, Na v 1.3-ir, in DRG neurons after axotomy using the double labeling method. We found a high percentage of coexpression in injured DRG neurons: 83.6+/-2.8% of neurons expressing β 3 mRNA were labeled for Na v 1.3-ir; 70.1+/-3.1% of Na v 1.3-ir neurons expressed β 3 mRNA. We also examined the expression of β 3 mRNA in DRG neurons in the SNI model, a neuropathic pain model. We used activating transcription factor 3 to identify axotomized neurons, and found that β 3 mRNA up-regulation occurred mainly in axotomized neurons in the neuropathic pain model. These data strongly suggest that β 3 expression in injured DRG neurons following axotomy might be an important pathomechanism of post-nerve injury pain in primary sensory neurons.