Although an increase in the excitability and ectopic spontaneous discharge (ESD) of primary sensory neurons can lead to abnormal burst activity, which is associated with neuropathic pain, the underlying molecular mechanisms are not fully understood. To investigate the relationship between these electrical abnormalities in injured neurons and voltage-gated calcium channel (VGCC) gene expression, reverse transcription-polymerase chain reaction (RT-PCR) was used to monitor the expression of the VGCC alpha(1) gene in the dorsal root ganglion (DRG) following chronic constriction injury (CCI) and axotomy of the rat sciatic nerve. Electrophoresis of the RT-PCR products showed the presence of multiple types of VGCC alpha(1) transcripts with various levels of basal expression in lumbar 4, 5, and 6 DRGs. CCI decreased alpha(1C), alpha(1D), alpha(1H), and alpha(1I) mRNA expression at 7 days in the ipsilateral DRG, to approximately 34-50% of the contralateral side. The same transcripts were repressed 7 days after sciatic axotomy and their reduction levels proved similar to those of CCI. Considering that changes of the intracellular calcium concentration modify the maintenance of ESD in injured DRG, these results suggest that the downregulation of alpha(1C), alpha(1D), alpha(1H) and alpha(1I) subunit gene expression in the rat DRG following peripheral nerve injury may contribute to the production of ESD associated with damaged nerves.